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Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions
Open accessAbstract
The amyloid hypothesis of Alzheimer’s disease has long been the predominant theory, suggesting that Alzheimer’s disease is caused by the accumulation of amyloid beta protein (Aβ) in the brain, leading to neuronal toxicity in the central nervous system (CNS). Because of breakthroughs in molecular medicine, the amyloid pathway is thought to be central to the pathophysiology of Alzheimer’s disease (AD). Currently, it is believed that altered biochemistry of the Aβ cycle remains a central biological feature of AD and is a promising target for treatment. This review provides an overview of the process of amyloid formation, explaining the transition from amyloid precursor protein to amyloid beta protein. Moreover, we also reveal the relationship between autophagy, cerebral blood flow, ACHE, expression of LRP1, and amyloidosis. In addition, we discuss the detailed pathogenesis of amyloidosis, including oxidative damage, tau protein, NFTs, and neuronal damage. Finally, we list some ways to treat AD in terms of decreasing the accumulation of Aβ in the brain.
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“The amyloid hypothesis emphasizes that the accumulation of Aβ plaques in the brain is a central event in the pathogenesis of AD, leading to neurodegeneration and cognitive decline.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [11]
In the citing paper
“The hydrophobic C-terminus of Aβ42 facilitates its aggregation and the formation of senile plaques.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [11]
In the citing paper
“Aβ originates from the processing of the amyloid precursor protein (APP) through sequential cleavage by β-secretase and γ-secretase, resulting in various lengths of Aβ fragments, with Aβ40 and Aβ42 being predominant.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [11]
In the citing paper
“However, the relationship between FAD mutations and Aβ levels is complex, and the plaque formation in sporadic AD is influenced by a dynamic imbalance between Aβ production and clearance mechanisms [11,12].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [11]
In the citing paper
“Mutations in presenilin-1 (PS1) can promote Aβ accumulation through increased production and impaired autophagy functions.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [11]
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Metadata
- Authors
- Ma, C., Hong, F., & Yang, S.
- Affiliations
- Nanchang University (CN)
- Experimental Center of Pathogen Biology, Nanchang University, Nanchang 330006, China
- Department of Physiology, College of Medicine, Nanchang University, Nanchang 330006, China
- ORCID
- Ma, Chen
- Venue
- Molecules
- Publisher
- MDPI AG
- Published
- 2022-02-11
- Volume
- 27
- Issue
- 4
- Pages
- 1210
- ISSN
- 1420-3049 (ISSN-L)
- PMC
- PMC8876037
- OpenAlex
- W4212889165
- Cited by
- 243
- References
- 83
- Citations by year
- 2026: 51 · 2025: 80 · 2024: 65 · 2023: 36 · 2022: 11
- FWCI
- 6.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Molecules (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- the National Natural Science Foundation of China (82060661,81660151 and 81660751)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloidosis, amyloid hypothesis, amyloid-beta, amyloid precursor protein, amyloid fibril formation, autophagy, cerebral blood flow, acetylcholinesterase, LRP1, oxidative damage, tau protein, neurofibrillary tangles, neuronal injury, Alzheimer's disease treatment
- MeSH terms
- Alzheimer Disease, Amyloid, Amyloidosis, Animals, Autophagy, Brain, Disease Susceptibility, Gene Expression Regulation, Humans, Risk Factors, Biomarkers, Amyloid beta-Peptides, Disease Management, Plaque, Amyloid
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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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