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Alzheimer's disease genes and autophagy
Abstract
Autophagy is a process to degrade and recycle cellular constituents via the lysosome for regulating cellular homeostasis. Its dysfunction is now considered to be involved in many diseases, including neurodegenerative diseases. Many features reflecting autophagy impairment, such as autophagosome accumulation and lysosomal dysfunction, have been also revealed to be involved in Alzheimer's disease (AD). Recent genetic studies such as genome-wide association studies in AD have identified a number of novel genes associated with AD. Some of the identified genes have demonstrated dysfunction in autophagic processes in AD, while others remain under investigation. Since autophagy is strongly regarded to be one of the major pathogenic mechanisms of AD, it is necessary to review how the AD-associated genes are related to autophagy. We anticipate our current review to be a starting point for future studies regarding AD-associated genes and autophagy. This article is part of a Special Issue entitled SI:Autophagy.
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Pathological proteins associated with familial Alzheimer's disease are either autophagy substrates, such as amyloid-β and tau, or linked to autophagy regulation, such as presenilin and clusterin.
“Moreover, pathological proteins associated with familial Alzheimer’s disease are either autophagy substrates, such as amyloid-β and tau, or linked to autophagy regulation, such as presenilin and clusterin [148].”
From Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases (2023) · cites this paper as [148]
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Metadata
- Authors
- Yoon, S.-Y., & Kim, D.-H.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2016-10
- Volume
- 1649
- Pages
- 201-209
- ISSN
- 0006-8993
- Cited by
- 42
- References
- 31
- Language
- en
- Funders
- Ministry of Science, ICT and Future Planning (2008-0062286)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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