A tiny percentage of our DNA—around 2%—contains 20,000-odd genes. The remaining 98%—long known as the non-coding genome, or so-called ‘junk’ DNA—includes many of the “switches” that control when and how strongly genes are expressed.

Now researchers from UNSW Sydney have identified the DNA switches that help control how astrocytes work—these are brain cells that support neurons, and are known to play a role in Alzheimer’s disease.

In research published in Nature Neuroscience, researchers from UNSW’s School of Biotechnology & Biomolecular Sciences described how they tested nearly 1,000 potential switches—strings of DNA known as enhancers—in human astrocytes grown in the lab. Enhancers can be located very far away from the gene they control, sometimes hundreds of thousands of DNA letters away—making them difficult to study.

New York State Psychiatric Institute and Columbia University Medical Center investigators, with co-authors across additional US centers, report greater cognitive worsening at 78 weeks with valacyclovir than with placebo among adults with early symptomatic Alzheimer’s disease and herpes simplex virus (HSV) seropositivity.

Infectious diseases may contribute to Alzheimer’s disease pathogenesis. HSV-1 can become latent after oral infection, enter the brain via retrograde axonal transport, infiltrate the locus coeruleus, and migrate to the temporal lobe.

β-amyloid plaques and tau neurofibrillary tangles are neuropathological features of Alzheimer’s disease. Animal models connect HSV-1 infection of neuronal and glial cells with a decrease in amyloid precursor protein, an increase in intracellular amyloid β-protein, and phosphorylation of tau protein.

One specific state, referred to as State 4, emerged as a key point of difference between the two groups. This state was characterized by strong connections between the left and right hemispheres of the brain. It specifically involved robust communication between the temporal and parietal regions, which are areas often associated with language and sensory processing.

The data showed that children with autism spent considerably less time in State 4 compared to the typically developing children. They also transitioned into and out of this state less frequently. The reduced time spent in this high-connectivity state was statistically distinct.

The researchers then compared these brain patterns to clinical assessments of the children. They found a correlation between the brain data and the severity of autism symptoms. Children who spent the least amount of time in State 4 tended to have higher scores on standardized measures of autism severity.

In the last few years, progress has been made in the fight against Alzheimer’s disease with a class of therapies called anti-amyloid antibodies (anti-Aβ). These monoclonal anti-Aβs are proteins made in a laboratory to stimulate the immune system to slow the progression of the disease by targeting amyloid plaques in the brain that are characteristic of Alzheimer’s.

Biomarkers, such as measures derived from PET scans that reflect amyloid plaques in the brain, were instrumental in FDA approval of anti-Aβ therapies, like lecanumab (Leqembi) and donanemab (Kisulna), and have been shown to reduce plaques in the brains of Alzheimer’s patients. Yet despite FDA approval, there is still a clinical need to better understand how to monitor the efficacy and safety of these treatments.

To this end, the Alzheimer’s Association convened a workgroup of scientists and clinicians with experience in Alzheimer’s disease, including clinical trials of anti-Aβ therapies and biomarkers, to propose a framework to characterize the response of patients receiving these treatments.

The spinal cord vasculature in development and pathophysiology.

In brain, retina, and spinal cord the vasculature plays an active role as regulator of homeostasis and repair, but vascular cells adopt region-specific traits.

However, vascular organization and properties of spinal cord remain understudied.

Although it is assumed that spinal cord and brain neurovascular systems are built and function in the same way, the researchers challenge this view by examining specific properties underlying spinal cord vascular development, physiology, and pathology.

They highlight unique angioarchitecture and homeostatic mechanisms, and discuss how neurovascular disruption contributes to spinal disorders and regenerative failure after injury. https://sciencemission.com/Neurovascular-dynamics-in-the-sc

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Ruiz de Almodóvar et al. review the unique properties of spinal cord vasculature and its interactions with neural tissue across development, physiology, and disease, highlighting future directions to address open questions in neurovascular biology and translation.

New research from the University of Virginia School of Medicine is revealing why traumatic brain injury increases the chance of developing Alzheimer’s disease—and the discovery is pointing to a potential strategy to prevent the progressive brain disorder.

John Lukens, director of UVA’s Harrison Family Translational Research Center in Alzheimer’s and Neurodegenerative Diseases—housed within the Paul and Diane Manning Institute of Biotechnology—and his team discovered that even one mild traumatic brain injury can set off damaging changes, paving the way for the development of Alzheimer’s.

“Our findings indicate that fixing brain drainage following head trauma can provide a much-needed strategy to limit the development of Alzheimer’s disease later in life,” said Lukens, part of UVA’s Department of Neuroscience and its Center for Brain Immunology and Glia, and author on the new study published in Cell Reports.

Lung cancer cells metastasizing to the brain can form real electrical synapses with neurons, not just hijack brain space — a discovery that may open new therapeutic targets. Researchers found that neuronal activity actually spurs tumor growth and that drugs reducing neuron signaling could slow cancer proliferation.

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Two teams discover how small cell lung cancer hijacks neural pathways to proliferate faster, especially to the brain. Common neuro drugs could be the answer.

Scientists at the University of Colorado Anschutz have discovered that while brain neuron changes, including cell loss, may begin in early life, a drug long-approved for other conditions might be repurposed to slow this damage, offering new hope for those with Alzheimer’s disease (AD) and other cognition issues.

The study was published today in the journal Cell Reports Medicine.

“This drug improved one measure of cognition and reduced a blood measure of neuron death in people with AD in a relatively short period of time in its first clinical trial,” said the study’s senior author Professor Huntington Potter, Ph.D., director of the University of Colorado Alzheimer’s and Cognition Center at CU Anschutz.