We review the genetic risk factors for late-onset Alzheimer’s disease (AD) and their role in
AD pathogenesis. More recent advances in understanding of the human genome—…

Abstract Development of tau-based therapies for Alzheimer’s disease requires an understanding
of the timing of disease-related changes in tau. We quantified the phosphorylation state …

Genome-wide association studies (GWAS) have identified several risk variants for late-onset
Alzheimer's disease (LOAD) 1 , 2 . These common variants have replicable but small effects …

The impact of apolipoprotein E ε4 (APOE4), the strongest genetic risk factor for Alzheimer's
disease (AD), on human brain cellular function remains unclear. Here, we investigated the …

We developed stable isotope labeling and mass spectrometry approaches to measure the
kinetics of multiple isoforms and fragments of tau in the human central nervous system (CNS) …

Alzheimer's disease (AD) is a clinically heterogeneous neurodegenerative disease with a
strong genetic component. Several genes have been associated with AD risk for nearly 20 …

Alzheimer’s disease (AD) is the most prevalent cause of dementia 1 . Although there is no
effective treatment for AD, passive immunotherapy with monoclonal antibodies against …

Macrophages are important players in the maintenance of tissue homeostasis 1 .
Perivascular and leptomeningeal macrophages reside near the central nervous system (CNS) …

Alzheimer’s disease (AD) pathology develops many years before the onset of cognitive
symptoms. Two pathological processes—aggregation of the amyloid-β (Aβ) peptide into plaques …

Background Identifying individuals at risk for developing Alzheimer disease (AD) is of utmost
importance. Although genetic studies have identified AD-associated SNPs in APOE and …