Stanford Bio-X Researchers’ “Decoy Drug” Could Someday Do Wonders For Alzheimer’s Disease

Stanford Bio-X Researchers’ “Decoy Drug” Could Someday Do Wonders For Alzheimer’s Disease
A recent study revealed the mechanism to restore the capability of neurons to form new synapses, entitled, "Blocking PirB up-regulates spines and functional synapses to unlock visual cortical plasticity and facilitate recovery from amblyopia," which was published in Science Translational Medicine by David Bochner and Richard W. Sapp, first co-authors from the work, part of the group of Dr. Carla Shatz, from the Department of Biology and Bio-X, Stanford University, CA, U.S.A. the findings of the study suggest that the newfound capability may have the potential to be applied to clinical conditions such as stroke, forms of blindness, or Alzheimer's disease. During brain development, the neurons respond to various stimuli by forming new synapses, although this capacity decreases substantially in adults. Dr. Shatz and collaborators described previously a protein called Paired-immunoglobulin-like receptor B (PirB), a major histocompatibility complex class I (MHCI) receptor, localized in mice on the surface of neurons and immune cells. The PirB protein seems to control the time “window” for synapse formation. When there is no stimulation of PirB, the neurons are able to form new synapses. But when there is stimulation, other proteins latch onto PirB and the “window” is closed -- a process that occurs mostly during adult life -- and there is inhibition of synapse formation. PirB is essentially an on/off switch system for synapse formation. Therefore, the million dollar question has been what controls that “window” and how can we open it during adulthood and mainly during disabling conditions such as stroke, some forms of blindness, Alzheimer's disease and other neurodegenerative conditions. "To me, this is amazing because what this is saying is that it
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