The effect of BAP31 on Alzheimer's disease

What is it about?

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder, which affects more than 30 million people worldwide. The clinical symptoms result from the deterioration of selective cognitive domains, together with impairments in behavior, language, and visuospatial skills, culminating in the premature death of the individual particularly those related to memory. These traits are accompanied by neuropathological features observed in postmortem AD brains, including a selective neuronal and synaptic loss in cortical and subcortical regions, deposition of extracellular senile plaques, mainly composed of amyloid β (Aβ) peptide, presence of intracellular neurofibrillary tangles (NFT) containing hyperphosphorylated tau protein, and cerebral amyloid angiopathy. The amyloid cascade hypothesis is the dominant explanation of AD etiology. It indicates that a chronic imbalance between production and clearance of Aβ peptides results in intracerebral accumulation of Aβ. This leads to a cascade of events that cause AD. Understanding the molecular mechanism by which affects the amyloidogenic pathway has been a long-standing goal of AD research.

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Why is it important?

The ER plays a key role in maintaining the cell homeostasis and directly influences protein folding and subsequently, ER stress and apoptosis. BAP31 is an essential component of the ER quality control (QC) system that prevents the export of misfolded and incompletely folded glycoproteins as well as non-glycosylated proteins. Here, we found that BAP31 was involved in the pathological process of AD by preventing both RTN3 aggregation and amyloid protein generation.

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