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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Effects of multi-mode physical stimulation on APP/PS1 Alzheimer's disease model mice
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Meshref, M. M., Ghaith, H. S., Hammad, M. A., Shalaby, M. M. M., Ayasra, F., Monib, F. A., Attia, M. S., Ebada, M. A., Elsayed, H., Shalash, A., et al. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03802-0 · Cited by 12
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“In addition to neuritic plaque (NP) and neurofibrillary tangles, the insoluble aggregation of Aβ can trigger peripheral microglia infiltration, which in turn leads to the continuous secretion of inflammatory factors and further aggravates degenerative neuronal injury (22).”
Background
Protein Kinase C Involvement in Neuroprotective Effects of Thymol and Carvacrol Against Toxicity Induced by Amyloid-β in Rat Hippocampal Neurons
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“One of these pathways includes Protein Kinase C (PKC), a central kinase in intracellular signal transduction (Crews & Masliah, 2010; LuckeWold et al., 2015).”
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Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach
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“…disease (AD) was first described by German neuro-psychiatrist Alois Alzheimer in 1906, and till today it represents the most common form of dementia in the elderly—a progressive, neurodegenerative disease characterized by synaptic alterations, neuronal loss, and cognitive dysfunction [1].”
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“Alzheimer's disease (AD), with the clinical manifestation characterized by cognitive disorder and memory dysfunction, is the most common form of senile dementia [1].”
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“The etiology of this condition is multifactorial inﬂuenced by the genetic background, sex, environment, and injury, among other factors [2].”
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“Monomeric Aβ aggregates into oligomers and protofibrils, while insoluble amyloid beta-fibril aggregates form amyloid plaques that interfere with signaling at the synapse (Chen and Yan, 2010; Crews and Masliah, 2010).”
Background
Monoterpenes and Diterpenes in Combating Alzheimer Disease, Mechanisms, and Clinical Insights: A Comprehensive Review
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Optimizing Diagnosis and Management in mild-to-moderate Alzheimer’s Disease
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“The tau hypothesis suggests that accumulation of hyperphosphorylated tau as paired helical filaments within neurofibrillary tangles and in neuritic processes is linked to neuronal dysfunction and death [3, 4].”
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Regulation of extracellular Zn2+homeostasis in the hippocampus as a therapeutic target for Alzheimer’s disease
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“Individuals with MCI have 32% fewer neurons in the entorhinal cortex and show synaptic loss in the dentate gyrus, which correlates with cognitive deficits [66-68].”
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Markers of Alzheimer’s Disease in Primary Visual Cortex in Normal Aging in Mice
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“It has been demonstrated that an abnormal increase in p-Tau affects the normal functioning ofmicrotubules, impairs intracellular communication, and, finally, induces cell death [31, 32].”
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Epigenetic processes in Alzheimer's disease
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“Investigations support the notion that the synaptic pathology and defective neurogenesis in AD are related to progressive accumulation of Aβ oligomers rather than fibrils (Leslie and Eliezer, 2010).”
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“AD is characterized pathologically by the extracellular accumulation of beta-amyloid neurite plaques and intra-cellular formation of phosphorylated tau neurofibrillary tangles ( Crews & Masliah, 2010; Perl, 2010).”
Background
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“Dys-regulated Aβ plaque clearance and subsequent inflammation are the classic pathological mechanism of neurodegeneration in AD, inducing oxidative stress and activating neuronal apoptotic pathways [93].”
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“Stable microglial- astrocyte-neuronal structure and function are critical for normal neurocognitive function (Bano et al., 2011; Brundel et al., 2012 ; Crews & Masliah, 2010 ; Jellinger & Stadelmann, 2001 ; Okouchi et al., 2007 ).”
Background
Mapping Molecular Association Networks of Nervous System Diseases via Large-Scale Analysis of Published Research
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“Again, these findings are supported by other research [13,15,16].”
Result
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Self-citation
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Pyroglutamate-Amyloid-β and Glutaminyl Cyclase Are Colocalized with Amyloid-β in Secretory Vesicles and Undergo Activity-Dependent, Regulated Secretion
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“AD is characterized by pathological changes that include amyloid-β (Aβ) deposition, marked neuronal loss, and tau hyperphosphorylation (Gomez-Isla et al., 1996; Scheff et al., 2006; Crews and Masliah, 2010).”
Background
Nonselective Cation Channels and Links to Hippocampal Ischemia, Aging, and Dementia
MacDonald, J. F., Belrose, J. C., Xie, Y., & Jackson, M. F. (2012) · Advances in experimental medicine and biology · doi:10.1007/978-1-4614-4756-6_37 · Cited by 8
Uncontrolled SFK-mediated protein trafficking in prion and Alzheimer's disease
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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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Molecular mechanisms of neurodegeneration in Alzheimer's disease

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