Cited by 78Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

The DOI matches its Crossref record; 150 of the 156 references it cites were found in a registry or an index.

Cycles of Aberrant Synaptic Sprouting and Neurodegeneration in Alzheimer's and Dementia with Lewy Bodies

Hashimoto, Makoto, Masliah, Eliezer·2003·Neurochemical Research

Abstract

Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the most common neurodegenerative disorders affecting the elderly. The cognitive and motor deficits in these diseases are associated with the disruption of neuritic substructure, loss of synaptic contacts in selectively vulnerable circuitries, and aberrant sprouting. Where as in AD, accumulation of misfolded forms of Abeta triggers neurodegeneration, in DLB accumulation of alpha-synuclein might play a central role. The mechanisms by which oligomeric forms of these proteins might lead to cycles of synapse loss and aberrant sprouting are currently under investigation. Several possibilities are being considered, including mitochondrial damage, caspase activation, lysosomal leakage, fragmentation of the Golgi apparatus, interference with synaptic vesicle transport and function, and interference with gene transcription and signaling. Among them, recent lines of research support the possibility that alterations in signaling pathways such extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 relevant to synaptic plasticity and cell survival might play a pivotal role. A wide range of cellular functions are affected by the accumulation of misfolded Abeta and alpha-synuclein; thus it is possible that a more fundamental cellular alteration may underlie the mechanisms of synaptic pathology in these disorders. Among them, one possibility is that scaffold proteins, such as caveolin and JNK-interac…

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Crossref · 10.1023/a:1026073324672

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Research works printed but not linked: 9

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Metadata

Authors
Hashimoto, M., & Masliah, E.
Affiliations
University of California San Diego (US)
Corresponding author
Masliah, Eliezer
Venue
Neurochemical Research
Published
2003-11
Volume
28
Issue
11
Pages
1743-1756
ISSN
  • 0364-3190 (ISSN-L)
  • 1573-6903
OpenAlex
W321625949
Cited by
78
References
156
Citations by year
2025: 1 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 2
FWCI
2.30
Type
journal article
Language
en
Open access
closed
Locations
  • Neurochemical Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r29ag010869-05)
  • National Institute on Aging (P50AG005131, AG-5131, AG 18440, AG10869)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
Alzheimer's disease, dementia with Lewy bodies, synaptic loss, neurodegeneration, amyloid-beta, alpha-synuclein, protein oligomers, ERK signaling, JNK signaling, p38 MAPK, caveolin, synaptic plasticity, mitochondrial damage, Golgi fragmentation, synaptic vesicle transport, axonal plasticity
MeSH terms
Alzheimer Disease, Animals, Humans, Memory Disorders, Nerve Degeneration, Nerve Tissue Proteins, Neural Pathways, Synaptic Transmission, Neuronal Plasticity, Amyloid beta-Peptides, Neurites, Lewy Body Disease, Synucleins, alpha-Synuclein

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