Alzheimer's disease clinical research

Alzheimer's disease clinical research

As of August 2010 there were more than 800 clinical trials under way to understand and treat Alzheimer's disease. 149 of these studies were human phase three trials, the last step before U.S. Food and Drug Administration approval and marketing. [1]

There are different approaches. One approach is to reduce Amyloid beta, for example with bapineuzumab, an antibody in phase III studies for patients in mild to moderate stage; semagacestat, a γ-secretase inhibitor, MPC-7869; and acc-001, a vaccine to amyloid beta in phase II studies used in mild stage. However, in a recent study, a vaccine cleared patients of amyloid plaques, but had no effect on their dementia, suggesting this approach won't work.[2] It has been argued that anti-Aβ therapies currently under research may be highly effective at preventing or delaying the development of the disease when administered to asymptomatic patients or at the earliest stages of the disease, but much less effective or completely uneffective in advanced stages.[3] [4]

Other approaches are neuroprotective agents, like AL-108 (phase II completed); or metal-protein interaction attenuation, as is the case of PBT2 (phase II completed).

Finally, there are basic investigations on the origin and mechanisms of Alzheimer's disease.


Treatments in clinical development

Multiple potential treatments for Alzheimer's disease are currently under investigation, including several compounds being studied in phase 3 clinical trials. The most important clinical research is focused on potentially treating the underlying disease pathology, for which reduction of amyloid beta is a common target of compounds under investigation.

Immunotherapy to amyloid beta

Immunotherapy or vaccination for Alzheimer's stimulates the immune system to attack beta-amyloid. One approach is active immunization, which would stimulate a permanent immune response.[5] The vaccine AN-1792 showed promise in mouse and early human trials, but in a 2002 Phase II trial, 6% of subjects (18 of 300) developed serious brain inflammation resembling meningoencephalitis, and the trial was stopped. In long-term followups, 20% of subjects had developed high levels of antibodies to beta-amyloid. While placebo-patients and non-antibody responders worsened, these antibody-responders showed a degree of stability in cognitive levels as assessed by the neuropsychological test battery (although not by other measures), and had lower levels of the protein tau in their cerebrospinal fluid. These results may suggest reduced disease activity in the antibody-responder group. Autopsies found that immunization resulted in clearance of amyloid plaques, but did not prevent progressive neurodegeneration.[6]

A Phase IIA study of ACC-001, a modified version of AN-1792, is now recruiting subjects.[7]

One Aβ vaccine was found to be effective against inclusion body myositis in mouse models.[8]

Passive immunotherapy

Also derived from the AN-1792 immunotherapy program, there is an infused antibody approach termed a passive vaccine in that it does not invoke the immune system and would require regular infusions to maintain the artificial antibody levels. Micro-cerebral hemorrhages may be a threat to this process.

The most advanced such candidate is known as bapineuzumab or aab-001, and this antibody is designed as essentially identical to the natural antibody triggered by the earlier AN-1792 vaccine. The aab-001 antibody is in Phase 3 clinical trials for both Apolipoprotein E4 gene carriers,[9] and Apolipoprotein E4 gene non-carriers.[10]

Gamma secretase inhibition

Gamma secretase is a protein complex thought to be a fundamental building block in the development of the amyloid beta peptide. A gamma secretase inhibitor known as LY451039 is in Phase 3 trials.[11]

Gamma secretase modulation

Tarenflurbil (MPC-7869, formerly R-flubiprofen) is a gamma secretase modulator sometimes called a selective amyloid beta 42 lowering agent. It is believed to reduce the production of the toxic amyloid beta in favor of shorter forms of the peptide.[12] Negative results were announced regarding tarenflurbil in July 2008 and further development was canceled.

Metal-protein interaction attenuation

PBT2 is an 8-hydroxy quinoline that removes copper and zinc from cerebrospinal fluid, which are held to be necessary catalysts for amyloid beta aggregation.[13] This drug has been in a Phase II trial for early Alzheimers and which has reported preliminarily promising, but not detailed, results.


Simvastatin, a statin, stimulates brain vascular endothelial cells to create a beta-amyloid ejector.[14] The use of this statin may have a causal relationship to decreased development of the disease.[15]


Several other pharmaceuticals are under investigation to treat Alzheimer's disease.


A 2006 pilot study showed small but significant improvements in various cognitive rating scales in patients with Alzheimer's disease after treatment with etanercept, a Tumor necrosis factor-alpha receptor fusion protein, which binds to tumor necrosis factor-alpha, and decreases its role in inflammation of nervous tissue.[16] Etanercept was administered by perispinal infusion to 15 AD patients which resulted in sustained improvement in cognitive function;[17] however it is not clear if this was temporary or not. A small trial consisting of 50 patients has commenced.[18] A 12 person replication study is being run by Griffith University, Australia.[19] A study published in 2008 of etanercept, administered to a single AD patient via perispinal infusion, showed rapid (within 10 minutes) and significant improvement in Alzheimer's symptoms that lasted until the end of the study, which involved weekly injections.[20] [21] [22]

Methylthioninium chloride

In July 2008, researchers announced positive results from methylthioninium chloride (MTC), (trade name: rember) a drug that dissolved Tau polymers. Phase II results indicate that it is the first therapy that has success in modifying the course of disease in mild to moderate AD.[23]


Also in July 2008 results were announced of a study in which an antihistamine that was formerly available in Russia, Dimebon, was given to a group of AD patients. The group receiving Dimebon improved somewhat over the 6 months of the study (and this continued for the next six months), whereas those on placebo deteriorated.[24] Unfortunately the consecutive phase-III trial failed to show significant positive effects in the primary and secondary endpoints.[25] The sponsors acknowledged in March 2010 that initial results of the phase III trial showed that while the drug had been well tolerated, its outcomes did not significantly differ from the placebo control.[26]

Antibiotic therapy

Only one clinical trial is being done (at McMaster University) to investigate the efficacy of antibiotic therapy.[27] The authors of the study indicated that it was effective in delaying the progress of the disease: "In conclusion, a 3-month course of doxycycline and rifampin reduced cognitive worsening at 6 months of follow-up in patients with mild to moderate AD."[28] A re-examination of the same data using: "...AUC analysis of the pooled index showed significant treatment effect over the 12-month period".[29]

Several studies using minocycline and doxycycline, in an animal model of Alzheimer's Disease, have indicated that minocycline [30][31] and doxycycline [32][33] exerts a protective effect in preventing neuron death and slowing the onset of the disease.

Antiviral therapy

The possibility that AD could be treated with antiviral medication is suggested by a study showing colocation of herpes simplex virus with amyloid plaques.[34]

Angiotensin receptor blockers

A retrospective analysis of five million patient records with the US Department of Veterans Affairs system found that different types of commonly used anti-hypertensive medications had very different AD outcomes. Those patients taking angiotensin receptor blockers (ARBs) were 35—40% less likely to develop AD than those using other anti-hypertensives.[35]


The endocannabinoid system may have a role in AD.[36][37]


Allopregnanolone has been identified as a potential drug agent. Levels of neurosteroids such as allopregnanolone decline in the brain in old age and AD.[38] Allopregnanolone has been shown to aid the neurogenesis that reverses cognitive deficits in a mouse model of AD.[39]

Insulin sensitizers

Recent studies suggest an association between insulin resistance and AD (fat cell sensitivity to insulin can decline with aging): In clinical trials, a certain insulin sensitizer called "rosiglitazone" improved cognition in a subset of AD patients;[40][41] in vitro, beneficial effects of Rosiglitazone on primary cortical rat neurons have been demonstrated[42][43]

Table of advanced disease-modifying drug (DMD) candidates

Table - Disease-Modifying Candidates in Late-Stage Clinical Trials for Alzheimer's Disease
Target/Approach Notes (Theoretical) Candidate Name Trial Phase Trial Start Date Expected End Date Planned Enrollment AD population targeted (severity) AD population targeted (genetic) Comments
Gamma Secretase Modulator/NSAID Shifts A-Beta production to shorter and less toxic species MPC-7869[44] Phase III Feb 2005 May 2008 1,600 Mild n/a 800-patient Trial also underway worldwide.[45]
Gamma Secretase Inhibitor Inhibits Gamma Secretase, believed crucial to pathology LY451039[46] Phase III March 2008 March 2012 1,500 Mild-to-Moderate n/a smaller trial completed '07, data not out.[47]
Antibody to Amyloid-Beta Mimics Natural Antibody triggered by AN-1792 aab-001[9] Phase III Dec 2007 Dec 2010 800 Mild-to-Moderate Apolipoprotein E4 Carriers only Identical Trial also underway in Europe
Antibody to Amyloid-Beta Mimics Natural Antibody triggered by AN-1792 aab-001[48] Phase III Dec 2007 Dec 2010 1,250 Mild-to-Moderate Apolipoprotein E4 Non-Carriers only Identical Trial also underway in Europe
Metal-Protein Interaction Attenuation Primary Targets Copper & Zinc PBT2[49] Phase II (completed) Dec 2006 Dec 2007 80 early Alzheimer's disease n/a Deemed a Success; Phase III to start
Fibrilization of Amyloid-Beta Prevents/Reverses Fibrilization of A-Beta AZD-103[50] Phase II Dec 2007 May 2010 340 Mild-to-Moderate n/a Phase I was success
Neuroprotection Neuroprotective Peptide, intra-nasal AL-108[51] Phase II (completed) Jan 2007 Jan 2008 120 Mild Cognitive Impairment n/a Deemed a Success; Phase III to start
Brain Cell Apoptosis Inhibitor Blocks Mitochondrial Pores Dimebon[52] Phase II (completed) Sept 2006 Nov 2007 (actual) 183 Mild-to-Moderate n/a Deemed a Success; Phase III completed but failed
Natural Antibodies to A-Beta human plasma source limits supply IVIg[53] Phase II (completed) Feb 2006 June 2007 24 Mild-to-Moderate n/a Deemed a Success; Phase III to start
Vaccine to Amyloid-Beta Injects modified A-Beta (active vaccine) acc-001[7] Phase II Nov 2007 Mar 2012 228 Mild-to-Moderate n/a Sequel to famous AN-1792 Vaccine Trial


  1. ^ "Clinical Trials. Found 812 studies with search of: alzheimer". U.S National Institutes of Health. Retrieved 2010-08-16. 
  2. ^ Holmes C, Boche D, Wilkinson D, Yadegarfar G, Hopkins V, Bayer A, Jones RW, Bullock R, Love S, Neal JW, Zotova E, Nicoll JAR (July 2008). "Long-term effects of Aβ42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial". The Lancet 372 (9634): 216–233. doi:10.1016/S0140-6736(08)61075-2. PMID 18640458. 
  3. ^ Todd E. Golde et al (2011). "Anti-Aβ Therapeutics in Alzheimer's Disease: The Need for a Paradigm Shift". Neuron. 
  4. ^ Eric M Reiman et al (2010). "Alzheimer’s Prevention Initiative: a proposal to evaluate presymptomatic treatments as quickly as possible". Biomarkers in Medicine. 
  5. ^ Dodel r, Neff F, Noelker C, Pul R, Du Y, Bacher M Oertel W. (2010). "Intravenous Immunoglobulins as a Treatment for Alzheimer's Disease: Rationale and Current Evidence". Drugs 70 (5): 513–528. doi:10.2165/11533070-000000000-00000. PMID 20329802. 
  6. ^ Vaccination:
  7. ^ a b "Study Evaluating ACC-001 in Mild to Moderate Alzheimers Disease Subjects". Clinical Trial. FDA/ 2008-03-11. 
  8. ^ Kitazawa M, Vasilevko V, Cribbs DH, LaFerla FM (13 May 2009). "Immunization with amyloid-β attenuates inclusion body myositis-like myopathology and motor impairment in a transgenic mouse model". The Journal of Neuroscience 29 (19): 6132–41. doi:10.1523/JNEUROSCI.1150-09.2009. PMC 3049190. PMID 19439591. Lay summary. "Inclusion body myositis...features include T-cell mediated inflammatory infiltrates and aberrant accumulations of proteins, including amyloid-β (Aβ), tau, ubiquitinated proteins, apolipoprotein E, and β-synuclein in skeletal muscle. ... active immunization markedly reduces intracellular Aβ deposits and attenuates the motor impairment compared with untreated mice...Aβ oligomers contribute to the myopathy process as they were significantly reduced in the affected skeletal muscle from immunized mice. In addition, the anti-Aβ antibodies produced in the immunized mice blocked the toxicity of the Aβ oligomers in vitro, providing a possible key mechanism for the functional recovery." 
  9. ^ a b "Bapineuzumab in Patients With Mild to Moderate Alzheimer's Disease/ Apo_e4 carriers". Clinical Trial. FDA/ 2008-02-29. 
  10. ^ "Bapineuzumab in Patients With Mild to Moderate Alzheimer's Disease/ Apo_e4 non-carriers". Clinical Trial. FDA/ 2008-02-29. 
  11. ^ "Effect of LY451039 on the Long Term Progression of Alzheimer's Disease". Clinical Trial. FDA/ 2008-01-11. 
  12. ^ Tarenflurbil:
  13. ^ Strozyk D, Launer LJ, Adlard PA, et al. (2007). "Zinc and copper modulate Alzheimer Abeta levels in human cerebrospinal fluid". Neurobiol Aging 30 (7): 1069–77. doi:10.1016/j.neurobiolaging.2007.10.012. PMC 2709821. PMID 18068270. 
  14. ^ Whitfield JF (2007). "The road to LOAD: late-onset Alzheimer's disease and a possible way to block it". Expert Opinion on Therapeutic Targets 11 (10): 1257–1260. doi:10.1517/14728222.11.10.1257. PMID 17907956. 
  15. ^ Li G, Larson EB, Sonnen JA, Shofer JB, Petrie EC, Schantz A, Peskind ER, Raskind MA, Breitner JC, Montine TJ (2007). "Statin therapy is associated with reduced neuropathologic changes of Alzheimer disease". Neurology 69 (9): 878–85. doi:10.1212/01.wnl.0000277657.95487.1c. PMID 17724290. 
  16. ^ Tobinick E, Gross H, Weinberger A, Cohen H (2006). "TNF-alpha modulation for treatment of Alzheimer's disease: a 6-month pilot study". MedGenMed 8 (2): 25. PMC 1785182. PMID 16926764. 
  17. ^ Griffin WS (2008). "Perispinal etanercept: potential as an Alzheimer therapeutic". J Neuroinflammation 5: 3. doi:10.1186/1742-2094-5-3. PMC 2241592. PMID 18186919. 
  18. ^ Tobinick E (2007). "Perispinal etanercept for treatment of Alzheimer's disease". Curr Alzheimer Res 4 (5): 550–2. doi:10.2174/156720507783018217. PMID 18220520. 
  19. ^ Bedo, S. (18/9/11). "Dementia drug on trial". Goldcoast Bulletin. Retrieved 18/9/11. 
  20. ^ "Alzheimer's treatment: hope behind the hype?". New Scientist. 2008-04-15. 
  21. ^ See videos at [1].
  22. ^ Tobinick Edward L., Gross H. (2008). "Rapid cognitive improvement in Alzheimer's disease following perispinal etanercept administration". J. Neuroinflammation 5 (2): 2. doi:10.1186/1742-2094-5-2. PMC 2211476. PMID 18184433. 
  23. ^ Wischik CM, Bentham P, Wischik DJ, Seng KM (2008). "Tau aggregation inhibitor (TAI) therapy with rember arrests disease progression in mild and moderate Alzheimer's disease over 50 weeks". Alzheimer’s Association.{E7C717CF-8D73-41E0-8DB0-FA92205978CD}&SKey={68E04DB5-AB1C-4F7B-9511-DA3173F4F755}&MKey={CFC5F7C6-CB6A-40C4-BC87-B30C9E64B1CC}&AKey={50E1744A-0C52-45B2-BF85-2A798BF24E02}. Retrieved 2008-07-29. 
  24. ^ Doody RS, Gavrilova SI, Sano M, Thomas RG, Aisen PS, Bachurin SO, Seely L, Hung D; dimebon investigators (2008). "Effect of dimebon on cognition, activities of daily living, behaviour, and global function in patients with mild-to-moderate Alzheimer's disease: a randomised, double-blind, placebo-controlled study". The Lancet 372 (9634): 207–15. doi:10.1016/S0140-6736(08)61074-0. PMID 18640457. 
  25. ^ Dimebon Disappoints in Phase 3 Trial
  26. ^ "Pfizer And Medivation Announce Results From Two Phase 3 Studies In Dimebon (latrepirdine*) Alzheimer's Disease Clinical Development Program" (Press release). 3 March 2010. 
  27. ^
  28. ^ Loeb MB, Molloy DW, Smieja M, et al. (March 2004). "A randomized, controlled trial of doxycycline and rifampin for patients with Alzheimer's disease". J Am Geriatr Soc 52 (3): 381–387. doi:10.1111/j.1532-5415.2004.52109.x. PMID 14962152. 
  29. ^ Carusone SC, Goldsmith CH, Smieja M, Loeb M (April 2006). "Summary measures were a useful alternative for analyzing therapeutic clinical trial data". J Clin Epidemiol 59 (4): 387–392. doi:10.1016/j.jclinepi.2005.05.009. PMID 16549261. 
  30. ^ Choi Y, Kim HS, Shin KY, et al. (November 2007). "Minocycline attenuates neuronal cell death and improves cognitive impairment in Alzheimer's disease models". Neuropsychopharmacology 32 (11): 2393–2404. doi:10.1038/sj.npp.1301377. PMID 17406652. 
  31. ^ Hunter CL, Quintero EM, Gilstrap L, Bhat NR, Granholm AC (June 2004). "Minocycline protects basal forebrain cholinergic neurons from mu p75-saporin immunotoxic lesioning". Eur. J. Neurosci. 19 (12): 3305–16. doi:10.1111/j.0953-816X.2004.03439.x. PMID 15217386. 
  32. ^ Jankowsky JL, Slunt HH, Gonzales V, et al. (December 2005). "Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease". PLoS Med. 2 (12): e355. doi:10.1371/journal.pmed.0020355. PMC 1283364. PMID 16279840. 
  33. ^ Khlistunova I, Biernat J, Wang Y, et al. (January 2006). "Inducible expression of Tau repeat domain in cell models of tauopathy: aggregation is toxic to cells but can be reversed by inhibitor drugs". J. Biol. Chem. 281 (2): 1205–1214. doi:10.1074/jbc.M507753200. PMID 16246844. 
  34. ^ Wozniak M, Mee A, Itzhaki R (2008). "Herpes simplex virus type 1 DNA is located within Alzheimer's disease amyloid plaques". J Pathol 217 (1): 131–138. doi:10.1002/path.2449. PMID 18973185. 
  35. ^ "Angiotensin receptor blockers are lower incidence, progression of Alzheimer's disease"
  36. ^ Benito C, Núñez E, Pazos MR, Tolón RM, Romero J (August 2007). "The endocannabinoid system and Alzheimer's disease". Mol Neurobiol 36 (1): 75–81. doi:10.1007/s12035-007-8006-8. PMID 17952652. 
  37. ^ Campbell VA, Gowran A (November 2007). "Alzheimer's disease; taking the edge off with cannabinoids?". Br J Pharmacol 152 (5): 655–62. doi:10.1038/sj.bjp.0707446. PMC 2190031. PMID 17828287. 
  38. ^ Marx C, Trost W, Shampine L, Stevens R, Hulette C, Steffens D, Ervin J, Butterfield M et al. (December 2006). "The Neurosteroid Allopregnanolone Is Reduced in Prefrontal Cortex in Alzheimer’s Disease". Biological Psychiatry 60 (12): 1287–94. doi:10.1016/j.biopsych.2006.06.017. PMID 16997284. 
  39. ^ Wang JM, Singh C, Liu L, Irwin RW, Chen S, Chung EJ, Thompson RF, Brinton RD. (2010). "Allopregnanolone reverses neuron and cognitive deficits in a mouse model of Alzheimer's disease". Proc Natl Acad Sci U S A 107 (14): 6498–6503. doi:10.1073/pnas.1001422107. PMC 2851948. PMID 20231471. 
  40. ^ Watson GS, Cholerton BA, Reger MA, Baker LD, Plymate SR, Asthana S, Fishel MA, Kulstad JJ, Green PS, Cook DG, "et al." (2005). "Preserved cognition in patients with early Alzheimer disease and amnestic mild cognitive impairment during treatment with rosiglitazone: a preliminary study". Am J Geriatr Psychiatry 13 (11): 950–958. doi:10.1176/appi.ajgp.13.11.950. PMID 16286438. 
  41. ^ Risner ME, Saunders AM, Altman JFB, Ormandy GC, Craft S, Foley IM, Zvartau-Hind ME, Hosford DA, Roses AD (2006). "Efficacy of rosiglitazone in a genetically defined population with mild-to-moderate Alzheimer's disease". Pharmacogenomics J 6 (4): 246–254. doi:10.1038/sj.tpj.6500369. PMID 16446752. 
  42. ^ Brodbeck J, Balestra M, Saunders A, Roses A, Mahley R, Huang Y (2008). "Rosiglitazone increases dendritic spine density and rescues spine loss caused by apolipoprotein E4 in primary cortical neurons". Proc Natl Acad Sci U. S. A. 105 (4): 1343–1346. doi:10.1073/pnas.0709906104. PMC 2234140. PMID 18212130. 
  43. ^ "Alzheimer's 'is brain diabetes'". BBC News. 2009-02-03. [unreliable medical source?]
  44. ^ "Efficacy Study of MPC-7869 to Treat Patients With Alzheimer's". Clinical Trial. FDA/ 2007-12-11. 
  45. ^ "Global Efficacy Study of MPC-7869 to Treat Patients With Alzheimer's". Clinical Trial. FDA/ 2007-12-11. 
  46. ^ "Effect of LY451039 on the Long Term Progression of Alzheimer's Disease". Clinical Trial. FDA/ 2008-01-11. 
  47. ^ "Effects of LY450139 Dihydrate on Subjects With Mild to Moderate Alzheimer's Disease". Clinical Trial. FDA/ 2007-05-24. 
  48. ^ "Bapineuzumab in Patients With Mild to Moderate Alzheimer's Disease Apo_e4 non-carriers". Clinical Trial. FDA/ 2008-02-29. 
  49. ^ "Study Evaluating the Safety, Tolerability and Efficacy of PBT2 in Patients With Early Alzheimer's Disease". Clinical Trial. FDA/ 2008-01-13. 
  50. ^ "ELND005 in Patients With Mild to Moderate Alzheimer's Disease". Clinical Trial. FDA/ 2008-02-29. 
  51. ^ "Safety, Tolerability and Efficacy Study to Evaluate Subjects With Mild Cognitive Impairment". Clinical Trial. FDA/ 2008-03-11. 
  52. ^ "Double-Blind, Placebo-Controlled Study of Oral Dimebon in Subjects With Mild to Moderate Alzheimer's Disease". Clinical Trial. FDA/ 2007-12-27. 
  53. ^ "Phase II Study of Intravenous Immunoglobulin (IVIg) for Alzheimer's Disease". Clinical Trial. FDA/ 2007-08-03. 

Wikimedia Foundation. 2010.

Look at other dictionaries:

  • Alzheimer's disease — Alzheimer redirects here. For other uses, see Alzheimer (disambiguation). Alzheimer s disease Classification and external resources …   Wikipedia

  • Early-onset Alzheimer's disease — Early onset Alzheimer s disease, also called early onset Alzheimer s, or early onset AD, is the term used for cases of Alzheimer s disease diagnosed before the age of 65. It is an uncommon form of Alzheimer s, accounting for only 5 10% of all… …   Wikipedia

  • Biochemistry of Alzheimer's disease — The biochemistry of Alzheimer s disease (AD), one of the most common causes of adult dementia, is as yet not well understood at the molecular level. It has been identified as a protein misfolding disease due to the accumulation of abnormally… …   Wikipedia

  • Clinical trial — Clinical trials are a set of procedures in medical research and drug development that are conducted to allow safety (or more specifically, information about adverse drug reactions and adverse effects of other treatments) and efficacy data to be… …   Wikipedia

  • Alzheimer-Krankheit — Vergleichende Klassifikation nach DSM IV   ICD 10 …   Deutsch Wikipedia

  • Alzheimer's Association — Infobox NPO organization name = Alzheimer s Association organization organization motto = Our vision is a world without Alzheimer s. organization type = NPO founded = 1980 location = key people = fields = services = num members = homepage =… …   Wikipedia

  • Clinical Neurochemistry — Progression of Huntington s Diesase. A microscope image of Medium spiny neurons (yellow) with nuclear inclusions (orange), which occur as part of the disease process. Clinical Neurochemistry is the field of neurological biochemistry which relates …   Wikipedia

  • Clinical neuroscience — For the journal, see Clinical Neuroscience (journal). Clinical neuroscience is a branch of neuroscience that focuses on the fundamental mechanisms that underlie diseases and disorders of the brain and central nervous system.[1] It seeks to… …   Wikipedia

  • Parkinson's disease — Parkinson s redirects here. For other uses, see Parkinson s (disambiguation). Parkinson s disease Classification and external resources …   Wikipedia

  • Enfermedad de Alzheimer — Para el neurólogo que dio nombre a la enfermedad, véase Alois Alzheimer. Enfermedad de Alzheimer …   Wikipedia Español

Share the article and excerpts

Direct link
Do a right-click on the link above
and select “Copy Link”