Alzheimer's, ADHD, Parkinson’s and other Neurodegenerative disorders

Paul L. Reller L.Ac. / Last Updated: August 03, 2017

Sections

Information Resources and Additional Information with Links to Scientific Studies

  1. A 2014 population-based retrospective study at the Seoul National University College of Medicine, in Seoul, South Korea, found that lower serum thyroid stimulating hormone (TSH), produced by the hypothalamus/pituitary in the brain, was independently associated with the risk of mild cognitive impairment (MCI), an early stage of Alzheimer's disease. These levels indicated a subclinical hyperthyroid syndrome (normal thyroid hormones but lowered TSH), largely ignored in standard medicine, with almost no effective treatment options, and associated with a wide range of potential causes, including deficient hypothalamic function, adrenal stress syndrome, improper dosage of synthetic thyroid hormone in treating hypothyroid conditions, chronic iodine deficiency, side effects of medications affecting glucocorticoids such as dopamine and norepinephrine (adrenaline), and chronic euthyroid conditions with neurohormonal dysfunction: http://www.ncbi.nlm.nih.gov/pubmed/24285689
  2. A 2015 population-based retrospective study at the Seoul National University College of Medicine, in Seoul, South Korea, found that the hormone Vitamin D deficiency was independently associated with mild cognitive impairment (MCI), an early stage of Alzheimer's disease, in the aging population. Such study links broader chronic hormone imbalance of a subclinical nature to neurodegeneration: http://www.ncbi.nlm.nih.gov/pubmed/25641087
  3. A 2014 study at Instanbul University, in Istanbul, Turkey, found that the association between the hormone Vitamin D deficiency and Alzheimer's disease involves more than just a dietary deficiency, but a broader chronic dysfunction in the hormone Vitamin D metabolism: http://www.ncbi.nlm.nih.gov/pubmed/24413618
  4. A 2013 study at the Karolinska Institute and Stockholm University, in Sweden, and the University of Perugia, in Italy, found that relatively higher levels of tocopherols (Vitamin E molecules) in relation to lower levels of cholesterol was associated with reduced risk of mild cognitive impairment (MCI), an early stage of Alzheimer's disease. Alpha-tocopherol has been shown to be one of the few proven preventive measures for future Alzheimer's disease: http://www.ncbi.nlm.nih.gov/pubmed/24113154
  5. A 2015 muticenter study of the pathogenesis of Alzheimer's disease, by experts at the University of Bonn, Massachusetts General Hospital, the University of Illinois, Stanford University School of Medicine, the David Geffen School of Medicine at UCLA, Duke University School of Medicine, and other institutions, noted that "increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain." A broader and more holistic approach in Neurohormonal Immunology is needed to really prevent the widespread incidence of progression to true neurodegenerative dementia in the younger population: http://www.ncbi.nlm.nih.gov/pubmed/25792098
  6. A 2008 study at the University of British Columbia, in Canada found a clear association between low grade bacterial and spirochete infections and expression of the amyloid beta proteins that form the classic plaques in the brain associated with Alzheimer's disease and other neurodegnerative disorders:http://www.ncbi.nlm.nih.gov/pubmed/18487847
  7. A 2014 review of studies of the pathogenesis of Alzheimer's disease at the King Abdulazziz University School of Medicine in Saudi Arabia found that low-grade infections with bacteria and spirochetes have been linked to excess production of amyloid beta proteins in plaques and hyperphophorylation of Tau proteins, the key factors in the pathologies of a number of neurodegeneratve disrorders: http://www.ncbi.nlm.nih.gov/pubmed/25230225
  8. A 2016 study at the Harvard University School of Medicine and Massachusetts General Hospital found that in the human and animal immune system that amyloid beta proteins serve to encapsulate bacteria in low-grade infections to protect the host and allow the normal immune cytokines to destroy them. This could be the key finding in explaining the accumulation of amyloid beta plaques over long periods of time, indicating a deficiency in both the immune responses and clearing of these amyloid beta: http://www.ncbi.nlm.nih.gov/pubmed/27225182
  9. A 2007 study at the National Institutes of Pediatrics, in Mexico
    City, Mexico, showed that exposure to high levels of fine particulate matter (PM) in Mexico City, one of the most polluted cities in the world for some time, leads to disruption of immune protection in respiratory membranes, systemic inflammation, dramatic upregulation of inflammatory mediators such as COX2, IL-1beta, and increased formation of amyloid beta plaques in the brain. This is a direct link between rising rates of Alzhemimer's disease and air pollution: http://www.ncbi.nlm.nih.gov/pu...http://www.ncbi.nlm.nih.gov/pubmed/17325984
  10. A 2016 controlled study by experts at the Boise State University School of Medicine, in Idaho, U.S.A. outlines the strong pathophysiological connection between air pollutants, especially fine particulate matter, and dramatically increased risk of Alzheimer's disease, a slowly developing pathology. Brain matter in laboratory animals was analyzed, and compared to healthy controls, the exposure to fine particulate matter and air pollution caused poor vascular health, a breakdown of protective barriers in the brain, and increased amyloid beta plaque in response. Damage to neurovascular health points to a number of strategies with CIM/TCM that could be used to prevent or correct this pathology: http://scholarworks.boisestate...http://scholarworks.boisestate.edu/math_facpubs/173/
  11. A 2009 study at the Whitehead Institute for Biomedical Research at Cambridge, Massachusetts, U.S.A. showed that beta-amyloid accumulation was not the cause of Alzheimer's disease, but instead a protective response to toxins in brain tissues: http://www.ncbi.nlm.nih.gov/pu...http://www.ncbi.nlm.nih.gov/pubmed/19411847
  12. The causes of Parkinsonism, or neurodegeneration of the dopaminergic neurons and support cells in the midbrain, especially the substantia nigra, a small area of the brain the is rich in dopamine and melanin, and contains a high iron content, are still unclear. This 2005 article by Buck Institute for Aging, Novato, California, U.S.A., outlines what was known of the basic pathophysiology: http://www.ncbi.nlm.nih.gov/pubmed/15743669
  13. Environmental neurotoxins are now a primary cause of concern concerning the multifaceted origins of neurodegenerative disorders. This report from researchers at the Worcester Polytechnic Institute in Massachusetts, U.S.A., from 2009, outlines some of the concerns at that time. Note that at the end of this article, which focused on lead, mercury, PCBs, and organochlorines, it is noted that iodine deficiency is one of the most noted widespread causes of neurodegeneration: http://www.wpi.edu/Pubs/E-project/Available/E-project-042808-121944/unrestricted/Neurotoxic_Chemicals_in_the_Environment.pdf
  14. Such seemingly harmless chemicals as fluoride, a halogen competitor to iodide, and iodine, is focus of much study regarding neurotoxicity in the environment, and proof of this problem finally resulted in new U.S. federal guidelines for fluoride levels, which have risen in recent decades in drinking water due to the profitable sale of industrial fluorides to local water agencies: http://ehp.niehs.nih.gov/1104912/
  15. A review of theories and approaches to Parkinson's treatment from the National Institute of Neurological Disorders and Stroke: http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease_backgrounder.htm
  16. An August 18, 2010 article in the New York Times outlines the current failures and reasons for failure in new drugs developed to treat Alzheimer's: http://www.nytimes.com/2010/08/19/health/19alzheimers.html
  17. An August 29, 2010 article in the New York Times outlines the findings of the recent NIH panel on risks, prevention and treatment of Alzheimer's, finding that there is no pharmaceutical treatment that is effective in prevention or treatment, and no single health measure that is proven to prevent neurodegenerative disease on its own: http://www.nytimes.com/2010/08/29/health/research/29prevent.html
  18. A multicenter study, with contributions from 26 University Medical School and other healthcare systems in the United States, released in January of 2014, and published in the Journal of the American Medical Association (JAMA), concluded that 2000 IU of d-alpha tocopherol Vitamin E was shown to significantly slow the progression of Alzheimer's disease in mild to moderate stages, while one of the widely prescribed drugs, memantine (Axura, Akatinol, Namenda, Ebixa, Abixa, Memox), an NMDA glutamine receptor inhibitor, had no effect. Foods containing tocopherol include sunflower seeds, whole wheat, asparagus, sweet potato, flax seed, whole buckwheat, bell pepper, cayenne pepper, lentil, banana, cashew, and nopal cactus, indicating the importance of a plant-based whole grain, and varied diet: http://jama.jamanetwork.com/article.aspx?articleid=1810379
  19. A study in 2007 at Texas Christian University found that a combination of factors was responsible for the dopamine depletion and neurological impairment of Parkinsonism, and that research was lacking that explored multiple factors of causation acting synergistically. Here, systemic bacterial endotoxicity producing low-grade inflammatory responses, when combined with a neurotoxin (MPTP), reproduced the dopamine depletion and neurological impairments of Parkinsons, while each individual factor did not: http://gradworks.umi.com/32/75/3275084.html
  20. A study in 2007 at Tohoku University in Japan explored the role of liver dysfunction and Metabolic Syndrome in the pathology of Alzheimer's disease. Poor clearance of amyloid beta peptide may contribute to excess amyloid beta accumulation in the brain and deficient LRP (low density lipoprotein receptor protein), which is induced by excess insulin that occurs with insulin resistance and Metabolic Syndrome: http://www.ncbi.nlm.nih.gov/pubmed/17609417
  21. A 2009 article by Zina Kroner, DO, medical director of Advanced Medicine of New York, outlines the findings of a succession of research studies demonstrating how insulin metabolism dysfunction and advanced glycation endproducts lead to the progression of Alzheimer's disease and other neurodegenerative states: http://acam.typepad.com/blog/2010/04/the-relationship-between-alzheimers-disease-and-diabetes-type-3-diabetes-.html
  22. A 2004 review of all scientific studies concerning the potential for the Major Histocompatibility Complex (MHC) to be involved in a genetic explanation for Alzheimer's disease, by experts at the University of Palermo, in Italy, found that many studies confirm links to this important part of our genetic code that is responsible for autoimmune regulation and much of the complement system of the adaptive immune system, but that subsequent studies often fail to duplicate these results. The problem, according to these experts, is that a complex combination of genetic alleles (as well as the epigenetic regulation of gene expression) may be responsible for genetic susceptibiltiy, and that a more holistic, or quantum, research protocol will have to be used: http://www.ncbi.nlm.nih.gov/pubmed/15050301
  23. By 2010, not only the whole human genome, including "junk DNA", and the epigenome, but also the 'second genome', or mitochondrial DNA, which is more variable, but still in each human cell, was shown to be linked to Alzheimer's disease. This research, at the University of California Irvine, reveals that indeed there is no simple promise of a single genetic pathway that needs to be corrected to treat the disease, and that the ongoing promise of such a miracle cure is false: http://www.ncbi.nlm.nih.gov/pubmed/20538375
  24. A 2013 review of all published scientific study of the risk of acquiring Parkinson's Disease from exposure to pesticides, herbicides and solvents, by 2 institues in Italy, including the Parkinson Institute and Foundation IRCCS Polyclinic of San Matteo, found that all current pesticides, as well as most herbicides and industrial solvents do increase risk of Parkinsonism, but that the common herbicide Paraquat doubled the risk of acquiring this neurodegenerative disease: http://www.ncbi.nlm.nih.gov/pubmed/23713084
  25. A 2010 review of the scientific study of acupuncture and its effects on the brain by Harvard Medical School reveals that correct stimulation and sensation from needle stimulation is proven to significantly effect the brain with an integrated response at multiple levels, especially with evoking deactivation of a hyperreactive limbic to cortical response, as well as activation of key somatosensory areas in the brain. The researchers found that acupuncture mobilizes the functionally anti-correlated networks of the brain to correct such disease states as Alzheimer's, depression, schizophrenia, autism, and chronic pain syndromes: http://www.ncbi.nlm.nih.gov/pubmed/20494627
  26. A 2005 study of acupuncture with functional MRI imaging proved that different acupuncture points activated specific areas of the brain. The intelligent choice of acupuncture points, individualized to the patient, as well as the correct stimulation techniques, also individualized and performed with proper patient feedback during therapy, is proven to be very important to treatment outcomes: http://www.ncbi.nlm.nih.gov/pubmed/15876491
  27. A 2015 study at the Beijing Key Laboratory for Parkinson's Disease, at Capital Medical University, and the Beijing Institute for Brain Disorders, in Beijing, China, showed that electroacupuncture possesses the ability to ameliorate mutant alpha synuclein-induced motor abnormalities and enhance both anti-inflammatory and antioxidant activities in laboratory animals with induced Parknson's neurodegeneration, and also suppress aberrant glial support cell activities in diseases areas of the brain: http://www.ncbi.nlm.nih.gov/pubmed/26016857
  28. A 2015 study at Fujian University of Traditional Chinese Medicine, in Fuzhou, China, found that electroacupuncture stimulation improved memory impairment of laboratory animals with induced Alzheimer's disease, and reduced excess production of amyloid beta proteins and BACE1 proteins in the hippocampus: http://www.ncbi.nlm.nih.gov/pubmed/26283960
  29. A 2014 randomized controlled study in China found that electroacupuncture stimulation at just 4 points, DU20, DU14, ST36 and UN17, daily for just 15 days, significantly improved brain function, memory, and lowered hippocampal excess of norepinephrine, dopamine and serotonin (5-HT) in laboratory animals with induced vascular dementia. Such effects could have profound benefit in a holistic treatment protocol for Alzheimer's disease: http://www.ncbi.nlm.nih.gov/pubmed/24818499
  30. A 2010 study at the Capital Medical University of Beijing, China, of specific electroacupuncture effects on laboratory animals with Parkinsons disease found that 100 Hz stimulation at specific points normalized the GABA content in specific parts of the brain associated with poor motor control, while not affecting other parts of the brain, exerting GABAergic inhibition in the output nuclei of the basal ganglia: http://www.ncbi.nlm.nih.gov/pubmed/20364891
  31. A 2009 study at the Capital Medical University of Beijing, China, of specific electroacupuncture effects on laboratory animals with Parkinsons disease found that 100 Hz stimulation at specific points protected dopaminergic neurons from degeneration in the substantia nigra, and reversed excess substance P and deficient glutamate decarboxylase in the midbrain, showing modulatory affects to restore motor function in Parkinsons disease: http://www.ncbi.nlm.nih.gov/pubmed/19549545
  32. A 2014 study at the Capital Medical University of Beijing, China, and the Key Laboratory fo Neurodegenerative Disease, with the General Hospital of the Chinese People's Armed Police Forces, showed that a simple acupuncture treatment at just 2 common points, LI4 and LV3, produced a significantly increased functional connectivity in key areas of the hippocampus associated with Alzheimers's disease. The effects were measured before, during and 10 minutes after stimulation, with functional MRI (fMRI), with the pre-stimulation resting state compared to the post acupuncture state, and compared to healthy controls: http://www.ncbi.nlm.nih.gov/pubmed/24603951
  33. A 2013 study at Zhejiang Chinese Medical University, Hangzhou, China, found that electroacupuncture at 2 hertz and 1 milliamp at the points DU16 and LV3 for 20 minutes daily for 14 days decreased the inflammatory cytokine COX-2 expression and upregulated T helper cell expression in the Substantia Nigra of laboratory animals with induced Parkinson's disease: http://www.ncbi.nlm.nih.gov/pubmed/24006664
  34. A 2013 study at Shaanxi University, in Xi'an, China, found that a combination of acupuncture (Xiu 3 needle technique) and eugenol (found in the herbs Xin yi hua, or Magnolia flower, Qu mai, and Ding xiang, or clove), decreased malondialdehyde toxicity of the hippocampus, increased super oxide dismutase and glutathione detoxification, and increased learning and memory function in laboratory animals with induced Alzheimer's disease. The combination of the acupuncture with herbal chemicals was proven to be more effective than either treatment protocol alone: http://www.ncbi.nlm.nih.gov/pubmed/24024340
  35. A 2016 study at the Tianjin University of TCM and the Nankai University College of Medicine, in China, showed that a key active chemical in the herb Trypterygium wilfordii, or Lei gong teng, called triptolide, protected brain cells against cytotoxicity of excess amyloid beta plaque accumulation in the brain, a key factory in the pathology of Alzheimer's disease, decreasing oxidative stress and inhibition cell death, or apoptosis of PC12 cells: http://www.ncbi.nlm.nih.gov/pubmed/26679104
  36. A 2012 meta-review of published scientific study of acupuncture and electroacupuncture to treat Alzheimer's disease, by Shanghai University of Chinese Medicine, Shanghai, China, showed that numerous studies have explored the many treatment goals with acupuncture, with 7 sets of beneficial treatment effects studied, affecting neurotransmitter modulation, cell apoptosis (programmed cell death), inflammatory mediation, neural growth factors genetically expressed, effects on beta-amyloid and other proteins, and immune modulation, as well as more general neuroprotective effects. So far, these studies are hampered by limited funding and difficulty in designing specific study measurements, as well as the complicated pathological mechanisms involved in the disease, but such a review shows that many scientists consider acupuncture and electroacupuncture treatments very promising in addressing the multifactorial disease: http://www.ncbi.nlm.nih.gov/pubmed/23342786
  37. A 2012 study of acupuncture at LV3 and LI4 and the measurable effects in the brain, studied with functional MRI imaging, at Capital Medical University, Beijing, China, showed that this simple and common treatment protocol activates specific cognitive-related areas of the brain in laboratory subjects with Alzheimer's disease and mild cognitive impairment, such as the frontal and temporal lobes. This is just one of many studies proving that specific acupuncture and electroacupuncture stimulations positively effects specific areas of the brain in a positive manner that are degenerated and dysfunctional in these disorders: http://www.ncbi.nlm.nih.gov/pubmed/22916152
  38. A 2014 study of acupuncture at LV3 and LI4 and the measurable effects in the brain, studied with functional MRI imaging, at Capital Medical University, Beijing, China, showed that this treatment also could increase the connectivity of the hippocampus to benefit Alzheimer's patients. The interaction of the hippocampus with the cortex is integral to successful memory formation and recall, as well as associative function, and degeneration of the hippocampus is associated with Alzheimer's disease: http://www.ncbi.nlm.nih.gov/pubmed/24603951
  39. A 2014 review of scientific studies concerning acupuncture as an adjunct therapy in a holistic protocol to treat Neurodegenerative Disease, at China Medical University, in Taichung, Taiwan, found that a number of studies have demonstrated that electroacupuncture may exert significant effects in mobilization of stem cells and proliferation of progenitor cells in the brain: http://www.ncbi.nlm.nih.gov/pubmed/24636189
  40. A 2013 study at Kyung Hee University, in Seoul, South Korea, found that stimulation at various points associated with neurogenesis, such as DU20 and ST36, instigated various physiological mechanisms for regeneration of brain tissue and function, such as upregulation of brain-derived neurotrophic factor, glial cell line neurotrophic factor, basic fibroblast growth factor, neuropeptide Y, and activation of the vascular system: http://www.ncbi.nlm.nih.gov/pubmed/24215918
  41. The National Institute on Aging (NIA), part of the National Institutes of Health (NIH) maintains an Alzheimer's Disease Education & Referral Center that provides a conservative source of research news and data, as well as referrals to caregivers in your area: http://www.nia.nih.gov/Alzheimers/
  42. An excellent overview of the subject of excitotoxins as food additives in a majority of processed foods, and the research links to neurodegenerative conditions, is available at the website of Dr. Russel Blaylock: http://docs.google.com/viewer?a=v&q=cache:Jg9An6V9RJ4J:landofpuregold.com/
  43. Published research into the neurodegenerative effects of excitotoxins and altered glutamate molecules in food additives has been paltry, given the evidence of its neurotoxicity. This research article from 1996, at Humbolt University in Germany, confirms the seriousness of this problem, though: http://www.ncbi.nlm.nih.gov/pubmed/8971131
  44. A 2014 study at the Benedictine University, in Lisle, Illinois, USA, notes that a number of studies have linked sodium benzoate preservatives with ADHD, and found in a survey of college students that a significant association existed between level of intake of beverages with sodium benzoate preservative and symptoms of ADHD. Strong research has been published showing the causative links between artificial food coloring and benzoate preservatives with ADHD, but subsequent studies were financed to show that no such link exists: http://www.ncbi.nlm.nih.gov/pubmed/22538314
  45. A 2010 study at University College Dublin, Dublin, Ireland, Institute of Food and Health, noted that a previous double-blind randomized study found that 7 common food additives were associated with childhood onset of ADHD, and devised this study to see how many Irish children and teens actually consumed these 7 additives together in the dose used in the study. While most of the study participants consumed foods with at least one of the additives, no food consumed contained the mix of all 7, and 6 of the additives consumed were below the prior study levels for all participants. The one additive associated with ADHD that was consumed at higher levels than the prior study was sodium benzoate preservative: http://www.ncbi.nlm.nih.gov/pubmed/20013441
  46. A 2007 randomized controlled human clinical trial of 153 children, conducted by the University of Southampton, UK, found that artificial colors and sodium benzoate preservatives in the diet resulted in increased hyperactivity in both 3 year olds and 8-9 year old children: http://www.ncbi.nlm.nih.gov/pubmed/17825405
  47. The initial research in 1995 at Humbolt University in Germany, shows that strong and specific explanations existed for the link between ecxitotoxins and gradual neurodegeneration, although the only suggestion for remedy by such research is the development of new drugs that act as glutamate antagonists, which were developed due to the soundness of this research, but proved to be problematic in therapy: http://www.ncbi.nlm.nih.gov/pubmed/8845937
  48. A 2001 review of the class of drugs called glutamate antagonists, by the Neurological Clinic of RWTH Aachen, in Germany, reveals that this class of drugs are widely prescribed in serious neurological disease, but not found to be effective as a neuroprotective agent in chronic neurodegenerative disease, and come with serious side effects, that include agitation, disorientation, and psychosis: http://www.ncbi.nlm.nih.gov/pubmed/11433698
  49. A 2009 mega-analysis of the drug class called glutamate antagonists, found that use of these drugs has fallen with findings of failure to work in clinical studies due to nonselective or competitive antagonism, and serious side effects, such as loss of cognitive function, sedation, and psychomimetic effect. Nevertheless, the subject of glutamate metabolites, and glutamate accumulation in brain tissues, was still taken seriously, and a class of new drugs called NMDA receptor antagonists, and other drugs, were developed and marketed for central nervous system pathology: http://www.ncbi.nlm.nih.gov/pubmed/19538098
  50. A 2008 review of Parkinson's research from Australia reveals how a more holistic approach to understanding the pathophysiology leads us to interrealated neurohormonal imbalance and eventual stimulation of hyperplasia due to improper circadian melatonin levels may be responsible: http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=20083925
  51. A 2013 randomized, placebo-controlled human clinical trial, conducted by the Jikei University School of Medicine, in Tokyo, Japan, of the hormone Vitamin D3 supplementation in the treatment of both mild and advanced Parkinson's disease, found that supplementation may stabilize Parkinson's Disease for short periods even in advanced disease when Fokl TT and CT genotypes, associated with hormone Vitamin D receptor dysfunctions, are found: http://www.ncbi.nlm.nih.gov/pubmed/23485413
  52. A 2012 meta-review of scientific study of CoQ10 supplementation for Parkinson's Disease, by Chinese PLA General Hospital, in Beijing, China, found that measures of Activities of Daily Living (ADL) and functional status showed significant improvement with a 16 month course of supplementation of 1200 mg/day, with only mild elevation of minor risk factors of diarrhea and pharyngitis, in 4 quality randomized, placebo-controlled human clinical trials published: http://www.ncbi.nlm.nih.gov/pubmed/22592726
  53. A 2012 study of antioxidant deficiencies, conducted by Bastyr University Research Institute, a premier Naturopathic Medical School in Seattle, Washington, U.S.A., found that measurable CoQ10 (coenzyme Q10) deficiency was significantly greater in patients with Parkinson's Disease than in healthy control subjects, recorded in 4 separate assessments in randomized studies between 2004 and 2008. Other studied antioxidants, including selenium, lipoic acid, Vitamin E, and glutathione, showed no significantly higher rate of deficiency than the control population. This does not mean that these other antioxidants will be ineffective in the overall treatment protocol, but it does indicate that CoQ10 may be an important supplement for many patients, both as a treatment and as a preventive measure: http://www.ncbi.nlm.nih.gov/pubmed/22542608
  54. A 2011 meta-review of scientific study of disease modification of Parkinson's Disease, by the Keck/USC School of Medicine, Los Angeles, California, U.S.A., found that quality human clinical trials show that CoQ10 was one of only 3 medications proven to slow progression of the disease, along with levadopa and pramipexole: http://www.ncbi.nlm.nih.gov/pubmed/22035026
  55. An excellent report on CoQ10 deficiencies is found on the LifeExtension magazine website: http://www.lef.org/magazine/mag2000/july2000_review.html
  56. A 2013 study at the University of Rochester, Centers for Neurodegenerative and Vascular Brain Disorders, in Rochester, New York, U.S.A. found that problems with copper homeostasis and accumulation in the brain capillaries and parenchyme (neurons and glial cells) is linked to higher accumulation of the protein tangles with amyloid-beta. The exact mechanism of this problem, and how to correct it was not elucidated, though: http://www.ncbi.nlm.nih.gov/pubmed/23959870
  57. A 2008 study at the University of Oregon, Portland, Oregon, U.S.A. found that the copper transporting protein enzyme ATP-ase was essential for various aspects of copper homeostasis as well as CNS function and development, and could be a link between neurodegenerative disorders and altered copper homeostasis: http://www.ncbi.nlm.nih.gov/pubmed/18534184
  58. Research publication on progesterone and pregnenelone therapy in relation to dopamine metabolism in the corpus striatum in Parkinson's: http://lib.bioinfo.pl/pmid:17535560
  59. Research in 2008 at USC Program in Neuroscience revealed the many ways that normal estrogen levels signal CNS pathways to prevent neurodegeneration, suggesting that restoration of estrogen homeostasis may be a key part to restoring mitochondrial function and neurological health; since estrogen mechanisms may have a negative impact on unhealthy degenerated neurons, a cautious approach is recommended with estrogen therapies: http://lib.bioinfo.pl/pmid:17535560
  60. A study by Thomas Jefferson University Medical College in Pennsylvania concerning the efficacy of herbal chemicals as neuroprotective antioxidants, especially reservatrol in Hu Zhang: http://www.ncbi.nlm.nih.gov/pubmed/11897104
  61. A 2013 study at the University Complutense Madrid, Department of Pharmacology, in Spain, showed that a standardized extract of St. John's Wort (Hypericum perforatum) with the Chinese herbal chemical quercetin, is proven to provide the effects needed to reverse or reduce neuron damage in neurodegenerative disease, diminishing substantia nigra cell death (apoptosis): http://www.ncbi.nlm.nih.gov/pubmed/23469842
  62. A 2012 study at the University of Quebec, Department of Biochemistry, Quebec, Canada, found that the herbal chemicals quercetin, a phytoestrogen and antioxidant, and sesamin, a potent plant lignan, not only decreased inflammatory oxidative cell damage in microglial cells of the brain, but also rescued PC12 neurons from early programmed cell death (apoptosis) induced by this inflammatory damage (MPP+), making these herbal chemicals potent, safe, and natural anti-inflammatory chemicals to protect dopaminergic cells in Parkinsonism. The PC12 cell line is used in scientific study to as a model cell to test for problems related to nerve growth factor (NGF). Quercetin is also found in steel cut oats, onions, shallots, green tea, sunflower seeds, cranberries, cabbage, kale, brussel sprouts, and chives, although the effective dose would be small. Sesamin is found in unprocessed sesame oil, and the bark of the herbs in the Xanthoxylum family (Hu jiao, Xiagn jiao zi, Chuan jiao): http://www.ncbi.nlm.nih.gov/pubmed/22919443
  63. A 2012 study of the herbal chemical quercetin on cognitive function in Parkinsonism, conducted by the faculty at Khon Kaen University School of Medicine, in South Korea, found that quercetin enhanced cognitive function in laboratory animals, increased superoxide dismutase activity, and glutathione peroxidase, as well as the activity of acetylcholinesterase: http://www.ncbi.nlm.nih.gov/pubmed/21792372
  64. A 2010 study at Qingdao University, in China, found that an active chemical in the Chinese herb Scutellaria baicalensis (Huang qin) called baicalein, prevented cell degeneration from oxidant stress, acting as an antioxidant, but also improving mitochondrial function and cell membrane function, as well as being a potent anti-inflammatory agent. These experts tested baicalein in PC12 cells, normally seen in kidney cancer and disease, or pheocrhomocytoma, that were cultured in the laboratory. Such herbal chemicals could play an important role in both preventing and treating neurodegeneration: http://www.ncbi.nlm.nih.gov/pubmed/19731100
  65. A 2004 study at the University of Southampton, UK, University of Dusseldorf, Germany, and the Institute of Neurology, London, England, found in double-blinded placebo-controlled clinical trials that the herb Mucuna pruriens (Velvet bean), a plant source of L-Dopa, had a quicker onset of effect and performed better than pharmaceutical L-Dopa in the treatment of Parkinson's disease. The flowers of the Fava bean plant are also excellent sources of L-Dopa, and may be added to tincture : http://jnnp.bmj.com/content/75/12/1672
  66. Research in 2007 concludes that deficiency in DHA and EPA, or Omega-3 essential fatty acid, is linked to Parkinson's, and that a balance between Omega-6 and Omega-3 fatty acids is essential to Neuronal health.: http://www.medicalnewstoday.com/articles/89928.php
  67. Research in 2013, at Kyoto University in Japan, found that various herbal and nutrient chemicals activate the innate cellular antioxidant and detox pathway of Nrf2 expression to protect dopaminergic neurons in the substantia nigra, achieving similar results as proteasome inhibitors. These researchers at the School of Pharmaceutical Sciences identified chemicals in the Chinese herb green perilla leaf (Zi su ye), also widely used fresh in the Japanese diet, as potent activators of the Nrf2 antioxidant response element (ARE): http://www.ncbi.nlm.nih.gov/pubmed/23995806
  68. Research in 2013, at the Bharathiar University Department of Biotechnology, found that the chemical quercetin, found in a number of Chinese medicinal herbs, and not standardized in medicines, often combined with the Chinese herbal chemical resveratrol, modulates pathological alterations of the antioxidant response in the brain via activation of the Nrf2 pathway of cellular detox and antioxidant effect: http://www.ncbi.nlm.nih.gov/pubmed/23994659
  69. A 2009 review of the research on common herbal and nutrient medicines widely used to treat Alzheimer's disease, from researchers at the Mayo Clinic Department of Neurology, shows much bias against these medicines, but a grudgingly genuine acknowledgement of their modest proven efficacy and overall safety. We must also realize that no pharmaceutical medicine to date has been proven to have more than mild effectiveness in the treatment of Alzheimer's disease: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731997/
  70. A 2015 report from the U.S. Veteran's Administration (VA) and the Geriatric Research Education and Clinical Center, in Los Angeles, California, U.S.A. noted that the Chinese herbal chemical curcumin, now standardized as well as a key component of various Chinese herbs, has shown remarkable potential in the treatment of Alzheimer's disease. Curcumin may help decrease beta-amyloid plaque, clear oxidative damage, chelate iron, and help restore inflammatory homeostasis: http://www.ncbi.nlm.nih.gov/pubmed/26035622
  71. A 2015 randomized controlled human clinical trial at Shanghai University of TCM and Tianjin University of TCM, in China, showed that the Chinese herbal formula Yishen Huazhuo significantly improved cognitive function in patients with mild Alzheimer's disease, performing better over 24 weeks than the standard medicine Donepezil hydrochloride. This formula, consisting of Yin yang huo (Epimedium), Bu gu zhi (Psoralea fruit), Nu zhen zi (Ligustri lucidum), He shou wu (Polygoni multiflorum), Huang qi (Astagalus), and Chuan xiong (Ligusticum) is representative of a variety of herbal formulas used to treat vitality and cognitive function in aging, and presents no adverse side effects. Such study proves that integration of courses of herbal formula in the treatment of mild Alzheimer's disease would be beneficial: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0130353
  72. A 2011 meta-review of scientific study of TCM herbal medicine and treatment of neurodegeneration, Alzheimer's Disease, and vascular dementia, by experts at the University of Hong Kong Pokfulan, in China, shows how a variety of single herb extracts and herbal formulas have been proven to aid treatment and prevention in a number of ways: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097009/
  73. A double-blind placebo study of Alzheimer's patients and patients with diagnosis of mild cognitive impairment in 2008 showed that the Omega-3 fatty acid EPA, used alone, produced significant improvement in cognitive function in the patients with mild cognitive impairment and overall improvement in the severe Alzheimer's patients as noted by the clinical physician. EPA and DHA, in krill oil, is thus an effective part of the holistic protocol in treatment of Alzheimer's and neurodegenerative disease: http://www.ncbi.nlm.nih.gov/pubmed/18573585
  74. A 2015 study at the Touro University College of Pharmacology, in Vallejo, California, found that a review of scientific studies indicated that the mineral lithium significantly stabilized mood and benefited cognition in both animal and human studies, exerting neuroprotective and antioxidant effects and stabilizing membranes. A safe low-dose lithium orotate could be integrated with a more holistic therapy to increase overall efficacy: http://www.ncbi.nlm.nih.gov/pubmed/25696782
  75. A 2014 study at the University of Sao Paolo, Brazil, noted the long history and study of the natural mineral lithium to successfully treat bipolar disorder mania, and recent research finding much potential in the treatment of neurodegenerative disorders such as Alzheimer's and Parkinson's disease, providing an array of benefits to improve brain health and function: http://www.ncbi.nlm.nih.gov/pubmed/24766396
  76. A 2008 study at UCLA Institute for Neurological Research found that the TNF-alpha inhibitor Enbrel (etanercept) exerted potent benefits in reducing neurodegenerative effects with injection around the cervical spine. While this drug is the subject of a number of lawsuits over injury from long term use, a number of Chinese herbs have been proven to have potent TNF-alpha inhibiting effects: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2491668/
  77. 2010 research at Harvard Medical School revealed that a genetic link exists between immune disorder and Alzheimer's pathology, with so-called sticky protein (beta-amyloid) generated in response to a variety of pathogens infecting the brain. The problem with such genetic causes are the findings of numerous mutations of the genes involved, and as stated, the effects of various pathogens, environmental chemicals, and epigenetic triggers involved. The research does point to the potential for reduction of pathogens, as well as immunomodulatory effects with Chinese herbs: http://www.nytimes.com/2010/03/09/health/09alzh.html
  78. A 2004 study by the Eve Topf and USA National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research found that iron overload, or iron cytotoxicity, was integral to the etiopathology of Parkinson's disease and other neurodegenerative diseases, both by inducing "sticky protein" accumulation and promoting oxidative stress that may degenerate neurons and inhibit protein regulation in the brain cells: http://www.ncbi.nlm.nih.gov/pubmed/15655262
  79. A 2010 article in the New York Times outlines how new imaging techniques are proven to accurately diagnose Alzheimer's disease now, but using a radioactive dye that reveals the amyloid plaques. Misdiagnosis, revealed in autopsy studies, was a huge problem up to now, and resulted in a high percentage of cases being given the wrong therapy. This improved diagnosis also helps the provider of integrated Complementary Medicine improve the treatment strategy, and perhaps provide preventative treatment for patients with early asymptomatic stages of Alzheimer's: http://www.nytimes.com/2010/06/24/health/research/24scans.html?pagewanted=2&ref=health
  80. The U.S. NIH website provides an outline of the disease mechanism called Alzheimer's and reveals that we are certain that the disease process starts 10-20 years before its manifestation as symptoms. The time to start reversing this neurodegeneration is at an early stage, and the preventative medicine provided by Complementary Medicine physicians such as Licensed Acupunturists and herbalists not only helps prevent neurodegeneration, but is a very healthy form of medical care with many positive benefits and not side effects: http://www.nia.nih.gov/Alzheimers/Publications/adfact.htm
  81. In vitro studies in 2007 proved that S-allyl-L-cysteine, found in water extract of aged garlic, inhibited beta-amyloid (Abeta) accumulation, or sticky protein plaques, that are linked to Alzheimer's: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=18023978
  82. A 2012 study at Columbia University, headed by Dr. Nikolaos Scarmeas, showed that a dietary deficiency of omega-3 fatty acids was highly correlated with excess levels of problematic beta-amyloid proteins in circulation: http://www.medpagetoday.com/Neurology/AlzheimersDisease/32466
  83. A 2009 joint study at Arizona State University and the University of Colorado Departments of Chemistry found that the chemical curcumin, found in the Chinese herbs E zhu, Yu jin and Jiang huang, reduces alpha-synuclein induced cytotoxicty, which is related to the "sticky protein" accumulation of beta-amyloid plaque in Parkinson's and Alzheimer's diseases: http:/http://
  84. Studies in 2008 revealed that the amino acid Carnosine was effective to reduce glutamate neurotoxicity as well as the reduction of plaques accumulating in brain tissue. Drugs to antogonize glutamate receptors, or NMDA glutamate receptor blockers, are widely used in therapy for various neurodegenerative conditions today: http://www.ncbi.nlm.nih.gov/pubmed/18027086
  85. Research in 2010 at the Rensslaer Polytechnic Institute in the United States found that resveratrol, a chemical extracted from the Chinese herbs Hu zhang, was effective in remodeling of 3 types of misshapen proteins found in the brain cells of Alzheimer's patients, and did so in a modulatory fashion: http://www.ncbi.nlm.nih.gov/pubmed/20511235
  86. A 2014 study at the Sun Yat Sen University School of Pharmaceutical Science, in Guangzhou, China, found that a combination of resveratrol and clioquinol, a hydroxyquinolone found to halt cognitive decline in Alzheimer's disease by acting as a potent chelator of copper and zinc, provided a number of therapeutic benefits when combined, inhibiting amyloid beta plaque, chelating copper accumulation that contributed to amyloid beta aggregation, and providing antioxidant effects. By combining this herbal chemical with the pharmaceutical, the clioquinol dose could be reduced to lower toxicity, and no adverse effects were noted. Such study of integrative treatments may provide the best way forward to treat this difficult disease: http://www.ncbi.nlm.nih.gov/pubmed/24986600
  87. Research in 2001 showed that standardized extract of Gingko biloba, or AGb761 was significantly effective in partial prevention of dopamine depletion of corpus striatum cells subjected to neurotoxicity.: http://www.springerlink.com/content/l18dtptbnlvb6g4e/
  88. A 2012 study at China Pharmaceutical University, in Nanjing, China, found that a saponin chemical in the herb Akebia (Ba ye zha is the fruit), and in the herb Dipsacus asper Wall. (Xu duan) provided a number of beneficial effects in the care of Alzheimer's disease, exerting anti-inflammatory and neuroprotective effects that benefit cognitive function and memory. Measures on laboratory animals in studies showed modulation of excessive glial activity, decrease in the expression of inflammatory cytokines TNF-alpha, IL-1beta, and NF-kB, which are known to be induced in Alzheimer's disease induced by Abeta1-42, the beta-amyloids that create plaques in the brain: http://www.ncbi.nlm.nih.gov/pubmed/?term=IKK+beta+hippocampus+herbal
  89. Research in 2002 at the University of California at Berkeley, The Children's Hospital in Oakland, and the Buck Institute of Aging in Novato, California revealed that R-Lipoic Acid is a potent preventative supplement for neurodegnerative conditions: http://www.sciencedirect.com/science
  90. Research at the University of Massaschusetts Center for Cellular Neurobiology and Neurodegenerative Research in 2009 found that a formula comprised of alpha-lipoic acid (R-lipoic acid is the more active metabolite), acetyl-L-carnitine, phosphatidylcholine, phosphatidylyserine, and DHA (an omega 3 fatty acid found concentrated in krill oil) reduced ROS (reactive oxygen species) in the mouse brain with induced neurodegneration by 57% and markedly prevented cognitive decline; another study at the University of Toronto found that phosphatidylserine, Gingko biloba, Vit E, and P5P (B6) markedly increased cognitive function in dog brains: http://www.naturalnews.com/025616_brain_nutrients_supplement.html
  91. Research in 2000 showed that neurodegeneration spread from the corpus striatum to the cortex and thalamus over time with the progression of the disease.: http://www.neurology.org/cgi/content/abstract/54/7/1482
  92. Research in 2009 at the University of Columbia in Vancouver found that chronic adrenal stress could desensitize serotonergic 5HT receptors in the hypothalamus and cause endocrine suppression. Such findings may implicate adrenal stress in the suppression of dopamine receptors as well.: http://www.sciencedirect.com/science
  93. Research in 2005 at the Neuroendocrine Research Laboratory in Budapest, Hungary, revealed that hypothalamic response to stress includes increased prolactin and corticosterone, and that inhbition of the NMDA glutamate receptor decreased these circulating neurohormones, linking the pathology of neurodegenerative diseases, as well as some of the symptoms, to the pathology of deficient hypothalamic function and adrenal stress syndrome: http://www.springerlink.com/content/6653053k623937r1/
  94. Research in 2005 at the State University of New York Department of Neurology and Sleep Medicine, coordinated with studies at universities around the world, found that melatonin exerts a potent antioxidant and detoxifying effect in the brain, and deficiency of melatonin in the circadian cycle and sleep disorders may be a primary cause of neurodegeneration.: http://www.springerlink.com/content/m25357432233607m/
  95. Research review in Parkinson's treatment approaches in 2007 is outlined in this article and shows that adrenal stress is now a primary focus in study of the pathology, and the the neuroprotective and adaptive approaches of herbal medicine are now being explored by modern pharmacology: http://vml.med.uoc.gr/molmedgp-guide-2007/molmedgp_guide_2007_page_076-080.pdf
  96. In vivo studies in 2005 found that curcumin, from the Chinese herbs Yu jin and E zhu (curcuma zedoaria), both broke up and inhibited beta-amyloid (Abeta) accumulation, or sticky protein plaques, that are linked to Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/15590663
  97. For a complete research review of Attention Deficit and Hyperactivity Disorder and the complex science of potential causes: http://www.acnp.org/asset.axd?id=26c3b427-a7b2-4e3b-9c5f-8245305786bb
  98. A small human clinical trial of Huperzine A, an herbal cholinesterase inhibitor that has shown great benefit in neurodegeneration in clinical trials in China, as well as potent acetylcholinesterase activity in vitro, was conducted at the University of California San Diego School of Medicine, in La Jolla, California. The trial showed modest benefits compared to placebo, with a 2.27 point improvement in the ADAS-Cog scale at 11 weeks versus a 0.29 point decline with use of placebo. This shows that, while Huperzine A does not by itself show a statistically significant benefit, that it compares in statistical benefit to the widely prescribed cholinesterase inhibitor Aricept, which scored a 2.49 difference from placebo. This herbal extract has no side effects, and is combined with a variety of herbs and supplements to increase effectiveness in Chinese Medicine. The mean score at baseline for Alzheimer's patients on the ADAS-cognitive scale is about 27.: http://www.ncbi.nlm.nih.gov/pubmed/21502597
  99. In 2006, the Academy of Sciences in Shanghai, China, released a meta-review of studies of Huperzine A, a constituent of a Chinese herb standardized from a type of Club moss, Huperzia serrata. The findings stres that Huperzine A is an effective cholinesterase inhibitor, but this effect alone will not cure Alzheimer's disease, and have a limited effect on cognitive function. The alkaloid Huperzine A was also found to exert neuroprotective effects, modify beta-amyloid processing, reduce oxidative stress, protect against early programmed cell death (apoptosis), and regulate expression and secretion of nerve growth factor and NGF signaling. These benefits make Huperzine A an ideal part of a comprehensive long-term treatment protocol, as well as an effective preventive medicine: http://www.ncbi.nlm.nih.gov/pubmed/17056129
  100. In 2011, research at China Medical University showed that Huperzine A decreases the amyloid plague tangles and supports the nonamyloidogenic pathway, as well as enhancing the beta-catenin signaling that is important for neural and vascular epithelium, regulating cell growth and adhesion. Huperzine A is shown in animal studies to enhance the Wnt pathway of beta-catenin, which is deficient, or depleted in Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/21289607
  101. In 2003, the chemical galantamine, from a Chinese herb Lycoris radiata (Shi suan), was licensed to treat Alzheimer's Disease, exerting significant anticholesterinase activity. This review of scientific study from the Royal Botanic Gardens, Jodrell Laboratory, in Surrey, England, reveals that a number of Chinese herbs have shown pharmacological activities relevant to the treatment of cognitive disorders: http://www.ncbi.nlm.nih.gov/pubmed/12895669
  102. In 2012, studies at Punjab University Department of Biochemistry, in Chandigarh, India, showed that the Ayurvedic herb Bacopa monnieri (Brahmi) was potentially effective in the treatment of Alzheimer's Disease (AD) with cognitive decline. Bacopa showed neuroprotective effects, antioxidant effects, improvement in neural cell functions, restoration of neural membrane enzymes, acetyl cholinesterase and ATPase, and improvement in memory and cognitive functions in laboratory studies: http://www.ncbi.nlm.nih.gov/pubmed/22700087
  103. In 2011, studies at the National Institute of Mental Health and Neuroscience in Kamtaka, India, found that both Bacopa monnieri (Brahmi) and Centella asiatica (Gotu kola) possess significant neuroprotective effects, and aid memory loss. Bacopa monnieri is a more potent herbal medicine in this regard, but Gotu kola is well known for its benefits with tissue regeneration and antioxidant effects: http://www.ncbi.nlm.nih.gov/pubmed/22074576
  104. A research report in 2013, reviewing 10 years of research on the Ayurvedic herb Bacopa monieri (Brahmi) at Swinburne University, and Swansea University, Wales, United Kingdom, confirmed that this herbal extract improved cognition in the elderly and with patients suffering from neurodegenerative diseases, and that the herbal extract had several mode of action on the human brain: http://www.ncbi.nlm.nih.gov/pubmed/23958194
  105. In 2012, a large randomized, placebo-controlled human clinical trial was started to confirm the efficacy of a combination of the Ayurvedic herb Bacopa monieri and Pycnogenol (derived from Maritime Pine bark, with standardized OPCs, or oligomeric proanthocyanidins) to treat cognitive dysfunction, as well as cardiovascular health, showing the belief even in standard medicine that these herbal extracts will be able to effectively treat patients with neurodegenerative disorders and dementia where standard pharmaceuticals have failed: http://www.ncbi.nlm.nih.gov/pubmed/22390677
  106. In 2011, chemicals in the common Chinese herb Salvia miltiorrhiza (Dan shen), tanshinones and polyphenols, demonstrated remarkable acetylcholinesterase activity in vitro, compared to the drug galanthamine hdrobromide, as well as reducing amyloid beta plaques. This research was conducted at the New Medicine Research and Develpment Center for the Disha Pharmaceutical Group in Weihai, Chinaz: http://www.ncbi.nlm.nih.gov/pubmed/21787715
  107. In 2011, chemicals in the Chinese herb Gentiana rhodantha (mangiferrin and rhodanthenone), were found to be effective acetylcholinesterase inhibitors as well, by the Chinese Academy of Sciences, in Kunming, China. The chemcial mangiferrin exhibited a 13.4 percent ACHE inhibitory effect, and is also found in the herbs Anemarrhena asphodeloides (Zhi mu), Gentiana rhodantha, Swertia punica (Zi Hong Chang Ya Cai), and Mangiferrin indica. : http://www.ncbi.nlm.nih.gov/pubmed/22006717
  108. In 2003, research at the Shanghai Second Medical University in China found that the Chinese herb Anisodamine (aniso), from the Chinese herb Anisodus tanguticus, ameliorated the side effects of the cholinomimetic drug pilocarpine, a muscarinic agonist used to treat Alzheimer's, but discouraged due to side effects. : http://www.ncbi.nlm.nih.gov/pubmed/12812833
  109. A 2010 study of aging individuals in New York, conducted by Columbia University, found that a diet rich in folates, essential fatty acids and Vitamin E, or rich in dark, leafy greens, hearty salads with oil and vinegar dressing, fresh fruit, fresh nuts, fish and poultry had over a 30% decreased risk of developing Alzheimer's: http://www.nytimes.com/2010/04/20/health/research/20aging.html
  110. A type of shitake mushroom, the Yamabushitake (Hericium erinaceus) was proven in a double-blind placebo study in Japan to significantly increase cognitive function in 50-80 year old patients diagnosed with neurodegenerative cognitive impairment, such as in Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/18844328
  111. A 2012 double-blinded placebo-controlled study at Swinburne University, Hawthorn, Australia, found that even an 8-week supplementation with Vitamin B12, folate (5MTHF), and essential minerals, combined with herbal medicine, significantly improved cognitive function and memory in male patients between the ages of 50 and 74 years of age, reducing high homocysteine levels, and improving memory: http://www.ncbi.nlm.nih.gov/pubmed/22711385
  112. A study in 2010 at the Medical School of Xian Jiatong University in China revealed that a chemical in the herb Polygonum cuspidatum (Hu zhang, the common source of resveratrol) called Emodin, protected brain cells against beta-amyloid neurotxicity seen in Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/20573598
  113. A study in 2011 at the Institute for Functional Neurosurgery PLA and the Institute for Functional Brain Disorders in Xi'an, China, found that laboratory animals with induced hypoperfusion of the cerebrum and neurodegeneration, in a controlled study, benefited significantly from a saponin extract of the Chinese herb Jiao gu lan, or Gynostemma pentaphylum, called gypenoside. These study animals showed remarkable improvement in cognitive function with antioxidant effects and decreases in lipid peroxidation and oxidative DNA damage, and decrease in inflammatory astrocytes (brain glia support cells). These effects were dose-dependent, though, with 100 mg/kg of body weight for 2 months ineffective, but 200 mg/kg effective: http://www.ncbi.nlm.nih.gov/pubmed/21897202
  114. Food preservatives, such as benzoic acid, produce oxidative stress and disruption of cellular membranes, and the science is available to utilize healthier alternatives in the food industry to decrease incidence of neurodegeneration: http://aem.asm.org/cgi/reprint/70/8/4449.pdf
  115. Scientific study in 2007 uncovered the role of chronic inflammatory cytokines and the link to viral lipopolysaccharides as both a direct stimulation of symptoms of hyperactivity and a major cause of dopaminergic neurotoxicity. Of course, the recommendation was to increase use of corticosteroids that have harsh side effects, but Complementary Medicine offers safe effective alternative to this approach: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2442423
  116. A 2013 study at Xi'an Jiao Tong University, in China, found that electroacupuncture stimulation at SP6, GB34 and ST36, at 100 Hz, effectively enhanced survival of dopaminergic neurons in the substantia nigra, reduced motor deficits, and increased dopamine transport protein 254 percent in the striatum. This treatment also increased dopamine receptor type 1 (D1) and suppressed dopamine receptor type 2 (D2) expression in laboratory animals with induce Parkinson-like lesions. This type of therapy is thus shown potentially very helpful in the treatment and prevention of Parkinson's disease, as well as other diseases associated with depressed levels of dopamine and imbalance of D2 over D1 receptors, such as ADHD: http://www.ncbi.nlm.nih.gov/pubmed/23036843
  117. A 2012 study at Capital Medical University, in Beijing, China, found that electroacupuncture stimulation of 100 Hz at DU20 and DU14 significantly decreased excess glutamate and acetylcholine in the brains of laboratory animals with induced Parkinsonism, exerting a neuroprotective effect on dopaminergic neurons and reducing symptoms associated with Parkinson's disease. While prior evidence showed that this type of acupuncture stimulation improved symptoms in human patients with Parkinson's disease, the exact mechanisms of benefit were not known, as this stimulation does not directly increase dopamine levels: http://www.ncbi.nlm.nih.gov/pubmed/22583765
  118. A 2013 study at Peking University, Key Laboratory for Neuroscience, in Beijing, China, found that electroacupuncture at ST36 and SP6, 12 treatments at 100 Hz, improved striatal dopamine content by 36 percent and decreased striatal dopamine turnover in laboratory animals with Parkinsonism induced by MPTP. The motor function in these animals, damaged by the MPTP, improved significantly in total movements, movement time and velocity, and distance in walking. The dopaminergic cell metabolism appears to be modulated in a healthy manner, suggesting that the electroacupuncture might exert a neuroprotective and and striatal regulatory effect. Of course, the application of this treatment on laboratory animals suggests that it is not just a placebo effect: http://www.ncbi.nlm.nih.gov/pubmed/23737982
  119. A 2013 study at Konkuk University College of Veterinary Medicine examined the effects of electroacupuncture at ST36 on the brain activity of a group of dogs, inducing Parkinsonism with MPTP and dividing the dogs into 2 groups, half receiving acupuncture with needle retention at ST36 and half at a sham point. Only the dogs with the acupuncture retained at ST36 showed significantly decreased brain activity in the basal ganglia, limbic system and cerebellum, as seen with functional MRI, reducing symptoms associated with Parkinson's disease, and demonstrating the modulating effects of acupuncture. Studies show that degeneration of of dopaminergic neurons in the substantia nigra of Parkinson's patients triggers hyperactivity in the circuit of the medial globus pallidus and substantia nigra pars reticulata: http://www.ncbi.nlm.nih.gov/pubmed/23578167
  120. A 2006 paper by experts at Julius-Maximilians University in Wuerzburg, Germany, demonstrates that the pathology of Parkinson's disease involves a dopamine-induced dysbalance of the basal ganglia, and reduction of the positive feedback controls that results in an overactive system in the basal ganglia output sites, with hyperactivity of the D2 (dopamine type 2) receptors also seen in schizophrenia and ADHD: http://people.stfx.ca/x2008/x2008nhx/schiz%20and%20parkinsons.pdf
  121. A 2013 study at the Federal University of Minas Gerai, Brazil, found that there may be a strong link between inflammatory processes, immune function and the central nervous system (CNS) in Alzheimer's Disease. NK-cells, or Natural Killer Cells, showed a unique and profound increase in 5HT2C receptors in Alzheimer', linking these 2 mechanisms together in the pathology: http://www.ncbi.nlm.nih.gov/pubmed/22766135