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Study links glucose/protein complexes to Alzheimer's disease
A Correspondent, N.J. | Wednesday, August 8, 2001, 08:00 Hrs  [IST]

Alteon Inc reported that a team of researchers at Case Western Reserve University have provided further evidence that Advanced Glycation End-products (A.G.E.s) are a critical factor in the early progression of Alzheimer's disease (AD). The authors suggest that therapeutic strategies aimed at ameliorating the A.G.E. pathway hold substantial promise in the management of the disease.

A.G.E.s are naturally formed throughout the body when blood sugar (glucose) reacts with proteins, such as collagen or elastin. A.G.E.s further crosslink with each other, forming bonds that lead to a loss of flexibility and function of body tissues, organs and vessels. The formation and crosslinking of A.G.Es. is an inevitable part of the aging process, and are accelerated in diabetes, where higher sugar levels are present. The scientific literature points to A.G.E.s as a causative factor in many complications of aging and diabetes, including heart, kidney and eye diseases.

Alteon's approach is to inhibit or "break" A.G.E.s and their chemical crosslinks, thereby potentially impacting such disease states. The company is a worldwide leader in the research and development of compounds that target the A.G.E. pathway.

The researchers examined postmortem human tissue samples from 27 pathologically confirmed AD cases. Their results suggest that A.G.E.s produce deleterious biochemical consequences, and are a factor in the accumulation of neurofibrillary tangles in AD. Their data also confirms that active glycation is still occurring in AD lesions throughout their existence.

"Furthermore, A.G.E.s predate the formation of the pathological lesions of Alzheimer's disease, suggesting they play an early and detrimental role in the disease process," said George Perry, Professor and Chair of Pathology, Case Western Reserve University.

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