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Updated: Jan 14, 2026

Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
Published on: February 18, 2014
Tubular ER dysfunction in neurodegenerative diseases
Md Golam Sharoar1, Riqiang Yan2
1Alzheimer's disease Research Program, Corewell Health Research Institute (CHRI), Corewell Health East, 3811 W 13 Mile Road, Royal Oak, MI 48073, United States of America; Department of Internal Medicine, Oakland University William Beaumont School of Medicine (OUWB), Corewell Health East, 3811 W 13 Mile Road, Royal Oak, MI 48073, United States of America.
Abstract:
Endoplasmic reticulum (ER) is the largest secretory organelle, and it regulates diverse cellular processes to support neuronal growth, development, and maintenance during the lifespan. Structural alterations to the ER network affect a multitude of functions and downstream events, which result in abnormalities in neuronal maintenance and neuronal death. Morphological and functional abnormalities in the tubular domain of ER or in tubular ER proteins have been linked to several major neurodegenerative diseases, including Alzheimer's disease (AD) and hereditary spastic paraplegias (HSPs). Tubular ER dysfunction in neurodegenerative diseases is manifested by elevated expression, abnormal aggregation, haplo-insufficiency, or functional deficiency in multiple ER tubule-shaping proteins. This review aims to highlight the involvement of ER tubule shaping and networking proteins that cause tubular ER dysfunction in AD and HSPs. The discussion of this review will also highlight the functional necessity of an integrated tubular ER network for axonal maintenance.
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