Protective effects of Humanin and calmodulin-like skin protein in Alzheimer's disease and broad range of abnormalities.
Matsuoka. Masaaki M
Key Findings
- Humanin blocks neuron death caused by Alzheimer’s‑linked genes via the htHNR receptor
- CLSP is a natural activator of the same receptor and is about 100,000 times more potent than Humanin
- Humanin may also protect against certain metabolic disorders
Practical Outcomes
- For biohackers, Humanin and especially its more potent cousin CLSP could be interesting targets for neuro‑protective or metabolic‑support strategies, but there are no clear dosing protocols yet. Until more human trials emerge, consider monitoring emerging peptide supplements that claim to activate the htHNR pathway, and stay aware of safety data before experimenting.
Summary
Humanin is a tiny protein that can protect brain cells from dying, especially in forms of Alzheimer’s linked to genetics, by attaching to a special receptor. A related skin protein, CLSP, does the same thing but is far more powerful. Humanin also shows some promise in helping with metabolic problems, though the exact ways and doses aren’t clear yet.
Abstract
Humanin is a 24-amino acid, secreted bioactive peptide that prevents various types of cell death and improves some types of cell dysfunction. Humanin inhibits neuronal cell death that is caused by a familial Alzheimer's disease (AD)-linked gene via binding to the heterotrimeric Humanin receptor (htHNR). This suggests that Humanin may play a protective role in AD-related pathogenesis. Calmodulin-like skin protein (CLSP) has recently been identified as a physiological agonist of htHNR with 10(5)-fold more potent anti-cell death activity than Humanin. Humanin has also shown to have protective effects against some metabolic disorders. In this review, the broad range of functions of Humanin and the functions of CLSP that have been characterized thus far are summarized.
Study Information
pubmed
2014
2014-06-27T00:00:00.000Z
10.1007/s12035-014-8799-1
1