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University of Alabama at Birmingham


Pathogenic Alzheimer's disease cascade is activated by faulty norepinephrine signaling

Scientists discovered a key mechanism underlying Alzheimer's pathology, revealing how amyloid-beta oligomers hijack norepinephrine signaling to activate GSK3-beta and hyper-phosphorylate tau protein. This rewiring of the alpha-2A adrenergic receptor may explain the failure of previous clinical trials targeting amyloid protein buildup.

SourceUniversity of Alabama at Birmingham·JournalScience Translational Medicine·DateJan 15, 2020

How IL-6 allows the immune response to develop for a key cell, the T follicular helper

A preclinical study shows that IL-6 protects T follicular helper cells from deleterious effects of IL-2 by interrupting a feedback loop, allowing them to receive sustained T-cell receptor stimulation. This finding has important therapeutic implications for autoimmune diseases like lupus and may lead to better treatment options.

SourceUniversity of Alabama at Birmingham·JournalScience Immunology·DateSep 13, 2019

A NEAT discovery about memory

A team of researchers has identified a tissue-specific non-coding RNA called NEAT1 that regulates memory formation in the hippocampus region of the brain. Increasing NEAT1 levels in younger mice impaired learning and memory, while decreasing NEAT1 levels improved cognitive function.

SourceUniversity of Alabama at Birmingham·JournalScience Signaling·DateJul 2, 2019

New research addresses incidence of atrial fibrillation after aortic valve replacement

Researchers found that approximately 50 percent of hospitalizations for both TAVI and surgical aortic valve replacement were associated with the development of new atrial fibrillation. Hospitalizations with new atrial fibrillation had higher odds of in-hospital stroke and in-hospital death compared to those without, highlighting the ne...

SourceUniversity of Alabama at Birmingham·JournalJAMA Internal Medicine·DateJun 3, 2019