| Literature DB >> 34794851 |
Karis Little1, María Llorián-Salvador1, Sarah Scullion1, Cristina Hernández2, Olga Simó-Servat2, Angel Del Marco3, Esmeralda Bosma4, Maria Vargas-Soria3, Maria Jose Carranza-Naval3, Tine Van Bergen5, Silvia Galbiati6, Ilaria Viganò6, Clara Alice Musi7, Reiner Schlingemann8, Jean Feyen5, Tiziana Borsello7, Gianpaolo Zerbini6, Ingeborg Klaassen4, Monica Garcia-Alloza3, Rafael Simó9, Alan W Stitt10.
Abstract
Type 2 diabetes (T2D) is associated with multiple comorbidities, including diabetic retinopathy (DR) and cognitive decline, and T2D patients have a significantly higher risk of developing Alzheimer's disease (AD). Both DR and AD are characterized by a number of pathological mechanisms that coalesce around the neurovascular unit, including neuroinflammation and degeneration, vascular degeneration, and glial activation. Chronic hyperglycemia and insulin resistance also play a significant role, leading to activation of pathological mechanisms such as increased oxidative stress and the accumulation of advanced glycation end-products (AGEs). Understanding these common pathways and the degree to which they occur simultaneously in the brain and retina during diabetes will provide avenues to identify T2D patients at risk of cognitive decline.Entities:
Keywords: Alzheimer’s disease; cognitive decline; diabetes; neurovascular unit
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Year: 2021 PMID: 34794851 DOI: 10.1016/j.tem.2021.10.008
Source DB: PubMed Journal: Trends Endocrinol Metab ISSN: 1043-2760 Impact factor: 12.015