While the abstract identifies autophagy/lysosome dysfunction as a consequence of PGRN insufficiency, the specific mechanisms linking this cellular dysfunction to the broader FTD pathology remain unclear. This knowledge gap limits therapeutic targeting of these pathways. Gap type: unexplained_observation Source paper: Approaches to develop therapeutics to treat frontotemporal dementia. (2020, Neuropharmacology, PMID:31962288)
Landscape Summary: How does autophagy and lysosome dysfunction mechanistically connect PGRN deficiency to FTD pathogenesis? is a 0.82 priority gap in neurodegeneration. It has 0 linked hypotheses with average composite score 0.000. Status: open.
Colonna, Sevlever, et al. (TREM2 biology)
How does autophagy and lysosome dysfunction mechanistically connect PGRN deficiency to FTD pathogenesis? — INVOKE-2 (completed)
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