What makes us unique? Different from most, yet similar to a few? What shapes our physical, behavioral, and even mental makeup? The answer lies in our genes.
Passed from parents to their offspring, genes contain the information that specifies physical and biological traits.
But that’s not all. Genes are also responsible for diseases. Faulty genes can cause all kinds of issues that can manifest as birth defects, chronic diseases, or developmental problems.
A new study by UCLA Health has discovered what researchers say is the first drug to fully reproduce the effects of physical stroke rehabilitation in model mice, following from human studies.
The findings, published in Nature Communications, tested two candidate drugs derived from their studies on the mechanism of the brain effects of rehabilitation, of which one resulted in significant recovery in movement control after stroke in the mouse model.
Stroke is the leading cause of adult disability because most patients do not fully recover from the effects of stroke. There are no drugs in the field of stroke recovery, requiring stroke patients to undergo physical rehabilitation which has shown to be only modestly effective.
Memory engrams are formed through experience-dependent plasticity of neural circuits, but their detailed architectures remain unresolved. Using three-dimensional electron microscopy, we performed nanoscale reconstructions of the hippocampal CA3-CA1 pathway after chemogenetic labeling of cellular ensembles recruited during associative learning. Neurons with a remote history of activity coinciding with memory acquisition showed no strong preference for wiring with each other. Instead, their connectomes expanded through multisynaptic boutons independently of the coactivation state of postsynaptic partners. The rewiring of ensembles representing an initial engram was accompanied by input-specific, spatially restricted upscaling of individual synapses, as well as remodeling of mitochondria, smooth endoplasmic reticulum, and interactions with astrocytes.
A study from Emory University suggests that levodopa, a medication that increases dopamine levels in the brain, may help treat individuals with depression who experience motivational impairments due to high inflammation. Researchers found that a common blood test measuring C-reactive protein (CRP), a blood biomarker of inflammation produced by the liver, could help determine which patients are most likely to respond to repeated doses of levodopa.
The findings, published in the March 2025 print edition of Brain, Behavior and Immunity, show that in participants with CRP levels above 2 mg/L, daily administration of levodopa improved connectivity within a key brain reward pathway—the ventral striatum to the ventromedial prefrontal cortex —after just one week of treatment across a range of doses.
While about half of the participants responded best to a lower dose of 150 mg/day, the other half required up to 450 mg/day for levodopa to effectively overcome the effects of inflammation on this dopamine-rich reward circuit.
