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Molecular mechanisms of neurodegeneration in Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-beta (Abeta)-containing plaques and neurofibrillary tangles composed of hyperphosphorylated tau. The neurodegenerative process in AD is initially characterized by synaptic damage accompanied by neuronal loss. In addition, recent evidence suggests that alterations in adult neurogenesis in the hippocampus might play a role. Synaptic loss is one of the strongest correlates to the cognitive impairment in patients with AD. Several lines of investigation support the notion that the synaptic pathology and defective neurogenesis in AD are related to progressive accumulation of Abeta oligomers rather than fibrils. Abnormal accumulation of Abeta resulting in the formation of toxic oligomers is the result of an imbalance between the levels of Abeta production, aggregation and clearance. Abeta oligomers might lead to synaptic damage by forming pore-like structures with channel activity; alterations in glutamate receptors; circuitry hyper-excitability; mitochondrial dysfunction; lysosomal failure and alterations in signaling pathways related to synaptic plasticity, neuronal cell and neurogenesis. A number of signaling proteins, including fyn kinase; glycogen synthase kinase-3beta (GSK3beta) and cyclin-dependent kinase-5 (CDK5), are involved in the neurodegenerative progression of AD. Therapies for AD might require the development of anti-aggregation compounds, pro-clearance pathways and blockers of hyperactive signaling pathways.
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“Due to cytosolic calcium overload, p35 splits into p25, which hyperactivates cyclin-dependent kinase-5 (CDK5) and leads to hyper phosphorylation of tau [6].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [6]
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Cites
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
The Ki-67 protein: From the known and the unknown
Scholzen, T. E., & Gerdes, J. (2000) · Journal of Cellular Physiology · doi:10.1002/(sici)1097-4652(200003)182:3 · Cited by 4,707
Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397
Self-citationCorrelative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Vassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A., Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., et al. (1999) · Science · doi:10.1126/science.286.5440.735 · Cited by 3,876
Shankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
More hippocampal neurons in adult mice living in an enriched environment
Kempermann, G., Kuhn, H. G., & Gage, F. H. (1997) · Nature · doi:10.1038/386493a0 · Cited by 3,586
Mechanisms and Functional Implications of Adult Neurogenesis
Zhao, C., Deng, W., & Gage, F. H. (2008) · Cell · doi:10.1016/j.cell.2008.01.033 · Cited by 3,007
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
Self-citationLee, V. M.-Y., Goedert, M., & Trojanowski, J. Q. (2001) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.24.1.1121 · Cited by 2,480
Research works printed but not linked: 9
- 1998, Trends in cell biology, 8, 125
- 2004, 127, 601
- 1997, 19, 939
- 2003, 37, 925
- 2006, 52, 831
- 2007, 55, 697
- Smith, 2001, Cell Growth & Differentiation, 12, 277
- 1997, 18, 29
- 2005, 48, 825
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Sepulveda-Diaz, J. E. (2013) · theses.fr (ABES) · doi:10.70675/56c42bcbz41dfz432bzbb78z77110b373285
Montecinos-Oliva, C. (2018) · theses.fr (ABES) · doi:10.70675/1cb0a505zb904z4045z83b4z7ec8f3bc62b9
Karameh, N. (2018) · theses.fr (ABES) · doi:10.70675/b70b7c03z8de8z4ee0z9848z381e95568515
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O’Brien, K., & Blair, P. (2026) · Springer eBooks · doi:10.1007/978-3-032-14521-5_9
Mahajan, S. (2026) · Glycobiology · doi:10.1093/glycob/cwag063
Momand, M. U. D., Macová, K., & Fričová, D. (2026) · Aging Cell · doi:10.1111/acel.70719
Vyas, C. M., Ostaszewski, B. L., Anderson, A. K., Cook, N. R., Kang, J. H., Mischoulon, D., Reynolds, C. F., Chang, G., Gatchel, J. R., Manson, J. E., et al. (2026) · Alzheimer s & Dementia Translational Research & Clinical Interventions · doi:10.1002/trc2.70312
Li, X., Rong-liang, G., Teng, Z., Liu, P.-P., & Liu, C. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103377
Richetti, S. K. (2010) · Americanae (AECID Library)
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Metadata
- Authors
- Crews, L., & Masliah, E.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Masliah, E.
- ORCID
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-04-15
- Volume
- 19
- Issue
- R1
- Pages
- R12-R20
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- PMC
- PMC2875049
- OpenAlex
- W2135957529
- Cited by
- 772
- References
- 175
- Citations by year
- 2026: 33 · 2025: 53 · 2024: 56 · 2023: 71 · 2022: 48 · 2021: 76 · 2020: 69 · 2019: 50 · 2018: 47 · 2017: 47 · 2016: 42 · 2015: 34 · 2014: 31 · 2013: 35 · 2012: 40
- FWCI
- 3.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Human Molecular Genetics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (AG5131, NS4 4233, AG‐18440, AG10435, AG11385)
- National Institute on Aging (P01AG010435, AG-11385, P50AG005131, AG-5131, AG 18440, AG10435)
- National Institute of Neurological Disorders and Stroke (P01NS044233, NS-44233)
- 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, neurodegeneration, amyloid-beta oligomers, amyloid plaques, tau hyperphosphorylation, neurofibrillary tangles, synaptic loss, adult hippocampal neurogenesis, glutamate receptors, excitotoxicity, mitochondrial dysfunction, lysosomal dysfunction, synaptic plasticity, Fyn, glycogen synthase kinase-3β, cyclin-dependent kinase 5, anti-aggregation therapy, amyloid-beta clearance
- MeSH terms
- Alzheimer Disease, Humans, Amyloid beta-Peptides, Neurogenesis
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