In a study from Augusta University, scientists found that a 50-year-old blood pressure drug could find a new purpose as a treatment to mitigate the often life-altering effects of increasingly prevalent PTSD.
Clonidine is commonly used as a high blood pressure medication and for ADHD.
It’s also already been studied in PTSD because clonidine works on adrenergic receptors in the brain, likely best known for their role in “fight or flight,” a heightened state of response that helps keep us safe.
These receptors are thought to be activated in PTSD and to have a role in consolidating a traumatic memory.
Clonidine’s sister drug guanfacine, which also activates these receptors, also has been studied in PTSD.
Conflicting results from the clinical trials have clonidine, which has shown promise in PTSD, put aside along with guanfacine, which has not.
In the study, the team found that while the two drugs bind to the same receptors, they do different things there.
Their results suggest that clonidine could provide immediate treatment to the significant number of people emerging from the current pandemic with PTSD, as well as from longer-established causes like wars and other violence.
The team says large-scale clinical trials of clonidine in PTSD are warranted.
Their studies also showed that other new therapies could be identified by looking at the impact on the activation of a key protein called cofilin by existing drugs.
The findings help clarify the disparate results in the clinical trials of these two similar drugs.
The U.S. Department of Veterans Affairs defines post-traumatic stress disorder as a mental health problem that some people develop after experiencing or witnessing a life-threatening or traumatic event.
While problems like feeling on edge, trouble sleeping, and/or nightmares may last a few weeks or more after the event, if symptoms like these, as well as flashbacks and increasingly negative thoughts, continue, it’s likely PTSD.
Sometimes symptoms don’t surface until months after the initial event.
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The study was conducted by Qin Wang et al and published in Molecular Psychiatry.
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