PhD Programs in Chemistry and Biochemistry, the Graduate Center of the City University of New York, New York, New York 10016, United States Department of Chemistry, York College of the City University ...

This manuscript provides fundamental studies to help us better understand the effects of mutations in the presenilin-1 (PSEN1) gene on proteolytic processing of the amyloid precursor protein (APP).

Diagnosis and monitoring of sporadic Alzheimer's disease (AD) have long depended on clinical examination of individuals with end-stage disease. However, upcoming anti-AD therapies are optimally ...

In humans, harmful tau protein deposits, known as tau tangles, appear early in life and spread widely through the brain, ...

Many of these treatments aim to modify the disease process itself. One of the hallmarks of Alzheimer’s disease is protein plaques that form between brain cells, made of beta-amyloid fragments. These ...

In contrast, these tangles are rare in non-human primates and typically confined to small regions of the brain. Clumps of ...

The drugs attack so-called amyloid plaques in the brain. But how can we reliably and cost effectively diagnose the presence of amyloid plaques in patients who show up at memory clinics with slight ...

Avoid fusions to the GFP fragments at the site of protein-protein interaction and consider optimizing the spacer length between the fusions and GFP fragments, if necessary. In the absence of ...

While primates may develop beta-amyloid deposits—fragments derived from amyloid precursor protein—these deposits are less toxic and do not interact with tau tangles to trigger Alzheimer’s ...

Two types of proteins play roles in the pathology of Alzheimer’s disease: fragments of beta-amyloid protein form plaques that disrupt nerve cell function, and another protein, named tau, forms threads ...