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View article: Pharmacologic reversal of advanced Alzheimer’s disease in mice and identification of potential therapeutic nodes in human brain
Pharmacologic reversal of advanced Alzheimer’s disease in mice and identification of potential therapeutic nodes in human brain Open
Alzheimer's disease (AD) is traditionally considered irreversible. Here, however, we provide proof of principle for therapeutic reversibility of advanced AD. In advanced disease amyloid-driven 5xFAD mice, treatment with P7C3-A20, which res…
View article: Astrocytic abnormalities in brain-specific <i>Cacna1c</i> -deficient mice: Implications for BBB impairment in neuropsychiatric diseases associated with <i>CACNA1C</i> mutations
Astrocytic abnormalities in brain-specific <i>Cacna1c</i> -deficient mice: Implications for BBB impairment in neuropsychiatric diseases associated with <i>CACNA1C</i> mutations Open
Intronic genetic variants within the CACNA1C gene, which encodes the pore-forming alpha 1c subunit of the Cav1.2 L-type calcium channel, are significant risk factors for a multitude of neuropsychiatric disorders. In most cases, these intro…
View article: Inhibiting 15-PGDH blocks blood–brain barrier deterioration and protects mice from Alzheimer’s disease and traumatic brain injury
Inhibiting 15-PGDH blocks blood–brain barrier deterioration and protects mice from Alzheimer’s disease and traumatic brain injury Open
Alzheimer’s disease (AD) and traumatic brain injury (TBI) are currently untreatable neurodegenerative disorders afflicting millions of people worldwide. These conditions are pathologically related, and TBI is one of the greatest risk facto…
View article: Deterioration of neuronal primary cilia in Alzheimer’s disease
Deterioration of neuronal primary cilia in Alzheimer’s disease Open
Background Emerging evidence links Alzheimer’s disease (AD) to dysfunction of the primary cilium, a historically overlooked organelle that serves as the neuron’s antenna. All neurons harbor a single primary cilium that projects from the me…