Читать книгу The SAGE Encyclopedia of Stem Cell Research - Группа авторов - Страница 92
Proposed Disease-Modifying Therapies
ОглавлениеImmunotherapy (bapineuzumab). Most target beta amyloid. Transgenic mice models showed improvement in behavior and clearance of plaques in some AD patients after administration of Aβ immunoglobulin, but there was an increased incidence of encephalitis in some study groups, thus, this therapy is of limited utility. Passive immunotherapy with Aβ antibodies is an ongoing research, however, its relevance is questionable because only a limited quantity can cross the blood–brain barrier.
Secretase inhibitors (tarenflurbil, semagacestat) aim to increase the concentration of Aβ 1–40 and to reduce Aβ 1–42.
Amyloid aggregators (tramiprosate) failed in three trials, thus they are of questionable benefit.
Copper or zinc modulators (PBT2). Experimental evidence exists that copper and zinc are found in abundance in amyloid plaques and interfere with NMDA receptor responses. Clinical benefit has been observed as decreased CSF Aβ following administration of PBT2/clioquinol.
Tau aggregation inhibitors (methylthioninium chloride, lithium and sodium valproate) have been known to target tau phosphorylation and aggregation in animal models.
Natural products and vitamins (vitamin E, ginkgo biloba, omega 3 fatty acids, and docosahexaenoic acid) have been of questionable efficacy in randomized controlled trials.
Diagram of how microtubules disintegrate with Alzheimer’s disease. Abnormal clusters of protein fragments, called plaque, build up between nerve cells. Dying nerve cells contain tangles, which are made up of twisted strands of another protein. Scientists are unsure what causes cell death and tissue loss in the Alzheimer’s brain, but plaques and tangles are prime suspects. (National Institute on Aging)
Suppression of brain inflammation. Epidemiologic studies suggest that some patients on long-term anti-inflammatory therapy have a decreased risk of developing AD. Nonetheless, no randomized clinical trial longer than 6 months has demonstrated efficacy of anti-inflammatory drugs in slowing the rate of progression of AD.
Nerve cell regeneration. Experts believe that transplanted healthy cholinergic neurons can restore normal acetylcholine levels in the brains of AD patients. This remains a major subject of research and debate whether this technique will be of any major benefit given that other neurotransmitter deficits, synaptic loss, and neuronal degeneration will not be affected. Therefore, it cannot be speculated to what extent dementia will be controlled.
Meta-analysis and systematic reviews of risk factors for dementia and Alzheimer’s disease hypothesize a decreased risk depending mostly upon lifestyle changes and improved treatment or prevention of medical conditions that pose additional risk. These include obesity, smoking, alcohol intake, physical activity, midlife hypertension, stroke, diabetes, and hypercholesterolemia.
Areej Tariq
Independent Scholar
Muhammad Ali Tariq
Sheikh Khalifa Bin Zayed Al Nahyan Medical and Dental College
See Also: Neural: Major Pathologies; Neural: Stem and Progenitor Cells in Adults; Neuralstem, Inc.; Parkinson’s Disease.