Role of extracellular vesicle–mediated neurodegeneration in substance use disorders
Year: 2025
Type: review
Abstract: Substance use disorders (SUDs) remain a complicated and widespread public health problem, characterized by obsessive drug and alcohol use, despite adverse consequences. Emerging research suggests that the extracellular vesicles (EVs) play a critical role in mediating drug addiction and several neurodegenerative processes associated with SUDs. EVs, which include exosomes, microvesicles, and apoptotic bodies, are lipid-bilayered vesicles that facilitate intracellular communication throughout the host by shuttling bioactive molecules, such as proteins, lipids, DNA fragments, and RNA, including both coding and noncoding RNAs across recipient cells. The current review is a comprehensive analysis highlighting the potential role of EVs in the onset and progression of SUD, specifically in the context of cocaine, cannabis, methamphetamine, opiates, alcohol, and tobacco. The goal is to offer valuable insights into the underlying mechanism(s) involving EVs in the pathogenesis of SUD, ultimately paving the way for new therapeutic avenues.
Source: Current Opinion in Physiology
Authors: Mohit Kumar, Arnab Saha, Agasou Alfonso Rameau, Susmita Sil, Shilpa Buch
Institution: University of Nebraska Medical Center
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $3,500
Awards: G1318492209, Mechanisms underlying dysregulated neuroimmune signaling and neuronal dysfunction in HIV (+) individuals with cART and cocaine, G2435025461, Combinatorial effects of HIV, cART, & morphine on neuroinflammation: implications for HAND, G2702422785, Molecular mechanisms underlying HIV & Cocaine-mediated microglial activation: Targeting NLRP3 inflammasome, G4998873175, Astrocytic HIF-1a as a therapeutic target for Alzheimer's-like comorbidity of HAND, HIV Tat and Opiate-mediated aberrations in glial-neuronal crosstalk: Implications for the role of extracellular RNA in HAND
OpenAlex ID: W4408862993
