Researchers at INSERM and collaborators have identified hypothalamic tanycytes as mediators of tau clearance and shown that their structural and genetic disruption may drive Alzheimer’s disease pathology.
Researchers at INSERM and collaborators have identified hypothalamic tanycytes as mediators of tau clearance and shown that their structural and genetic disruption may drive Alzheimer’s disease (AD) pathology. AD is characterized by the buildup of extracellular amyloid-β plaques and intracellular tau tangles, protein aggregates that disrupt neuronal function and drive neurodegeneration.
Tau is an intrinsically disordered protein that regulates the stability and dynamics of microtubules in physiological conditions. Recent work has revealed the involvement of tau in various neuronal processes. Researchers from the University of California and collaborators aimed to systematically investigate the cellular factors that control the accumulation of tau aggregates in human neurons.
Brain-derived tau, a protein that is exclusive to the brain and detectable in the blood, could serve as an indicator of brain damage after an ischemic stroke. The analysis of this special form of tau has revealed a relationship between high levels of the protein and extensive brain injury, a higher risk of complications, and poorer outcomes.
Experts agree that the earlier Alzheimer's disease is detected, the sooner action can be taken. And so, the key to preventing deterioration is identifying the most effective early biomarkers, those that can spot the disorder and help halt its progression. Recent advances in the field have pushed a new era of early detection through blood-based biomarkers and personalized medicine strategies based on each patient’s genetic, immunological and clinical profile.
Experts agree that the earlier Alzheimer's disease is detected, the sooner action can be taken. And so, the key to preventing deterioration is identifying the most effective early biomarkers, those that can spot the disorder and help halt its progression. Recent advances in the field have pushed a new era of early detection through blood-based biomarkers and personalized medicine strategies based on each patient’s genetic, immunological and clinical profile.
A little-known tissue composed of a cluster of immune cells could offer novel insights into the development of neurological disorders. Meninges' immune system changes with age and neurodegeneration. Are they protecting the brain or fueling disease?
The difference between the origin of Alzheimer's disease (AD) and its symptoms is an obstacle to finding effective treatments. Scientists focused on amyloid-β (Aβ) plaques and tau aggregates to slow neurodegeneration and cognitive decline. Without identifying what causes AD, approved treatments do not provide much benefit.
A little-known tissue composed of a cluster of immune cells could offer novel insights into the development of neurological disorders. Meninges' immune system changes with age and neurodegeneration. Are they protecting the brain or fueling disease? Mapping and analyzing the so-called ectopic lymphoid structures (ELSs) in the meninges at different ages in preclinical models of neurodegenerative diseases such as Alzheimer's may help clarify whether they are good, bad, or ugly, as in the iconic film by Sergio Leone.
The difference between the origin of Alzheimer's disease (AD) and its symptoms is an obstacle to finding effective treatments. Scientists focused on amyloid-β (Aβ) plaques and tau aggregates to slow neurodegeneration and cognitive decline. Without identifying what causes AD, approved treatments do not provide much benefit. However, new findings suggest that restoring lithium levels in the brain could prevent and treat AD. Not just any lithium would work, just the forms that do not bind to Aβ.
