RT Journal Article
T1 Synaptic Plasticity and Oscillations in Alzheimer's Disease: A Complex Picture of a Multifaceted Disease
T2 Plasticity and Oscillations Role in AD
A1 Andrade Talavera, Yuniesky
A1 Rodríguez-Moreno, Antonio
K1 Alzheimer’s disease
K1 Alzheimer’s disease models
K1 0scillations
K1 Plasticity
K1 Spike timing-dependent plasticity
K1 Transcranial magnetic stimulation
AB 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.
PB Frontiers
YR 2021
FD 2021
LK https://hdl.handle.net/10433/23719
UL https://hdl.handle.net/10433/23719
LA en
NO Departamento de Fisiología, Anatomía y Biología Celular
DS RIO
RD May 26, 2026