What the research examined
Early humanin research used cell-based screening to examine selected forms of neuronal injury associated with familial Alzheimer-related genes and amyloid. Later experiments investigated signaling pathways, including GP130-related responses, in cellular and animal systems.
How to interpret the findings
Protection in a selected experimental injury model does not establish treatment of a human neurodegenerative disease. The original effects were model-dependent, and pathway activation alone is not a clinical endpoint.
Research literature
- A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta.
Proceedings of the National Academy of Sciences of the United States of America · 2001 · PMID 11371646 - The mitochondrial-derived peptide humanin activates the ERK1/2, AKT, and STAT3 signaling pathways and has age-dependent signaling differences in the hippocampus.
Oncotarget · 2016 · PMID 27384491
Links open the indexed paper records. Summaries are based on those records and their available abstracts, not a systematic review or a full-text appraisal of every study.