Unscrambling the cellular and molecular threads of Neuroplasticity: Insights into Alzheimer’s disease pathogenesis

Abstract

Alzheimer’s disease (AD) is predominantly the most recurring and devastating neurological condition among the elderly population, characterized by the accumulation of amyloid-β (Aβ) and phosphorylated tau proteins, and is accompanied by progressive decline of learning and memory. Due to its complex and multifactorial etiology, a wide variety of therapeutic interventions have been developed. Despite constant advancements in the field, effective treatments that ameliorate the severity of Alzheimer’s symptoms or cease their progression are still insufficient. Mounting evidence suggests that synaptic dysfunction could be an essential component of AD pathogenesis as synapse signaling is impaired in the aging brain, which contributes to synaptic decline. Therefore, improving neuroplasticity such as synaptic plasticity or neurogenesis could be a promising therapeutic approach for alleviating the effects of AD. This article reviews the cellular and molecular threads of neuroplasticity as well as targets that restore neuronal survival and plasticity to provide functional recoveries, including receptors, downstream signaling pathways, ion channels, transporters, enzymes, and neurotrophic factors.