TREM2 levels tracked with tau, but varied widely among patients and carriers of different mutations, leaving it unclear whether TREM2 helps or hurts.
Probing this this Alzheimer’s risk factor, scientists find a novel variant, but no consensus yet on how this cell surface receptor increases risk for disease.
For the first time, scientists report a crystal structure of TSPO, a potential target for PET imaging of neuroinflammation.
Hoping for better luck in clinical trials than their Alzheimer’s colleagues had in the past decade, FTD researchers are now chasing biomarkers. It’s slim pickings so far, but neurofilament, tau PET, and MRI are showing promise.
Study improves confidence in three core biomarkers and five emerging markers, most in cerebrospinal fluid and one in blood.
Can proteins in the cerebrospinal fluid help tell movement disorders apart and predict who will develop dementia?
Identifying injuries that might lead to chronic traumatic encephalopathy or other neurodegenerative pathologies, and then treating those injuries, are two major challenges...
Individual labs are experimenting trying to improve the differential diagnoses of related dementias...
At a workshop on engaging more black Americans in ADRD research, new CSF findings stood out against a general dearth of data on Alzheimer’s disease in underrepresented minorities.
Despite having a higher incidence of Alzheimer’s or a related dementia, relatively few black people participate in research studies or drug trials. How to achieve full representation?
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.
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.
Large IDEAS data set establishes that PET scans are valuable in clinical practice. Other studies suggest CSF biomarker ratios perform nearly as well.
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.
In sporadic and familial forms of AD, progranulin climbs in the cerebrospinal fluid as disease progresses, perhaps reflecting microglial activation.