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Updated: May 6, 2026
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Assessing Lysosomal Alkalinization in the Intestine of Live Caenorhabditis elegans
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Autophagic/lysosomal dysfunction in Alzheimer's disease
Miranda E Orr1, Salvatore Oddo2
1Department of Physiology and The Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Alzheimer'S Research & Therapy
|November 1, 2013
Summary
Autophagic dysfunction contributes to Alzheimer's disease (AD) by causing toxic buildup. Restoring the autophagy pathway offers potential therapeutic strategies for AD.
Area of Science:
- Neurobiology
- Cellular Biology
- Pathology
Background:
- Autophagy is the primary cellular process for degrading damaged organelles and misfolded proteins.
- Dysfunctional autophagy is increasingly linked to neurodegenerative diseases, including Alzheimer's disease (AD).
- The autophagic/lysosomal system normally recycles cellular components but impaired function leads to toxic accumulation.
Purpose of the Study:
- To review the role of autophagic/lysosomal dysfunction in Alzheimer's disease pathogenesis.
- To identify potential therapeutic targets within the autophagy pathway for AD treatment.
Main Methods:
- Literature review of current research on autophagy and AD.
- Analysis of the molecular mechanisms linking autophagic dysfunction to amyloid-beta production.
- Exploration of therapeutic strategies targeting the autophagic/lysosomal pathway.
Main Results:
- Impaired autophagy leads to the accumulation of protein aggregates and dysfunctional vesicles.
- These vesicles contain enzymes capable of generating amyloid-beta, a key component of AD plaques.
- Autophagic dysfunction contributes significantly to the progression of Alzheimer's disease.
Conclusions:
- Autophagic/lysosomal pathway dysfunction is a critical factor in Alzheimer's disease.
- Targeting and restoring this pathway presents a promising therapeutic avenue for AD.
- Further research into modulating autophagy holds potential for novel AD treatments.
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