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Cited by 39Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeural dynamics and brain function

Synaptic Plasticity and Oscillations in Alzheimer’s Disease: A Complex Picture of a Multifaceted Disease

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Andrade-Talavera, Yuniesky, Rodríguez-Moreno, Antonio·2021·Frontiers in Molecular Neuroscience
DOI 10.3389/fnmol.2021.696476PMC PMC8248350
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Abstract

Brain plasticity is widely accepted as the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). By using diverse induction protocols like high-frequency stimulation (HFS) or spike-timing dependent plasticity (STDP), such crucial cognition-relevant plastic processes are shown to be impaired in Alzheimer’s disease (AD). In AD, the severity of the cognitive impairment also correlates with the level of disruption of neuronal network dynamics. Currently under debate, the named amyloid hypothesis points to amyloid-beta peptide 1–42 (Aβ42) as the trigger of the functional deviations underlying cognitive impairment in AD. However, there are missing functional mechanistic data that comprehensively dissect the early subtle changes that lead to synaptic dysfunction and subsequent neuronal network collapse in AD. The convergence of the study of both, mechanisms underlying brain plasticity, and neuronal network dynamics, may represent the most efficient approach to address the early triggering and aberrant mechanisms underlying the progressive clinical cognitive impairment in AD. Here we comment on the emerging integrative roles of brain plasticity and network oscillations in AD research and on the future perspectives of research in this field.

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  • 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.

    “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 [87]

    The Introduction (page unavailable) says functional and network changes can precede cognitive deficits and argues for earlier intervention. The Discussion (page unavailable) describes EEG and TMS–EEG as ways to assess connectivity and plasticity, but the retrieved passages do not support detection through functional imaging. The Introduction also cautions that some forms of plasticity appear affected only at later stages. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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Cited by

Sorted by citations

Authors
Andrade-Talavera, Y., & Rodríguez-Moreno, A.
Venue
Frontiers in Molecular Neuroscience
Publisher
Frontiers Media SA
Published
2021-06-17
Volume
14
Pages
696476-696476
ISSN
1662-5099 (ISSN-L)
DOI
10.3389/fnmol.2021.696476
PMC
PMC8248350
OpenAlex
W3174400192
Cited by
39
References
9
Citations by year
2026: 6 · 2025: 10 · 2024: 11 · 2023: 4 · 2022: 7 · 2021: 1
FWCI
3.52
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • RIO (Universidad Pablo de Olavide) (submittedVersion, cc-by-nc-nd)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Ministerio de Economía, Industria y Competitividad, Gobierno de España
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
Alzheimer's disease, synaptic plasticity, neuronal network oscillations, long-term potentiation, long-term depression, spike-timing-dependent plasticity, high-frequency stimulation, amyloid-beta, amyloid-beta 42, neuronal network dynamics, cognitive impairment, synaptic dysfunction

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