Synaptic loss is the strongest correlate of cognitive decline in Alzheimer's disease, and preserving synaptic function has emerged as a critical therapeutic strategy. AAIC 2026 features extensive programming on synaptic biology, including mechanisms of synaptic degeneration, protective interventions, and synaptic resilience approaches["@selkoe2024"].
Key Topics
Synaptic Vulnerability Mechanisms
Pre-Synaptic Terminal Dysfunction
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Conference: AAIC 2026 | Dates: July 12-15, 2026 | Location: Excel London, UK
Overview
Mermaid diagram (expand to render)
Synaptic loss is the strongest correlate of cognitive decline in Alzheimer's disease, and preserving synaptic function has emerged as a critical therapeutic strategy. AAIC 2026 features extensive programming on synaptic biology, including mechanisms of synaptic degeneration, protective interventions, and synaptic resilience approaches["@selkoe2024"].
Key Topics
Synaptic Vulnerability Mechanisms
Pre-Synaptic Terminal Dysfunction
Vesicle Cycling Impairment: Disruptions in synaptic vesicle release and recycling
neurotransmitter depletion: Reduced synthesis and packaging of neurotransmitters
[Unknown, Selkoe DJ. Alzheimer's disease: Genetically defined disorders that converge on amyloid-beta/synapse loss. Neuron. 2024 (2024)](https://doi.org/10.1016/j.neuron.2024.01.015)
[Hernandez FX, et al., Synaptic plasticity deficits in Alzheimer's disease models. Nat Rev Neurosci. 2023 (2023)](https://doi.org/10.1038/s41583-023-00727-0)
[Unknown, Tanzi RE. The synapse, tau, and amyloid: An updated view of Alzheimer's disease pathogenesis. Nat Med. 2024 (2024)](https://doi.org/10.1038/s41591-024-02967-0)