NfL in Blood Foretells Poor Brain Health After the Heart Stops
Neurofilament light protein in the serum registers the degree of axonal damage after cardiac arrest, and may help doctors predict long-term consequences for the brain.
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Neurofilament light protein in the serum registers the degree of axonal damage after cardiac arrest, and may help doctors predict long-term consequences for the brain.
Researchers gain traction in the study of these rare tau disorders, which are sometimes confused with Alzheimer’s disease.
International conference gives scientists hope for understanding and treating PSP and CBD.
International Symposium Puts PSP/CBD on the Map Can Clinical Trials and Longitudinal Studies Crack Rare Tauopathies? Tufted astrocytes? Astrocytic plaques? These tau pathologies mark progressive supranuclear palsy and corticobasal degeneration, respective
With plasma tests performing in AIBL staging, scientists are sharing data across platforms and cohorts, and tackling standardization to avoid time lost to irreproducibility.
Toxic Stew of Aβ Dimers Hides Out in Human Plaques How Immune Cells From Blood Beget Aging in Brain Toxic Tau: Who Are You, and Where Are You From? Tau Silences, Aβ Inflames; Hitting Excitatory Synapses Hardest When Glial Clocks Fall Out of Sync, Inflamma
Brains of Alzheimer’s patients contain Aβ dimers consisting of monomers Aβ37 to Aβ42 and held together by covalent bonds.
Scientists at CTAD were excited about postmortem validation of tau scans and new, more sensitive tracers. Others are exploring practical applications for live imaging of tau pathology.
People with a lot of neurofilament light protein in their spinal fluid are more likely to develop mild cognitive impairment in the next four years.
Cultured sensory neurons from ALS mouse models have truncated, less-complex neurites that grow slowly compared to controls.
Researchers are applying the proposed 2018 NIA-AA diagnostic criteria to three large, standing cohorts. How did the research framework perform?
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
At CTAD, intranasal insulin trial stumbles, pioglitazone gets a postmortem, a RAGE inhibitor tries to hang on.
At CTAD, researchers discussed baseline data from the first 500 participants in the EPAD cohort and, finally, the start of recruitment for TRC-PAD.
In sporadic and familial forms of AD, progranulin climbs in the cerebrospinal fluid as disease progresses, perhaps reflecting microglial activation.
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