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Category: neuroscience – Page 11

The neocortex is highly susceptible to metabolic dysfunction. When exposed to global ischemia or anoxia, it suffers a slowly propagating wave of collective neuronal depolarization that ultimately impairs its structure and function. While the molecular signature of anoxic depolarization (AD) is well documented, little is known about the brain states that precede and follow AD onset. Here, by means of multisite extracellular local field potentials and intracellular recordings from identified pyramidal cells, we investigated the laminar expression of cortical activities induced by transient anoxia in rat primary somatosensory cortex. Soon after the interruption of brain oxygenation, we observed a well-organized sequence of stereotyped activity patterns across all cortical layers.

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A new neuroimaging study from China has found that an eight-week course of bright light therapy helped reduce depressive symptoms in individuals with subthreshold depression. The treatment also altered dynamic functional connectivity in several brain regions associated with mood regulation. The study was published in the Journal of Affective Disorders.

Subthreshold depression refers to the presence of depressive symptoms that are clinically relevant but do not meet the full diagnostic criteria for major depressive disorder. Individuals with subthreshold depression may experience persistent sadness, fatigue, sleep disturbances, or concentration problems, but with fewer symptoms or a shorter duration than required for a formal diagnosis.

Despite being “subthreshold,” the condition can impair daily functioning and reduce quality of life. It is also linked to an increased risk of developing major depression in the future. Subthreshold depression is common—especially among adolescents, older adults, and individuals with chronic illnesses—and it often goes undiagnosed and untreated because the symptoms are perceived as mild or situational. However, research shows that even mild depressive symptoms can negatively affect social relationships, job performance, and physical health.

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As researchers work to improve treatment of Alzheimer’s disease, new research by UCLA Health identified a candidate drug that reduces levels of a toxic form of a protein in the brain caused by the disease and improved memory in mice by boosting production of a protective protein.

In a study published in npj Drug Discovery, UCLA Health researchers targeted the protein clusterin (CLU), which is crucial in preventing the build-up of amyloid-beta plaques and tau proteins that disrupt communication between and lead to memory impairment—a hallmark symptom of Alzheimer’s disease.

More than a decade ago, a variant of the gene that encodes clusterin was identified as the third strongest genetic risk factor for late-onset Alzheimer’s disease. It was recently reported that increased CLU protein could provide protection against Alzheimer’s disease and .

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