Gene therapy targeting synaptopathy linked with Alzheimer's and Parkinson's disease.

Synaptic Plasticity pertains to the synapse's tendency to adapt fresh information and is a crucial step in the establishment of brain circuits that aid in memory formation. It has become one of the most intensively researched topics in all of neuroscience. Pieces of evidence are accumulating that synaptopathy (altered synaptic plasticity) mechanisms contribute to Alzheimer's disease (AD) and Parkinson's disease (PD). Toxins responsible for synaptopathy and aberrant neurotransmitter (NT) release at synapses are the aggregates of amyloid-β (Aβ) (amyloidopathy) and hyperphosphorylated tau (tauopathy). Amyloidopathy and tauopathy contributes to synaptopathy in AD. Defective NT release at the synaptic interface generates various negative consequences related with changed activity of synaptic gene, proteins, and Ca