Research Keyword: long-term potentiation

PsilOCD: A Pharmacological Challenge Study Evaluating the Effects of the 5-HT2A Agonist Psilocybin on the Neurocognitive and Clinical Correlates of Compulsivity

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This study is investigating whether psilocybin (an active compound in magic mushrooms) can help people with obsessive-compulsive disorder (OCD) by improving their mental flexibility and brain plasticity. Participants will receive two doses of psilocybin—a low test dose and a slightly higher therapeutic dose—four weeks apart, while receiving professional psychological support. Researchers will measure changes in cognitive abilities and brain activity to understand how psilocybin might help reduce OCD symptoms like intrusive thoughts and repetitive behaviors.

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Impaired spatial memory in adult vitamin D deficient BALB/c mice is associated with reductions in spine density, nitric oxide, and neural nitric oxide synthase in the hippocampus

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This study found that adults with vitamin D deficiency have impaired spatial memory and reduced brain structures called dendritic spines in the hippocampus, the brain region responsible for learning and memory. The researchers identified that low vitamin D decreases nitric oxide production in the brain, which is important for forming and maintaining the synaptic connections needed for memory formation. Importantly, when vitamin D was supplemented back to deficient mice, the brain’s ability to produce nitric oxide was restored, suggesting vitamin D supplementation could potentially improve cognitive function in vitamin D-deficient individuals.

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Glutamate-specific gene linked to human brain evolution enhances synaptic plasticity and cognitive processes

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Scientists discovered that a human gene called GLUD2, which evolved as our brains expanded, makes synapses stronger and more plastic through a lactate-dependent process. When they added this gene to mice, the animals showed improved memory, better learning ability, and stronger brain connections. This research suggests that GLUD2 played a key role in the evolution of human intelligence by enhancing the brain’s ability to form new neural connections and adapt to new information.

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β-secretase inhibition prevents structural spine plasticity deficits in AppNL-G-F mice

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Researchers tested whether a drug that blocks BACE1 (an enzyme involved in Alzheimer’s disease) could protect nerve cell connections in a mouse model of Alzheimer’s disease. They found that at high doses, the drug significantly improved the formation of new dendritic spines (connection points between neurons) and restored synaptic activity to near-normal levels. These findings suggest that using BACE1 inhibitors early in Alzheimer’s disease development, before widespread neuronal damage occurs, might help prevent cognitive decline.

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Cerebral Hypoxia-Induced Molecular Alterations and Their Impact on the Physiology of Neurons and Dendritic Spines: A Comprehensive Review

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This review explains how low oxygen levels in the brain damage nerve cells and their connection points (dendritic spines) through a cascade of molecular changes. The brain normally has protective mechanisms, but severe or prolonged hypoxia overwhelms these defenses, leading to memory loss and cognitive problems. Several molecular pathways and supporting cells called astrocytes and microglia can help protect neurons. Understanding these protective mechanisms may lead to new treatments for brain conditions caused by low oxygen, such as stroke.

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New Positive TRPC6 Modulator Penetrates Blood–Brain Barrier, Eliminates Synaptic Deficiency and Restores Memory Deficit in 5xFAD Mice

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Researchers developed a new drug candidate called C20 that activates TRPC6 proteins in the brain. In studies with Alzheimer’s disease mouse models, C20 protected nerve connections from damage, restored memory function, and successfully crossed the blood-brain barrier. The compound shows promise as a potential treatment for Alzheimer’s disease by strengthening the connections between brain cells that are damaged in the disease.

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