AD is generally regarded as type 3 DM but this paper takes us close to a better understanding of how tau is related not only to AD but also to type 2DM.
We know also that PD patients are prone to get DM as is that DM patients are prone to get PD.
According to this paper, Tau is a therapeutic target in AD but now evidently also in T2DM. This will take ATH with its many iron and zinc chelating molecules to this interesting world of type 2 diabetes and metabolic syndrome. This is not only an animal study but this effect of tau could also be seen both in diabetic and healthy control populations, and so this evidence is very strong already today.
The patent applications of ATH do not target a single disease but diseases. Here we have once again evidence that "diseases" are the right targets.
Unfortunately, this paper is not free.Tau suppresses microtubule-regulated pancreatic insulin secretion
Salvatore P Mangiafico # 1, Qing-Zhang Tuo # 2, Xiao-Lan Li # 2, Yu Liu 2, Christian Haralambous 1, Xu-Long Ding 2, Scott Ayton 3, Qing Wang 2, D Ross Laybutt 4, Jeng Yie Chan 4, Xiang Zhang 2, Cameron Kos 5, Helen E Thomas 5, Thomas Loudovaris 5 6, Chieh-Hsin Yang 1, Christos N Joannides 1, Benjamin J Lamont 1, Lunzhi Dai 2, Hai-Huai He 2, Biao Dong 2, Sofianos Andrikopoulos 7, Ashley I Bush 8, Peng Lei 9 10AffiliationsDOI: 10.1038/s41380-023-02267-w
- PMID: 37735502
Abstract
Tau protein is implicated in the pathogenesis of Alzheimer's disease (AD) and other tauopathies, but its physiological function is in debate. Mostly explored in the brain, tau is also expressed in the pancreas. We further explored the mechanism of tau's involvement in the regulation of glucose-stimulated insulin secretion (GSIS) in islet β-cells, and established a potential relationship between type 2 diabetes mellitus (T2DM) and AD. We demonstrate that pancreatic tau is crucial for insulin secretion regulation and glucose homeostasis. Tau levels were found to be elevated in β-islet cells of patients with T2DM, and loss of tau enhanced insulin secretion in cell lines, drosophila, and mice. Pharmacological or genetic suppression of tau in the db/db diabetic mouse model normalized glucose levels by promoting insulin secretion and was recapitulated by pharmacological inhibition of microtubule assembly. Clinical studies further showed that serum tau protein was positively correlated with blood glucose levels in healthy controls, which was lost in AD. These findings present tau as a common therapeutic target between AD and T2DM.
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