A new method for accelerating the maturation of neuronal cell models and brain organoids is poised to make it possible to track the etiology of neurodegenerative diseases that develop over decades.
Microglia are the brain’s innate immune cells that maintain brain health and play a key role in Alzheimer's disease (AD). Triggering receptor expressed on myeloid cells 2 (TREM2) acts as a regulator of microglial cells and restores neuronal functioning.
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.
The Jackson Laboratory has disclosed short transient receptor potential channel 3 (TRPC3) and short transient receptor potential channel 6 (TRPC6) antagonists reported to be useful for the treatment of Alzheimer’s disease.
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.
Phosphorylation of the protein Tau is a key post-translational feature in tauopathies like Alzheimer’s disease (AD), which leads to microtubule dysfunction and Tau accumulation. Recent findings have suggested the blockade of the adenosine A2A receptor as an approach that improves the outcome in amyloid and Tau models.
Subtyping is what made precision medicine in cancer a reality. And for successful drug discovery in all its stages, finding subtypes in Alzheimer’s disease is all but imperative.
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.
Abnormal tau aggregation is a hallmark of Alzheimer’s disease (AD) and a major contributor to neurodegeneration, synaptic dysfunction, and progressive functional decline. Antibodies against extracellular tau represent a potential therapeutic approach aimed at reducing pathological spread and delaying the clinical progression of AD. Researchers from Merck & Co., Inc. presented the preclinical development of MK-2214, a murine IgG2a monoclonal antibody that selectively targets the pathological phospho-epitope pSer413 of the tau protein.
