Harvard Medical School other research news

Harvard researchers and colleagues published in Nature Genetics an association between a deletion in the A2M gene and increased risk of developing AD (p=0.001). A2M is thought to be involved in the clearance of beta-amyloid protein by both protease digestion and internalization from serum into cells via the LRP1 receptor (low-density lipoprotein receptor-related protein). A2M, apolipoprotein E (ApoE) and the beta- amyloid precursor protein APP all are ligands for the same receptor (LRP1) and all now are implicated in AD, leading the researchers to suggest that there may be a common neuropathogenic pathway leading to AD.

However, while the deletion in A2M was linked to AD it did not affect age of onset of AD, in contrast to the e4 allele of ApoE. The researchers concluded that A2M may influence whether, but not when, an individual will develop AD. ...