Biochemistry of Alzheimer's disease | Wikipedia audio article
Channel: wikipedia tts
Date: 2019-05-02

This is an audio version of the Wikipedia Article:
https://en.wikipedia.org/wiki/Biochemistry_of_Alzheimer%27s_disease


00:02:50 1 Neuropathology
00:03:50 2 Biochemical characteristics
00:07:09 3 Disease mechanism
00:08:04 3.1 Cholinergic hypothesis
00:10:09 3.2 Tau hypothesis
00:11:10 3.3 Amyloid hypothesis
00:14:10 3.4 Isoprenoid changes
00:15:25 4 Glucose consumption
00:18:45 5 Insulin signaling
00:20:11 6 Oxidative stress
00:21:11 7 Large gene instability hypothesis



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SUMMARY
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The biochemistry of Alzheimer's disease (AD), one of the most common causes of adult dementia, is not yet very well understood. AD has been identified as a possible protein misfolding disease due to the accumulation of abnormally folded amyloid beta protein in the brains of Alzheimer's patients. Amyloid beta, also written Aβ, is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid precursor protein (APP), whose function is unclear but thought to be involved in neuronal development.  The presenilins are components of proteolytic complex involved in APP processing and degradation.Amyloid beta monomers are soluble and contain short regions of beta sheet and polyproline II helix secondary structures in solution, though they are largely alpha helical in membranes; however, at sufficiently high concentration, they undergo a dramatic conformational change to form a beta sheet-rich tertiary structure that aggregates to form amyloid fibrils. These fibrils deposit outside neurons in dense formations known as senile plaques or neuritic plaques, in less dense aggregates as diffuse plaques, and sometimes in the walls of small blood vessels in the brain in a process called amyloid angiopathy or congophilic angiopathy.
AD is also considered a tauopathy due to abnormal aggregation of the tau protein, a microtubule-associated protein expressed in neurons that normally acts to stabilize microtubules in the cell cytoskeleton. Like most microtubule-associated proteins, tau is normally regulated by phosphorylation; however, in AD patients, hyperphosphorylated tau accumulates as paired helical filaments that in turn aggregate into masses inside nerve cell bodies known as neurofibrillary tangles and as dystrophic neurites associated with amyloid plaques. Although little is known about the process of filament assembly, it has recently been shown that a depletion of a prolyl isomerase protein in the parvulin family accelerates the accumulation of abnormal tau.Neuroinflammation is also involved in the complex cascade leading to AD pathology and symptoms. Considerable pathological and clinical evidence documents immunological changes associated with AD, including increased pro-inflammatory cytokine concentrations in the blood and cerebrospinal fluid. Whether these changes may be a cause or consequence of AD remains to be fully understood, but inflammation within the brain, including increased reactivity of the resident microglia towards amyloid deposits, has been implicated in the pathogenesis and progression of AD.