Alzheimer’s Disease affects millions of people. It is a neurodegenerative disease, characterized by plaques and tangles in the brain. Amyloid-beta is a protein that when accumulated in neurons forms plaques and results in neuronal dysfunction. NFTs (neurofibrillary tangles) are also present in individuals with AD.
New studies suggest that diabetes can influence cognitive performance and AD onset. Patients with diabetes also tend to develop AD more often than healthy individuals. Diabetes is characterized by abnormal glucose metabolism.
This study investigated the relationship between AD and some hormones that regulate metabolism, including: insulin, amylin, glucagon like peptide, asprosin and glucocorticoids.
The main cause/symptom of type 2 diabetes is insulin resistance. While insulin was considered a protein that rarely passes the blood brain barrier, more recent studies have shown that it does and that is has an effect on receptors in the brain. Additionally, the same effects of insulin resistance occur and affect brain cells in the same way as other cell types. And since the insulin receptor is involved in pathways (PI3K/Akt) that affect Amyloid-beta, there may be an effect and a potential treatment there.
Amylin is released with insulin to reduce orexis, gastric acid secretion, limits the rate of gastric emptying and diminishes pancreatic glucagon. The composition of Amyloid-beta and Amylin is very similar, meaning they can interact with each other and that the enzymes that degrade Amylin are also the ones that degrade Amyloid-beta. Like Amyloid-beta, Amylin is also overexpressed in AD patients, and can result in impaired cognition. Dysregulation in degrading enzymes may be the main cause of this, but still Amylin remains a valid target for research to develop potential treatments.
Glucagon like peptides.
GLP-1 and GLP-2 regulate blood glucose. Both are essential regulators of metabolism and growth in the body. GLP-1, can also act as a neurotransmitter in the CNS (central nervous system) and regulate, cell proliferation, apoptosis and neurogenesis. It has been shown that GLP-1 can improve neuronal health in AD brains.
Asprosin and glucocorticoids are also involved in similar pathways as the proteins mentioned above and as a result, they can influence metabolism and brain function.
The specific ways those proteins cause or prevent AD is very complex and still being studied. But we are getting closer to understanding AD and its causes. The article ends by mentioning how certain substances can help with AD, like curcumin, that can be introduced in the diet and improve memory as shown in mice.