Depression is not simply a mood disorder, a feeling of sadness, or being ill at ease. Depression can completely shut a person down, manifesting as an inability to make decisions, to take action, to think. Even sleep is affected by depression.
Researchers and clinicians who treat depression are learning that the physical manifestations can be mirrored by internal, cellular changes. Some people with depression have decreases in their gray matter volume, particularly in areas like the hippocampus (important to memory, learning, and emotions) and prefrontal cortex (where higher-level thought and planning abilities are based).
Additionally, imaging has shown a decrease in the number of synapses—the structures through which electrical or chemical signals are passed between neurons and other cells—in persons with chronic depression. Without the signals that synapses transmit, brain function is disrupted.
And without intervention in depression, synapse decrease can continue.
While there are drugs and behavioral therapies to treat depression, these therapies can be slow to act and sometimes ineffective. In addition, once synaptic loss has occurred, these therapies are less effective.
“It has long been recognized that these compounds (serotonergic psychedelics like psilocybin) may have therapeutic potential for neuropsychiatric disorders, including depression, obsessive-compulsive disorder and addiction”.
When researchers first identified a new family of seemingly non-functional “junk” RNA molecules, it’s unlikely they could have predicted the power and promise of these nucleic acids. The small, non-coding, single-stranded RNAs – typically 21-25 base pairs in length – were first discovered over 20 years ago in C. elegans, yet they were quickly found to be ubiquitous in species from worms to flies to plants to mammals. The role of these novel RNAs in the regulation of developmental pathways in worms, coupled with their prevalence, inspired researchers to better understand their significance.
We now know that miRNAs (for microRNAs) serve as post-transcriptional repressors of gene expression by targeting degradation of mRNA or interfering with mRNA translation. While small, each can have a big effect; a single miRNA can regulate dozens to hundreds of distinct target genes. They’ve been implicated in a variety of critical cellular processes such as differentiation, development, metabolism, signal transduction, apoptosis and proliferation.
Tissue-specific expression patterns revealed that specific miRNAs are enriched in mammalian tissues including adult brain, lung, spleen, liver, kidney and heart. More compelling was the identification of abnormal miRNA expression in tumorigenic cell lines. It’s no wonder that this growing family quickly became ripe for exploration in disease development.
Within only a few years, a rapidly expanding body of research supported the theory that miRNA expression may indeed play a role in the development of human diseases including cardiovascular disease, cancer, diabetes, cystic fibrosis, and liver disease. Investigations into the expression of miRNAs in cardiovascular disease, in particular, have demonstrated not only their value as disease markers, but also how their dysregulation is linked to disease processes.
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