Is there a causal relationship between depressive disorders and late-life neurodegenerative diseases? Or, is their co-occurrence due to confounding or common risk factors, such as aging?
Plasma tau phosphorylated at threonine 217 can be used to accurately differentiate Alzheimer’s disease from other neurodegenerative diseases.
Specific features of epileptiform abnormalities are associated with clinical seizures in Alzheimer disease, like right temporal hyperexcitability.
Anticholinergic medications are associated with an increased risk for incident mild cognitive impairment and cognitive decline in older adults.
There is no evidence supporting the causal role of disturbed sleep patterns on AD or between major depression and AD.
MRI-based cerebrovascular reactivity is associated with cognitive function independent of Alzheimer disease pathology.
The FDA has accepted for Priority Review the Biologics License Application for aducanumab for the treatment of Alzheimer disease.
The Lancet Commission added 3 new risk factors for dementia that coupled with the previous 9 lifestyle risk factors might prevent or delay up to 40% of dementias worldwide.
Years of education and the ε4 risk allele at APOE influence β-amyloid pathology in asymptomatic individuals with a parental history of sporadic AD, while only years of education influence β-amyloid pathology in presymptomatic autosomal dominant AD mutation carriers.
Plasma tau phosphorylated at threonine 217 (P-tau217) shows promise as a biomarker for Alzheimer disease (AD).
