Molecular medicine has come a long way.
When fighting afflictions of the mind a healthy dose of imagination is now understood to be imperative. Gut bacteria (bugs for drugs) for instance is currently being considered as a plausible method of combating depression in chronic sufferers.
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I recently reported on Dr. John Cryan’s optimism in utilizing unconventional methods against the silent killer. Observing mice, the Ireland based professor disclosed the gut microbita to be behind such mental disorders as Parkinson’s and Alzheimer’s.
Similarly, on February 18th molecular behavioral neuroscientist Dr. Xin-Yunn Lu successfully reversed depression in male mice by activating the gene responsible for exciting excitatory neurons.
The most obvious effect the report detailed was the turn around in symptoms like social isolation and a loss of interests. An inactive SIRT1 gene in excitatory neurons was found to lead to the most common features of depression disorders. The gene additionally affects the mitochondria, which is responsible for energy levels.
Dr. Xin-Yun Lu designed a drug that effectively activates it, and the results spoke for themselves.
“It has an antidepressant-like effect,” says Lu. “That means drugs that activate SIRT1 and enable the usual high level of activity of these excitatory neurons might one day be an effective therapy for some with major depression.”
Can it work on humans?
Unfortunately, these promising tests did not yield the same results in female mice. As far as the reasoning is concerned, the researchers can only hypothesize.
They suspect a disparity of neurons to be partially responsible. There are simply physical differences in the area of the brain targeted in males and females. Lu intends to delineate other potential sex-based differences in other regions of the hippocampus.
There are enough broad similarities between depressed humans and mice to revel in the recent report. Both express anhedonia when stressed, both lose sexual interest and both alienate.
All of these qualities were successfully repudiated by a jolt to neuron activity.
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