Topic: exosomes

Alzheimer's disease (AD) is a progressive degenerative disorder characterized by memory loss and cognitive decline. However, there are limited studies on preventing or stopping the advanced neuronal loss that occurs during or before the disease. Our project aims to provide a prophylactic application against AD and similar neurodegenerative diseases. Exosomes are small particles that can cross biological membranes like the blood-brain barrier. They are being used as drug carrier systems and have attracted attention recently. In AD and similar diseases, exposure to oxidant molecules increases in

Huntington Disease (HD) originates from the expansion of a polyglutamine (PolyQ) tract in the Huntingtin protein (Htt), that can assume a Coiled coil fold (Cc). We previously found that Cc structures mediate the aggregation and toxicity of Htt and hypothesize they might be implicated in other aspects of Htt dysfunction. There is evidence that expanded and aggregated Htt can be released by sick cells and taken up by healthy ones. With a prion-like mechanism, aggregated Htt can then seed the misfolding of normal Htt spreading the disorder.We hypothesize that Cc also mediate the intercellular pro

Intracellular membrane protein trafficking is crucial for both normal cellular physiology and cell-cell communication. It is now established that intracellular trafficking not only uses the conventional secretory pathway but also an alternative secretion pathway able to bypass the need for passage through the Golgi apparatus, which is collectively termed unconventional protein secretion. One of the major actors of this pathway is the vesicular SNARE VAMP7, which is involved in the secretion of extracellular vesicles of late endosomal origin called exosomes. It was recently shown that exosomes

Alzheimer’s disease (AD) presents a significant challenge to therapeutic interventions, necessitating the exploration of innovative strategies to manage its complex pathology. This study explores the relationship between autophagy and Transcription factor EB (TFEB) as a potential avenue for AD treatment. We demonstrate the therapeutic potential of TFEB in mitigating AD pathology by enhancing autophagy. Our strategy employs exosomes as vehicles for the targeted and efficient delivery of TFEB to affected cells. Exosomes, small extracellular vesicles, are recognized for their ability to cross bio