- Scientists found that a certain gene altered by heroin could be driving cravings
- Gene encoding tyrosine kinase FYN and the protein Tau were elevated in heroin-addicted brain cells
- Similar gene expression is seen in Alzheimer's, and its medication could potentially be repurposed for addicts
We all know about the detrimental effects of heroin on the human body, and new research found that its effect on the brain is similar to that of the neurodegenerative Alzheimer's disease.
Published in Nature Communications, scientists found that the gene encoding tyrosine kinase FYN is altered by the drug, and could be the driving force behind users' drug-taking behaviour, as well as explain their cognitive decline.
"Epigenetic mechanisms are dynamic processes that regulate gene expression and have recently emerged as key contributors to the molecular impairments caused by exposure to environmental factors such as abused substances," write the researchers.
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Answers lie in the striatum
The researchers used genome-wide direct assessment of the chromatin state in the striatum – the part of the brain in charge of motor functions, reward and inhibitions – of post-mortem humans as well as rats trained to self-administer heroin.
They found the FYN gene was hyper-expressed, which in turn elevated levels of the protein Tau. Found in brain cells, this protein can build-up and cause a variety of brain disorders, including Alzheimer's.
Heroin appears to stimulate this expression and build-up, and by introducing FYN inhibitor medication to the addicted rodents, they saw a reduction in cravings for heroin.
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Therefore, Alzheimer's medication that suppresses FYN could potentially be used to develop medication targeted at heroin addicts.
Similar results were also seen in laboratory-grown primary neurons chronically exposed to morphine in vitro.
"The mechanistic link we demonstrated between opioid exposure and dysregulated FYN and Tau pathology could also have marked implications for the large number of individuals exposed chronically to potent opioid analgesics during the past decade.
"Importantly, the fact that the FYN inhibitor saracatinib potently decreased addiction-like behaviours strongly suggests that FYN, and related network, is a key target for future therapeutic development.
"Although the potential efficacy of FYN inhibitors through current clinical trials for Alzheimer’s disease remains to be determined, most drugs targeting FYN appear to be well tolerated and could, therefore, be excellent candidates to repurpose for accelerated clinical studies focused on substance use disorders."
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