Multiple pathological processes are identified as contributing to depression in AD, but their relative contributions and potential synergistic interactions remain unexplained. This mechanistic understanding is essential for prioritizing therapeutic targets. Gap type: unexplained_observation Source paper: Pathogenesis of Depression in Alzheimer's Disease. (2024, Neurochemical research, PMID:38015411)
Landscape Summary: How do monoamine disruptions, glutamatergic dysfunction, and neuroinflammation interact to produce depression in AD? is a 0.76 priority gap in synaptic-biology. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
How do monoamine disruptions, glutamatergic dysfunction, and neuroinflammation interact to produce depression in AD? — INVOKE-2 (completed)
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