Astrocytes produced excessive amounts of immune messengers called chemokines, which can activate CXCR3 chemokine receptors typically found on infiltrating immune cells.
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Adam Orr, an assistant professor of research in neuroscience in the Feil Family Brain and Mind Research Institute and a member of the Appel Alzheimer’s Disease Research Institute at Weill Cornell Medicine, analyzed gene expression and found high levels of antiviral gene activities, even though no virus was present in the brain. To understand the causes of memory loss at the molecular level, co-senior author Dr. “Astrocytes in the hippocampus seem to be more vulnerable to this pathology.” she said. In mice, the build-up of TDP-43 in astrocytes was sufficient to cause progressive memory loss but not other behavioral changes. Robert Schwartz at Weill Cornell Medicine and Dr. Other senior investigators that contributed to the study include Dr.
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To understand the effects of this protein build-up, the team conducted a series of experiments in mouse models and brain cells grown in the laboratory. Avital Licht-Murava, a former postdoctoral associate in the Orr lab, examined tissue samples from deceased individuals who were diagnosed with either Alzheimer’s disease or frontotemporal dementia, they found an accumulation of a protein called TDP-43 in astrocytes within the hippocampus, a brain region crucial for memory. When the investigators, including first author Dr. “These cells are prevalent in the brain and perform various key functions, but their involvement in neurocognitive disorders like dementia are poorly understood.” “We are very interested in the roles of astrocytes in cognitive and behavioral disorders,” she said.
While neurons have been intensively studied in dementia and other diseases, much less research has focused on astrocytes, which many scientists viewed as playing only supporting roles to neurons in brain health. “We found, in mice, that astrocytes can cause cognitive decline through their antiviral activities, which can make neurons hyperactive.” Anna Orr, the Nan and Stephen Swid Assistant Professor of Frontotemporal Dementia Research in the Feil Family Brain and Mind Research Institute and a member of the Helen and Robert Appel Alzheimer's Disease Research Institute at Weill Cornell Medicine. “Astrocyte dysfunction alone can drive memory loss, even when neurons and other cells are otherwise healthy,” said co-senior author Dr. The discovery could lead to new treatments that reduce excess immune activity in astrocytes and their detrimental effects on other brain cells and cognition. But a new study, published in Science Advances on April 19, suggests that abnormal immune activity in non-neuronal brain cells called astrocytes is sufficient to cause cognitive deficits in dementia. People with dementia have protein build-up in astrocytes that may trigger abnormal antiviral activity and memory loss, according to a preclinical study by a team of Weill Cornell Medicine investigators.ĭysfunction in cells called neurons, which transmit messages throughout the brain, has long been the prime suspect in dementia-related cognitive deficits.
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