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  1. This is a most interesting finding. One important observation after gastric bypass surgery is that the patients are almost immediately relieved from being diabetic. This is linked to increased GLP-1 release (see, e.g., Morínigo et al., 2006). It is not understood why the intestine suddenly releases a lot more GLP-1 after this surgery, but GLP-1 re-sensitizes insulin signaling.

    Importantly, GLP-1 analogues also have neuroprotective properties and reduce amyloid synthesis, plaque load, and the inflammation response in animal models of AD. Nigel Greig's group from the NIH showed that the GLP-1 analogue exendin-4 has protective properties in a triple-Tg mouse model of AD (Li et al., 2010), and we showed that the GLP-1 analogue liraglutide has very clear protective properties in an APP/PS1 mouse model (McClean et al., 2011). Both drugs are already on the market as treatments for type 2 diabetes. This new study is an interesting confirmation of the idea that GLP-1 may be neuroprotective.


    . GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease. J Alzheimers Dis. 2010;19(4):1205-19. PubMed.

    . The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer's disease. J Neurosci. 2011 Apr 27;31(17):6587-94. PubMed.

    . Glucagon-like peptide-1, peptide YY, hunger, and satiety after gastric bypass surgery in morbidly obese subjects. J Clin Endocrinol Metab. 2006 May;91(5):1735-40. PubMed.

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  1. Research Brief: After Weight-Loss Surgery, AD-Related Proteins Drop