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Amyloid cascade hypothesis: Pathogenesis and therapeutic strategies in Alzheimer's disease
Abstract
Alzheimer's disease is an irreversible, progressive neurodegenerative disorder. Various therapeutic approaches are being used to improve the cholinergic neurotransmission, but their role in AD pathogenesis is still unknown. Although, an increase in tau protein concentration in CSF has been described in AD, but several issues remains unclear. Extensive and accurate analysis of CSF could be helpful to define presence of tau proteins in physiological conditions, or released during the progression of neurodegenerative disease. The amyloid cascade hypothesis postulates that the neurodegeneration in AD caused by abnormal accumulation of amyloid beta (Aβ) plaques in various areas of the brain. The amyloid hypothesis has continued to gain support over the last two decades, particularly from genetic studies. Therefore, current research progress in several areas of therapies shall provide an effective treatment to cure this devastating disease. This review critically evaluates general biochemical and physiological functions of Aβ directed therapeutics and their relevance.
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“Apart from the genetic mutations, many neuropeptides are likely to be involved in the formation of the plaque for e.g. low levels of corticotrophin-releasing hormone (CRH), somatostatin and neuropeptide Y levels whereas higher levels of Angiotensin II are likely to be involved in either irregular cleavage of the APP or impaired removal of Aβ1-42 fragment [2].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [2]
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“The Aβ plaque comprises of Aβ peptides obtained from amyloid precursor protein (APP) by the enzymatic cleavage via secretases (α, β and γ) [2].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [2]
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Metadata
- Authors
- Barage, S. H., & Sonawane, K. D.
- Affiliations
- Shivaji University (IN)
- Corresponding author
- Sonawane, Kailas D.
- Venue
- Neuropeptides
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 52
- Pages
- 1-18
- ISSN
- 0143-4179 (ISSN-L)
- OpenAlex
- W2099751992
- Cited by
- 579
- References
- 371
- Citations by year
- 2026: 22 · 2025: 57 · 2024: 75 · 2023: 69 · 2022: 58 · 2021: 67 · 2020: 59 · 2019: 58 · 2018: 51 · 2017: 33 · 2016: 24 · 2015: 5
- FWCI
- 4.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropeptides (publishedVersion)
- PubMed (publishedVersion)
- 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
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Keywords
- Alzheimer's disease, amyloid hypothesis, amyloid-beta, amyloid plaques, tau protein, cerebrospinal fluid biomarkers, cholinergic neurotransmission, neurodegeneration, Alzheimer's disease therapeutics, genetic risk factors
- MeSH terms
- Acetylcholine, Alzheimer Disease, Animals, Brain, Humans, Signal Transduction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, tau Proteins
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