Neuroplasticity in Alzheimer's disease
Open accessAbstract
Ramon y Cajal proclaimed in 1928 that “once development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably. In the adult centers the nerve paths are something fixed, ended and immutable. Everything must die, nothing may be regenerated. It is for the science of the future to change, if possible, this harsh decree.” (Ramon y Cajal, 1928). In large part, despite the extensive knowledge gained since then, the latter directive has not yet been achieved by ‘modern’ science. Although we know now that Ramon y Cajal's observation on CNS plasticity is largely true (for lower brain and primary cortical structures), there are mechanisms for recovery from CNS injury. These mechanisms, however, may contribute to the vulnerability to neurodegenerative disease. They may also be exploited therapeutically to help alleviate the suffering from neurodegenerative conditions. Published 2002 Wiley‐Liss, Inc.
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Aβ aggregates bind to neuronal and glial membranes, disrupting membrane integrity and receptor function.
“Mechanistically, Aβ aggregates bind to neuronal and glial membranes, disrupting membrane integrity and receptor function.”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [86]
Section 5.4 (page unavailable) says Aβ can alter membrane potential and synaptic transmission, supporting a general effect on neuronal function. It does not say that Aβ aggregates bind neuronal and glial membranes or that they disrupt membrane integrity or receptor function; those specific mechanisms are unsupported. (LLM, conf=0.83)
Experimental — accuracy not yet measuredEarly alterations in connectivity and plasticity, detectable through functional imaging or electrophysiological biomarkers, may precede clinical symptoms and represent a window of opportunity for intervention.
“Moreover, early alterations in connectivity and plasticity, detectable through functional imaging or electrophysiological biomarkers, may precede clinical symptoms and represent a window of opportunity for intervention [86, 87].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [86]
Section 3.3 describes altered plasticity-related proteins in early Alzheimer’s disease, and Section 10.1 discusses therapies targeting plasticity. The paper does not establish that connectivity or plasticity changes detectable by functional imaging or electrophysiological biomarkers precede clinical symptoms, or that such detection defines an intervention window. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAβ triggers maladaptive changes including activation of microglia and astrocytes with release of inflammatory cytokines, impaired glutamate clearance leading to excitotoxicity, and aberrant NMDA receptor hyperactivation.
“This triggers a cascade of maladaptive changes, such as (i) activation of microglia and astrocytes with release of inflammatory cytokines, (ii) impaired glutamate clearance leading to excitotoxicity, and (iii) aberrant NMDA receptor hyperactivation [86].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [86]
Section 5.4 (page unavailable) describes Aβ as neurotoxic and disruptive to synaptic activity. Section 2.4 (page unavailable) says activated microglia and astrocytes can inhibit neurite outgrowth and that glia secrete cytokines. Neither passage establishes that Aβ activates those cells to release inflammatory cytokines, impairs glutamate clearance, or hyperactivates NMDA receptors. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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Self-citation
- Authors
- Teter, B., & Ashford, J. W.
- Affiliations
- University of California, Los Angeles (US)
- University of Kentucky (US)
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2002-10-18
- Volume
- 70
- Issue
- 3
- Pages
- 402-437
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W1985802666
- Cited by
- 170
- References
- 40
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 7 · 2023: 9 · 2022: 28 · 2021: 4 · 2019: 20 · 2018: 3 · 2017: 5 · 2015: 7 · 2014: 4 · 2013: 4 · 2012: 7
- FWCI
- 0.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (K01AG000962)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neuroplasticity, Alzheimer's disease, neurodegeneration, central nervous system injury
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Brain, Estrogens, Humans, Neural Pathways, Neuronal Plasticity, Amyloid beta-Peptides, tau Proteins, Growth Cones
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