Researchers can use the 64-chip Pohoiki Beach system to make systems that learn and see the world more like humans.
The disability burden for people with multiple sclerosis (MS) can vary significantly depending on whether they have a relapsing/remitting form of the disease, where they experience periods of clinical remission, or a progressive form, where they have continued neurological deterioration without clinical remission. Effective therapies exist for managing relapsing/remitting MS, but treatment for progressive MS has proved more challenging. Now, a new paper published in the journal Brain from researchers at the Advanced Science Research Center (ASRC) at The Graduate Center, CUNY and Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai has identified potential mechanisms that may inform the development of therapies that effectively manage progressive MS.
Previous research had suggested that dysfunction of neuronal mitochondria—the energy-producing subcellular organelles—occurs in the brains of MS patients with progressive clinical disability. However, the molecular mechanisms underlying this process remained elusive.
“Because the brain is bathed by the cerebrospinal fluid (CSF), we asked whether treating cultured neurons with the CSF from MS patients with a relapsing/remitting or a progressive disease course would possibly elicit different effects on neuronal mitochondrial function,” said the study’s primary investigator Patrizia Casaccia, Einstein Professor of Biology at The Graduate Center and founding director of the Neuroscience Initiative at the ASRC. “We detected dramatic differences in the shape of the neuronal mitochondria and their ability to produce energy. Only exposure to the CSF from progressive MS patients caused neuronal mitochondria to fuse and elongate while rendering them unable to produce energy. We therefore searched for potential mechanisms of CSF-induced neurodegeneration with the intent to define therapeutic strategies.”
Senior mice treated with THC improved on learning and memory tests.
Optogenetic approaches are widely used to manipulate neural activity and assess the consequences for brain function. Here, a technique is outlined that upon in vivo expression of the optical activator Channelrhodopsin, allows for ex vivo analysis of synaptic properties of specific long range and local neural connections in fear-related circuits.
‘It is a real message of hope – I feel within my lifetime we can restore functional sight to the blind’, expert says of successful study.
Medical experts hail ‘paradigm shift’ of implant that transmits video images directly to the visual cortex, bypassing the eye and optic nerve.
We all have things we’d rather forget. But for over four million people in the US who suffer from post-traumatic stress disorder (PTSD), that need becomes very real.
Erasing memories has always been the stuff of science fiction and wishful thinking. After all, what happened, happened—your experiences are solidified in your head as part of your past, perhaps even molding your personality.
But does it have to be this way?
The past decade of Alzheimer’s disease research has been fraught with disappointment.
Years of focus on one hallmark of the disease ultimately resulted in no progress toward treatment or prevention.
But next week, when top scientists gather in Los Angeles at the Alzheimer’s Association International Conference, an annual meeting, many will present research on a different target: inflammation.
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