Parkinson's, Alzheimer's, ADD and Other Neurodegenerative Disorders

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

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Information Resources - Additional Information and Links to Scientific Studies

  1. 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
  2. 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
  3. 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/
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. A 2015 study at China Medical University in Taichung, Taiwan, found that patients taking Ambien (Zolpidem) for insomnia had a greater overall incidence of Parkinson's disease: http://www.ncbi.nlm.nih.gov/pubmed/25650675
  10. 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
  11. 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 (AGEs) 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
  12. 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 institutes 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
  13. A 2016 study at the University of Delaware School of Nursing found that noncompliance with medications prescribed to treat Parkinson's disease is a big problem. The reasons for this widespread noncompliance are complex, but rarely are considerations that the complex medication protocols are ineffective and come with considerable adverse health effects taken seriously. Patients obviously need a protocol of treatment that addresses the problem holistically and does not come with such problematic adverse side effects: http://www.ncbi.nlm.nih.gov/pubmed/27224682
  14. A 2006 review of stem cell research in Parkinson's disease, published in the journal Nature, showed that initial experiments with laboratory animals injected with dopamine producing neurons showed a remarkable initial success in relieving symptoms, but that many of the embryonic stem cells did not become neurons, and these cells kept dividing and grew into cancer, although the animals were killed before this cancerous growth took off, and the study designs do not explore the potential for this type of cancer, made from undifferentiated cells. Other intrinsic problems involve issues of long-term success, such as the inability of the body to properly regulate the new neurons, the difficulty in finding which type of dopamine producing cells would be needed in each case, and the risks and adverse effects of delivering the stem cells to the right area of the human brain. Stem cell transplant into laboratory animals that will soon be killed and dissected presents few of the challenges that such techniques would involve in human patients. In 2012 the U.S. FDA approved the first human clinical trial to assess stem cell therapy for autism, and small studies using endothelial stem cells to form increased blood vessel growth, and using bone marrow derived stem cells to increase immune cells in the brain have been conducted in China and India. The short term adverse effects were manageable, but the long-term effects, both adverse and beneficial, will not be known for a decade: http://www.nature.com/news/2006/061016/full/news061016-16.html
  15. A 2016 review of treatment for neurodegenerative diseases such as Parkinsonism and Alzheimer's disease, by experts at the University of Valencia College of Pharmacy, in Burjassot, Spain, found that herbal and nutrient medicines presented significant benefits in the overall treatment protocol, as neuroprotective agents, inflammatory modulators, inhibitors of alpha-synuclein condensation, antioxidants, and modulators of the dopamine metabolism: http://www.ncbi.nlm.nih.gov/pubmed/27224274
  16. 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
  17. A 2015 randomized controlled human study at the University of Arizona, in Tucson, Arizona, U.S.A. showed that short course of electroacupuncture significantly improved symptoms of rigidity and balance in patients with advance Parkinson's disease. This study showed that just a weekly acupuncture treatment for 3 weeks resulted in improvement: http://www.ncbi.nlm.nih.gov/pubmed/25341431
  18. A 2016 randomized controlled human clinical trial of electroacupuncture to improve the motor function of patents with Parkinson's disease, at the University of Arizona School of Medicine, showed with various measures of symptom improvement, including the monitoring of gait with sensors, that electroacupuncture is effective: http://www.ncbi.nlm.nih.gov/pubmed/27227460
  19. 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
  20. A 2016 study of the key area of the brain called the insula and its relationship to Parkinson's disease, by experts using functional MRI and other brain mapping technology at the University of Toronto, in Canada, and the University of Lyon, in France, noted that a number of loci in the insula were related to Parkinson's and symptoms of Parkinsonism. Such study design utilized Big Data approaches to gain more useful information for treatment and prevention: http://www.ncbi.nlm.nih.gov/pubmed/26800238
  21. A 2015 study at Kyung Hee University, in South Korea, showed that genuine manual stimulation and electroacupuncture stimulation at the points P6 and H7 exerted significant modulatory effects on the areas of the brain called the insula and cingulate gyrus that were significantly stronger than techniques of no or "pseudo-stimulation" at the points on control subjects. The stronger stimulation at the needles affected these deeper areas in the body, while the more superficial stimulation resulted in modulated activity in the cortex and some areas such as the insula that were not as dramatic. Many such studies are using fMRI and other technology to finally confirm that actual needle techniques produce that responses that we need to treat such diseases as Parkinsonism and Alzheimer's: http://www.ncbi.nlm.nih.gov/pubmed/26211895
  22. 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
  23. 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
  24. 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
  25. A 2014 randomized controlled study in China found that electroacupuncture at just 3 points, DU20, SP6 and LV3, daily for 14 days, significantly upregulated superoxide dismutase and glutathione metabolism in the dopaminergic neurons of the substantia nigra in laboratory animals with induced Parkinsonism, and downregulated cellular toxicity in these neurons as measured by malondialdehyde levels: http://www.ncbi.nlm.nih.gov/pubmed/25069193
  26. A 2015 study by UCSF and the Veterans Affairs Medical Center in San Francisco, California, U.S.A. and the Emory University School of Medicine, in Atlanta, Georgia, U.S.A. found that N-acetyl cysteine (NAC) presents a viable adjunct integrative role as part of a more holistic treatment of Parkinson's disease by restoring glutathione balance in the CNS, and could be measured with cerebrospinal fluid samples to adjust dosage. Of course, a more comprehensive treatment utilizing an array of herbs, nutrient medicines and acupuncture could achieve the goal of glutathione restoration even more. Proposals for early Alzheimer's disease screening includes testing cerebrospinal fluid for protein content and testing for NAC levels may improve outcomes: http://www.ncbi.nlm.nih.gov/pubmed/25765302
  27. A 2014 study at Kyung Hee University Hospital, in Seoul, South Korea, presented at the International Parkinson and Movement Disorder Society 18th Congress in Stockholm, Sweden, showed that the simple, safe and inexpensive treatment of bee venom acupuncture, which involves placing diluted bee venom under the skin at key acupuncture points, and then proceeding with a normal acupuncture course, provided significant benefits in a randomized controlled human clinical trial of Parkinson disease, with no serious adverse events: http://www.medscape.com/viewarticle/826810
  28. 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
  29. 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
  30. 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
  31. 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
  32. 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
  33. 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
  34. 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/
  35. 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/
  36. 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
  37. 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
  38. 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
  39. 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
  40. 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
  41. 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
  42. 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
  43. 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
  44. 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, a synthetic dopamine and a dopamine promoting drug. Dopaminergic herbs such as Mucuna pruriens, Muira puama and St. John's Wort may present a potential in therapy as well: http://www.ncbi.nlm.nih.gov/pubmed/22035026
  45. A 2004 study published in the British Journal of Pharmacology shows that an alcohol extract of St. Johns' wort, or Hypericum perforatum, selectively increases dopamine in the prefrontal cortex, and acts as a dopamine reuptake inhibitor. Such study shows the potential for St. Johns' wort tincture in the holistic protocol:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1574978/
  46. An excellent report on CoQ10 deficiencies is found on the LifeExtension magazine website: http://www.lef.org/magazine/mag2000/july2000_review.html
  47. 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
  48. 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
  49. 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
  50. 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
  51. A study by Thomas Jefferson University Medical College in Pennsylvania concerning the efficacy of herbal chemicals as neuroprotective antioxidants, especially reservatrol in the Chinese herb Hu Zhang (Polygonum cuspidatum): http://www.ncbi.nlm.nih.gov/pubmed/11897104
  52. 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). St. Johns wort is also proven to be dopaminergic: http://www.ncbi.nlm.nih.gov/pubmed/23469842
  53. 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
  54. 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
  55. 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
  56. A 2014 study of the benefits from use of the herb Mucuna pruriens, a dopaminergic herb with a significant amount of natural L-Dopa, for treatment of early Parkinsonism, by experts at the University of Cagliari School of Medicine, in Cagliari, Italy, and the Italian Institute of Technology, in Genoa, Italy, showed that an alcohol extract of this herb provided an array of benefits in Parkinson's Disease, improving motor, olfactory, mitochondrial and synaptic functions in laboratory animals: http://www.ncbi.nlm.nih.gov/pubmed/25340511
  57. A 2014 study at Kyung Hee University, in Seoul, South Korea, found that chemicals in the Chinese herb Gastrodia elata Blume (Tian ma) significantly alleviated the key side effects of the most longstanding drug used to treat Parkinsonism, L-Dopa, namely the induced dyskinesia (induced involuntary motor movements) with chronic use. These effects were linked to modulation of excess pERK1/2 and FosB induced by the drug, and clearly shows that avoidance of integration of professional Chinese Herbal Medicine may have been a big mistake for decades of care in Parkinson's disease: http://www.ncbi.nlm.nih.gov/pubmed/24650244
  58. A 2014 multicenter study of the effects of acupuncture stimulation to also alleviated the main adverse effects of chronic use of L-Dopa in the treatment of Parkinsonism was conducted at Kyung Hee Universtiy, the University of North Carolina Chapel Hill, and the Brown University Department of Neuroscience, in South Korea and the United States of America. This study clearly showed the potential in reduction of L-Dopa side effects with chronic use via a number of pathways, including modulation of GABA in the Substantia Nigra, and FosB expression. Clearly, an integration with both acupuncture and Chinese Herbal Medicine could have improve the outcomes and quality of life for so many patients with Parkinson's disease treated with standard medicine, yet this integrative therapy was highly discouraged by Medical Doctors: http://www.ncbi.nlm.nih.gov/pubmed/24321617
  59. A 2014 study at the Yale University School of Medicine in conjunction with Beijing Normal University, in New Haven, Connecticut, U.S.A. and Beijing, China, found that the Chinese Herbal Formula called Jitai tablet provided an array of benefits for Parkinsonism in laboratory animals, improving both behavioral and motor function via the dopaminergic pathways (DA system), and showed significant neuroprotective effects. The integration of such formulas into the treatment protocol provides significant potential with no adverse effects. The Jitai tablet (JTT) is a traditional herbal formula consisting of the following ingredients: Papaveraceae Corydalis (yan hu suo), 10.20%; Solanaceae Datura metel (yang jin hua), 2.18%; Lamiaceae Salvia Miltiorrhizae (Dan shen), 16.87%; Araliaceae Panax ginseng (Ren shen), 2.18%; Apiaceae Angelica sinensis (Dang gui), 10.20%; Apiaceae Ligusticum chuanxiong (Chuan xiong), 5.71%; Asteraceae Carthamus tinctorius (Hong hua), 10.20%; Ranunculaceae Aconitum (Fu zi), 2.18%; Myristicaceae Myristica cagayanensis (Dou kou), 2.18%; Asteraceae Aucklandia (Mu xiang), 5.71%; Thymelaeaceae Aquilaria, (Chen xiang), 4.35%; Zingiberaceae Zingiber (Gan jiang), 2.18%; Lauraceae Cinnamomum (Rou gui), 2.18%; Semen Persicae (Tao ren), 10.20%; Pearl powder (Zhen zhu fen), 13.47%: http://www.hindawi.com/journals/ecam/2014/542383/
  60. Research in 2012 at the Oxford University Hospitals and School of Medicine, in the United Kingdom, showed that Cholinesterase inhibitors presented a viable adjunct treatment for Parkinson's disease. Herbal chemicals have been FDA approved as cholinesterase inhibitors, and present almost no chance of adverse side effects that the drugs do. In China, the chemical Huperzine was proven to be effective, and this and other synergistic herbal chemicals is available as Vinpurazine, a formula from Health Concerns: http://www.ncbi.nlm.nih.gov/pubmed/22419314
  61. A 2005 study at the King's College London School of Pharmacy showed that a few herbal acyetlcholinesterase inhibitors and dopaminergic herbs show much potential in the treatment of both Parkinson's and Alzheimer's disease. Huperzine A, phytostigmine and galantamine are all proven and used in standard therapy, and a number of dopaminergic herbal chemicals were being studied at this time as well: http://www.ncbi.nlm.nih.gov/pubmed/15956811
  62. 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
  63. 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
  64. 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
  65. 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/
  66. 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
  67. 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/
  68. 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
  69. 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
  70. 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
  71. 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
  72. 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
  73. 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
  74. 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://
  75. 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
  76. 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
  77. 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/
  78. 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
  79. 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
  80. 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
  81. 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
  82. 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/
  83. 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/
  84. 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
  85. 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
  86. 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
  87. 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
  88. 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
  89. 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
  90. 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
  91. 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
  92. 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
  93. 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
  94. 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
  95. 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
  96. 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
  97. 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
  98. 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
  99. 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
  100. 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
  101. 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
  102. 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
  103. 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
  104. 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
  105. 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
  106. 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
  107. 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
  108. 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
  109. 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
  110. 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