Autophagy in Alzheimer's Disease and Its Models: Treatment Options
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 30 November 2024 | Viewed by 392
Special Issue Editor
Interests: brain ischemia versus Alzheimer's disease; brain ischemia; amyloid; tau protein; presenilins; α- and β-secretase; autophagy; mitophagy; apoptosis; apolipoproteins E, A1 and J; LRP1; RAGE; genes; neurodegeneration; dementia; Alzheimer's disease models
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Special Issue Information
Dear Colleagues,
Currently, Alzheimer's disease has become one of the most prevalent neurodegenerative diseases that seriously threaten the health and quality of life of older people. It is a disease characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain and the lack of causal treatment. The accumulation of amyloid plaques and neurofibrillary tangles ultimately leads to neuronal death. A natural process called autophagy occurs in the brain, and its task is to remove long-lived proteins, protein aggregates, folding proteins, dysfunctional cellular organelles and ultimately maintain cellular homeostasis. Moreover, autophagic mechanisms of cell apoptosis induced by amyloid have been revealed in Alzheimer's disease. Autophagy and apoptosis are the two main programmed mechanisms involved in neuronal death in Alzheimer's disease, and the balance between autophagy and apoptosis is essential for cellular homeostasis. The dysfunction of amyloid-induced autophagy has been found in late-stage Alzheimer's disease, causing autophagosome accumulation and amyloid deposition, which in turn promotes tau protein modifications, a neuroinflammatory response, and increases intracellular amyloid deposition, leading to neuronal apoptosis and the progression of Alzheimer's disease. The lysosomal autophagy pathway is believed to be one of the major amyloid degradation systems and is crucial in preventing amyloid deposition and pathological progression of Alzheimer's disease. It should also be mentioned that overactivated autophagy may also accelerate the cleavage of the amyloid protein precursor to form amyloid and increase its deposition. Therefore, by limiting the deposition of amyloid and modified tau protein in the brain through balanced autophagy activity, autophagy may reduce neurotoxicity in Alzheimer's disease. This points to one of many possible treatments for Alzheimer's disease, targeting amyloid and tau protein through autophagic degradation. Therefore, the study of the pathogenesis of autophagy and its prevention and treatment in Alzheimer's disease is of great practical importance for improving the quality of life of patients and reducing the burden of the disease on families and society. This Special Issue is intended to serve as a catalyst for further research into this important topic. This will be of great interest in the context of elucidating the behavior/balancing of autophagy activity in Alzheimer's disease and how and when to influence balanced autophagy activity with different therapeutic substances. This will allow us to better understand, in the future, which therapies may be most effective at specific points in the Alzheimer's disease continuum. I hope that each article on this topic will both expand knowledge and spark interest in autophagy, clarifying its role in the development of Alzheimer's disease and providing new insights for future treatment.
Prof. Dr. Ryszard Pluta
Guest Editor
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Keywords
- Alzheimer’s disease
- caenorhabditis elegans model of Alzheimer's disease
- transgenic models of Alzheimer's disease
- ischemic model of Alzheimer’s disease
- cells and mouse models of Alzheimer’s disease
- autophagy
- mitophagy
- amyloid
- tau protein
- necrosis
- apoptosis
- genes involved in Alzheimer’s disease
- dementia
- treatment
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