![]() To find out, they custom-designed electrodes to measure rhythmic activity simultaneously in all cortical layers of each hemisphere’s V1. Given the observations correlating reduced brain rhythm synchrony and memory performance in Alzheimer’s, the team wondered if that occurred in the mice, too. When they compared the incoming connections of healthy CH neurons to those in CH cells afflicted with Alzheimer’s, they found that cells in the disease condition had significantly less infrastructure for hosting incoming connections (measured in terms of synapse-hosting spines protruding from the vine-like dendrites that sprawl out of the cell body). The team examined the CH cells closely and found that they gather incoming input from a variety of other cells within their V1 and other regions in their hemisphere that process visual information. Unsurprisingly, Alzheimer’s mice fared much poorer in novelty discrimination tasks. ![]() The found that CH cell activity was significantly lessened amid the disease. Adaikkan also found that CH neurons were much more likely to be activated by a novelty discrimination task than V1 neurons in general or neurons in other regions heavily involved in memory such as the hippocampus or the prefrontal cortex.Ĭurious about how this might differ in Alzheimer’s disease, the team looked at the activity of the cells in two different Alzheimer’s mouse models. ![]() There, they found, the cross-hemispheric (CH) neurons forged connections, or synapses, with target cells, providing them with “excitatory” stimulation to drive their activity. In the study, Adaikkan, Tsai, Thomas McHugh, and co-authors discovered and traced V1 neurons that extended their axons all the way through the corpus callosum, which connects the brain’s hemispheres, to cells in the V1 on the brain’s other side. ![]() “It also demonstrates that the disruption of this circuit in AD mouse models is associated with specific behavioral deficits.” “This study demonstrates the propagation of gamma rhythm synchrony across the brain hemispheres via the cross hemispheric connectivity,” says study senior author Li-Huei Tsai, Picower Professor and director of The Picower Institute and MIT’s Aging Brain Initiative. Such recognition of novelty, which requires visual memory of what was there the prior day, is an ability commonly disrupted in Alzheimer’s. Specifically, Adaikkan’s work identified neurons that connect the primary visual cortex (V1) of each hemisphere and showed that when the cells are disrupted, either by genetic alterations that model Alzheimer’s disease or by direct laboratory perturbations, brain rhythm synchrony becomes reduced and mice become significantly less able to notice when a new pattern appeared on a wall in their enclosures. “In a way, we uncovered a fundamental biology that was not known before.” “We demonstrate that there is a functional circuit that can explain this phenomenon,” says lead author Chinnakkaruppan Adaikkan, a former Picower Institute postdoc who is now an assistant professor in the Centre for Brain Research at the Indian Institute of Science (IISc) in Bangalore. The results of the study, published in Neuron by a research team based at The Picower Institute for Learning and Memory, come from experiments in mice, but provide a physiological and mechanistic basis for prior observations in human patients: the degree of diminished brain rhythm synchrony between counterpart regions in each hemisphere correlates with the clinical severity of dementia. ![]() A new MIT study finds that Alzheimer’s disease disrupts at least one form of visual memory by degrading a newly identified circuit that connects the vision processing centers of each brain hemisphere. ![]()
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