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Molecular mechanism of Autophagy: Its role in the therapy of Alzheimer's disease.

07:00 EST 14th January 2020 | BioPortfolio

Summary of "Molecular mechanism of Autophagy: Its role in the therapy of Alzheimer's disease."

Alzheimer's disease (AD) is a neurodegenerative disorder of progressive dementia that is characterized by the accumulation of beta-amyloid (Aβ)-containing neuritic plaques and intracellular Tau protein tangles. This distinctive pathology indicates that the protein quality control is compromised in AD. Autophagy functions as a "neuronal housekeeper" that eliminates aberrant protein aggregates by wrapping then into autophagosomes and delivering them to lysosomes for degradation. Several studies have suggested that autophagy deficits participate in the accumulation and propagation of misfolded proteins (including Aβ and Tau). In this review, we summarize current knowledge of autophagy in the pathogenesis of AD, as well as some pathways targeting the restoration of autophagy. Moreover, we discuss how these aspects can contribute to the development of disease-modifying therapies in AD.

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This article was published in the following journal.

Name: Current neuropharmacology
ISSN: 1875-6190
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Medical and Biotech [MESH] Definitions

Abnormal structures located chiefly in distal dendrites and, along with NEUROFIBRILLARY TANGLES and SENILE PLAQUES, constitute the three morphological hallmarks of ALZHEIMER DISEASE. Neuropil threads are made up of straight and paired helical filaments which consist of abnormally phosphorylated microtubule-associated tau proteins. It has been suggested that the threads have a major role in the cognitive impairment seen in Alzheimer disease.

A precursor to the AMYLOID BETA-PROTEIN (beta/A4). Alterations in the expression of the amyloid beta-protein precursor (ABPP) gene, located on chromosome 21, plays a role in the development of the neuropathology common to both ALZHEIMER DISEASE and DOWN SYNDROME. ABPP is associated with the extensive extracellular matrix secreted by neuronal cells. Upon cleavage, this precursor produces three proteins of varying amino acid lengths: 695, 751, and 770. The beta/A4 (695 amino acids) or beta-amyloid protein is the principal component of the extracellular amyloid in senile plaques found in ALZHEIMER DISEASE; DOWN SYNDROME and, to a limited extent, in normal aging.

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A progressive form of dementia characterized by the global loss of language abilities and initial preservation of other cognitive functions. Fluent and nonfluent subtypes have been described. Eventually a pattern of global cognitive dysfunction, similar to ALZHEIMER DISEASE, emerges. Pathologically, there are no Alzheimer or PICK DISEASE like changes, however, spongiform changes of cortical layers II and III are present in the TEMPORAL LOBE and FRONTAL LOBE. (From Brain 1998 Jan;121(Pt 1):115-26)

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