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Maurice on
Conclusions: These data strongly suggest that GLP-1 functions as a humoral factor of remote ischaemic conditioning cardioprotection. Notably, they seem to
improve nearly all neuropathological features in AD and
cognitive functions as well. Long-term potentiation was significantly enhanced as well and synapse numbers increased
in the hippocampus and cortex (McClean and Holscher, 2014).
In another study, the same authors observed that
liraglutide might also protect from progressive neurodegeneration that develops in AD:
in 2-month old mice, liraglutide (once-daily intraperitoneally for
8 months) contrasted synaptic damage and improved memory.
The deficits in hippocampal late-phase long-term potentiation were reversed and p-PI3K and p-AKT growth factor kinases were up
regulated. The effects of GLP-1RAs on synaptic protection might involve the modulation of the brain-derived neurotrophic factor (BDNF), a trophic
factor which promotes neural progenitor cell
differentiation and survival. Despite the large amount of
evidence about the neuroprotective effects of GLP-1RAs in animal models of AD,
human studies are still scant.
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