Home > Research > Publications & Outputs > Neuroprotective effects of glucose-dependent in...

Electronic data

  • review_Liu_V4

    Accepted author manuscript, 532 KB, PDF document

    Available under license: CC BY-NC-ND: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License


Text available via DOI:

View graph of relations

Neuroprotective effects of glucose-dependent insulinotropic polypeptide in Alzheimer's disease

Research output: Contribution to journalJournal article

<mark>Journal publication date</mark>01/2016
<mark>Journal</mark>Reviews in the Neurosciences
Issue number1
Number of pages10
Pages (from-to)61-70
Publication StatusPublished
Early online date5/09/15
<mark>Original language</mark>English


Glucose-dependent insulinotropic polypeptide (GIP) is a member of the incretin hormones and growth factors. Neurons express the GIP receptor, and GIP and its agonists can pass through the blood brain barrier and show remarkable neuroprotective effects by protecting synapse function and numbers, promoting neuronal proliferation, reducing amyloid plaques in the cortex and reducing the chronic inflammation response of the nervous system. Long-acting analogues of GIP that are protease resistant had been developed as a treatment for type 2 diabetes. It has been found that such GIP analogues show good protective effects in animal models of Alzheimer's disease. Novel dual agonist peptides that activate the GIP receptor and another incretin receptor, glucagon-like peptide -1 (GLP-1), are under development that show superior effects in diabetic patients compared to single GLP-1 agonists. The dual agonists also show great promise in treating neurodegenerative disorders, and there are currently several clinical trials ongoing, testing GLP-1 mimetics in people with Alzheimer's or Parkinson's disease.