Harvard Scientists Clear Path For Study Of Early Onset Alzheimer's Disease


Beta-amyloid plaques found in Alzheimer's patients: image via wikipedia.comBeta-amyloid plaques found in Alzheimer's patients: image via wikipedia.comResearchers at Harvard University's Stem Cell Institute have converted skin cells of patients with early-onset Alzheimer's disease into neurons that are typically affected by the disease. This is the first time researchers have been able to study the disease in human, rather than animal, cells, and this ability enhances the possibilities for earlier treatments for the disease.

Experimental treatments for Alzheimer's disease have been hit or miss, often because testing is done on animal cells.  In this study, published in the journal Human Molecular Genetics and led by Dr. Tracy Young-Pearce, human skin cells, converted to Alzheimer's-affected neurons, confirmed what was found in mouse cells - a rise in neuronal Ab42 (amyloid-beta 42) that clumps together. Unexpectedly, however, researchers found a rise in Ab38, not typically a clumping amyloid-beta, but one which Young-Pearce suspects helps form the amyloid beta plaques common in Alzheimer's.

Another very important finding was that the tangled tau proteins present in the human cells could be 'rescued' by making adjustments to amyloid-beta, thereby indicating that tau proteins are distorted by the presence of amyloid-beta, and not the reverse - a controversy among Alzheimer's researchers.

“Not only is it important experimentally to show that tau elevation is due in some part to altered amyloid-beta accumulation, but it also shows that this is an excellent system for testing different therapeutic options,” said Young-Pierce.

Young-Pearce will be conducting further studies with patient-derived cells. She is particularly interested in learning why the hippocampus, the memory center of the brain, is affected by Alzheimer's cells, but other areas of the brain are not affected.  

An estimated 5 to 10 percent of all Alzheimer's disease cases are known as early-onset Alzheimer's disease.  It can start in one's 30's, 40's, or 50's, and it proceeds rapidly. Familial Alzheimer's also appears to have a different biochemical path than non-familial Alzheimer's; it is passed down by a dominant gene and there is a 50 percent chance that it will be expressed.


sources: Harvard Gazette, Human Molecular Genetics