Tau’s apparent lockstep with cognitive decline dominated the PET conversation. Piramal flaunted data, and Merck/Cerveau are close behind. A first stab at imaging synapses in the hippocampus drew notice, too.
In patients across a range of neurodegenerative diseases, NfL ramps up in the cerebrospinal fluid. Levels are higher in those with worse disease.
The awards total $52 million, divided among 17 early career investigators and nine collaborative science teams.
11th ICFTD Meeting in Sydney Sorts Out Clinical Subtypes Natural History Studies Provide Foundation for FTD Research Tracking Onset and Progression of Frontotemporal Dementia A Proteomics Dive into Cause of Frontotemporal Dementia Encompassing more than ...
Swine that express mutated human SOD1 exhibit the hallmarks of ALS pathology, including aggregates and degeneration in motor neurons, preceded by a lengthy preclinical phase.
At SfN, some scientists described how circulating immune cells deliver aging to the mouse hippocampus; others held off parkinsonism by blocking the effects of eotaxin’s rise in blood. Human trials are starting.
Researchers are applying the proposed 2018 NIA-AA diagnostic criteria to three large, standing cohorts. How did the research framework perform?
Five years after its creation, the WDC met in London to reflect, articulate next steps, and announce more sharing of BACE trial data.
Recent conferences revealed that tau is most toxic in oligomeric form, that tau oligomers propagate throughout the brain, and that tau oligomers might harm synapses from within or via astrocytes.
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, ...
Disrupting circadian clocks in astrocytes and microglia unleashed harmful responses in these glial cells, leading to neuronal damage.
By marrying iPSCs, human genomic data, and analysis of postmortem tissue, researchers tied loss of GABAergic signaling to tauopathies such as FTD and PSP, but not AD.
An ultrasensitive assay picked up elevated concentrations of N-terminal tau fragments in the blood of people with AD.
Recent failures of clinical trials targeting amyloid-β in mild to moderate Alzheimer’s disease (AD) have led to claims that the interventions are too little too late...
Absent the receptor, microglia ignore Aβ seeds and new plaques, which then absorb little ApoE and stay diffuse.