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

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 (H...

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Bibliographic Details
Published in:Frontiers in molecular neuroscience 2021-06, Vol.14, p.696476-696476
Main Authors: Andrade-Talavera, Yuniesky, Rodríguez-Moreno, Antonio
Format: Article
Language:English
Subjects:
Alzheimer's disease
Alzheimer’s disease models
Animal cognition
Brain research
Cognitive ability
Firing pattern
Hypotheses
Long-term depression
Long-term potentiation
Memory
Neurodegenerative diseases
Neuroplasticity
Neuroscience
Oscillations
Pathology
plasticity
Rhythm
spike timing-dependent plasticity
Synaptic plasticity
Synaptic strength
transcranial magnetic stimulation
β-Amyloid
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Summary: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.
ISSN:1662-5099
1662-5099
DOI:10.3389/fnmol.2021.696476