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Protein Turnover Disruptions in Alzh...

Rao, Nalini R.,

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Protein Turnover Disruptions in Alzheimer's Disease and Aging: Levetiracetam Prevents Aβ42 Production Through SV2a-Dependent Modulation of App Processing in Alzheimer's Disease Models & Derailed Protein Turnover in the Aging Mammalian Brain /

Record Type:	Electronic resources : Monograph/item
Title/Author:	Protein Turnover Disruptions in Alzheimer's Disease and Aging: Levetiracetam Prevents Aβ42 Production Through SV2a-Dependent Modulation of App Processing in Alzheimer's Disease Models & Derailed Protein Turnover in the Aging Mammalian Brain // Nalini R Rao.
Author:	Rao, Nalini R.,
Description:	1 electronic resource (168 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 86-09, Section: B.
Contained By:	Dissertations Abstracts International86-09B.
Subject:	Neurosciences. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31765691
ISBN:	9798310149878

Protein Turnover Disruptions in Alzheimer's Disease and Aging: Levetiracetam Prevents Aβ42 Production Through SV2a-Dependent Modulation of App Processing in Alzheimer's Disease Models & Derailed Protein Turnover in the Aging Mammalian Brain /
Rao, Nalini R.,

Protein Turnover Disruptions in Alzheimer's Disease and Aging: Levetiracetam Prevents Aβ42 Production Through SV2a-Dependent Modulation of App Processing in Alzheimer's Disease Models & Derailed Protein Turnover in the Aging Mammalian Brain /Nalini R Rao. - 1 electronic resource (168 pages)

Source: Dissertations Abstracts International, Volume: 86-09, Section: B.

Disrupted protein homeostasis, or proteostasis, is a hallmark of neurodegenerative diseases (NDs) and aging, and represents the delicate balance between protein synthesis, folding, and degradation. Protein turnover, involving coordinated waves of synthesis and degradation, is crucial for maintaining this balance, particularly in post-mitotic cells, such as neurons, which cannot dilute damaged proteins with cell division. In NDs, such as Alzheimer's disease (AD), compromised proteostasis leads to the accumulation of pathological plaques and tangles, however, the early protein turnover dysfunctions that may contribute to disease progression are not well understood. Building on our initial discovery that presynaptic terminal proteins, specifically synaptic vesicle (SV) proteins, experience impaired degradation before amyloid-beta (Aβ) accumulation, we explored targeting this site of dysfunction to modulate AD pathology. We found that the SV-targeting drug, levetiracetam, alters SV dynamics and influences App processing, effectively preventing pathological Aβ production and synapse loss. Importantly, age is the most significant known risk factor for many NDs. While impaired protein turnover is clearly linked to age-related diseases, the proteome-wide changes in turnover during aging are less understood. Using an in vivo pulse-step metabolic labeling paradigm, we discovered that proteome-wide changes in turnover during aging are non-linear and exhibit sex-specific and cellular compartmental fluctuations, potentially resulting from reduced proteasome fidelity. These studies underscore the multifaceted roles of protein turnover in both the progression of NDs and during normal aging, offering new insights that could inform future therapeutic strategies.

English

ISBN: 9798310149878Subjects--Topical Terms:

588700
Neurosciences.
Subjects--Index Terms:

Neurodegenerative diseases

Protein Turnover Disruptions in Alzheimer's Disease and Aging: Levetiracetam Prevents Aβ42 Production Through SV2a-Dependent Modulation of App Processing in Alzheimer's Disease Models & Derailed Protein Turnover in the Aging Mammalian Brain /
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