Alzheimer's disease, traumatic brain injury, and chronic traumatic encephalopathy represent conditions that have a profound socioeconomic impact for both the individual and the wider community. They are all characterized by specific protein aggregation that results in synaptic dysfunction, neuronal death, and consequent cognitive decline and memory loss. In this review, we present evidence to support the notion that the common pathologies found in all conditions, and indeed their associated cognitive deficits, may be linked by zinc (Zn²⁺) ion dyshomeostasis. Elucidation of this hypothesis may present new therapeutic avenues for these devastating conditions.
Keywords: Alzheimer’s disease; TDP-43; amyloid-β; brain injury; cognition; tau protein; zinc.