Proteomics

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Study of actin interactome in Alzheimers disease mouse model

ABSTRACT: Filamentous actin (F-actin) is one of the major cytoskeleton proteins present in dendritic spines and it is an essential component for defining dendritic spine morphology. We have shown that synaptosomal F-actin levels were significantly decreased in APP/PS1 mice as early as one month of age. The molecular mechanisms involved in F-actin loss in synaptosomes, the underlying factors and the functional consequence involved needs to be elucidated. Synaptic neurotransmission and synaptic plasticity are dependent on the dynamic regulation of the actin through actin interacting and actin-modulating proteins. F-actin nanoarchitecture is regulated by several factors, such as reactive oxygen species and cofilin and others that are present in the dendritic spines. Yet, the key players and their role in synaptosomal F-actin organization remains unknown. Here, we characterized actin interactome from wild type and APP/PS1 male mice.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain, Synapse

DISEASE(S): Alzheimer's Disease

SUBMITTER: Reddy Peera Kommaddi  

LAB HEAD: Reddy Peera Kommaddi

PROVIDER: PXD050802 | Pride | 2024-10-17

REPOSITORIES: Pride

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Dataset's files

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Action DRS
APPPS1_1.zip Other
APPPS1_1_DAT.zip Other
APPPS1_2.zip Other
APPPS1_2_DAT.zip Other
APPPS1_3.dat Other
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Publications

Mitigation of synaptic and memory impairments via F-actin stabilization in Alzheimer's disease.

P A Haseena H   Basavaraju Nimisha N   Chandran Mahesh M   Jaleel Abdul A   Bennett David A DA   Kommaddi Reddy Peera RP  

Alzheimer's research & therapy 20240907 1

<h4>Background</h4>Synaptic dysfunction, characterized by synapse loss and structural alterations, emerges as a prominent correlate of cognitive decline in Alzheimer's disease (AD). Actin cytoskeleton, which serves as the structural backbone of synaptic architecture, is observed to be lost from synapses in AD. Actin cytoskeleton loss compromises synaptic integrity, affecting glutamatergic receptor levels, neurotransmission, and synaptic strength. Understanding these molecular changes is crucial  ...[more]

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