aplasticity

Aplasticity is the reduced or absent capacity of a biological system to undergo plastic changes in response to experience, stimulation, or injury. In neuroscience, plasticity refers to the brain’s ability to modify synaptic connections and neural networks. Aplasticity thus describes conditions in which those adaptive changes are diminished compared with typical levels of plasticity. It is not a single disease but a state that can arise from aging, pathology, or damage to neural circuits.

In the nervous system, examples of aplasticity include attenuated synaptic potentiation and decreased structural remodeling after learning or rehabilitation. Age-related declines in synaptic efficacy, reduced long-term potentiation (LTP) or long-term depression (LTD) in certain brain regions, and impaired activity-dependent rewiring after stroke or spinal cord injury are cited in discussions of aplasticity. Neurodegenerative diseases such as Alzheimer’s disease can also involve impaired plastic responses, contributing to cognitive or motor deficits.

Mechanisms implicated in aplasticity include altered NMDA receptor function, changes in brain-derived neurotrophic factor (BDNF) signaling, disrupted excitatory–inhibitory balance, and reduced capacity for dendritic or synaptic remodeling. Metaplasticity, or the modulation of plasticity itself by prior activity, can also affect the expression of plastic changes, potentially contributing to anaplastic outcomes under certain conditions or during chronic stimulation.

Implications and approaches: aplasticity can constrain recovery after brain injury and limit adaptation to environmental changes. Interventions aiming to counteract aplasticity include pharmacological agents that enhance plasticity, noninvasive brain stimulation, intensive task-specific training, and aerobic exercise, often used in rehabilitation to promote reorganization and functional gains. Research continues to clarify when and how plasticity can be revived or supported.