Cited by 774Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Molecular mechanisms of neurodegeneration in Alzheimer's disease

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Crews, L., Masliah, E.·2010·Human Molecular Genetics

DOI 10.1093/hmg/ddq160PMC PMC2875049

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Abstract

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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“Amyloid plaques result from abnormal processing, excessive production, aggregation and improper clearance of the amyloid precursor protein (APP) [13, 14].”
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“(1-42)-induced proinflammatory cytokines in a primary microglia cell culture and the B92 rat microglia continuous cell line, using”
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“As a result of cytosolic calcium excess, p35 breaks into p25, which activates CDK5 and causes tau hyperphosphorylation (Crews & Masliah, 2010).”
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“Instead, in patients with Alzheimer's dementia, alterations of the neurotransmitter systems and the signal transduction mechanism are very frequent, altering the cholinergic signaling system, and the production of the neurotransmitter acetylcholine (Crews & Masliah, 2010).”
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“…extracellular amyloid deposits (senile plaques) containing misfolded amyloid-β (Aβ) peptides and (2) intracellular aggregates of hyperphosphorylated tau protein forms (neurofibrillary tangles) (Butterfield and Lauderback, 2002; Crews and Masliah, 2010; DeTure and Dickson, 2019; Price et al., 1991).”
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“For example, the brains of patients with Alzheimer’s disease (AD), a complex chronic neurodegenerative disease, exhibit significant neuronal loss along with proliferation of microglia and astrocytes [1–3].”
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“The etiology of AD is multifaceted, with prominent hypotheses including the amyloid cascade theory triggered by the deposition of amyloid-beta protein (Aβ) [1], tau protein hyperphosphorylation [2], cholinergic neuronal degeneration [3], oxidative stress [4], and neuroinflammation [5], among others.”
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Authors: Crews, L., & Masliah, E.
Affiliations: University of California San Diego (US)
Corresponding author: Masliah, E.
ORCID: Crews, L.
Masliah, E.
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
DOI: 10.1093/hmg/ddq160
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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