Researchers See Advanced Glycation End-Products as Critical in Alzheimer Progression

Researchers at Case Western Reserve University in Cleveland, Ohio have shown further evidence that Advanced Glycation End-products (A.G.E.s) are a critical factor in the early progression of Alzheimer's disease.

The researchers speculate that the ability to improve the A.G.E. pathway may hold substantial promise in the management of the disease.

A.G.E.s are formed in the body when glucose reacts with proteins, such as collagen. A.G.E.s further crosslink with each other, forming bonds that lead to a loss of flexibility and function of tissues, organs and vessels. The formation and crosslinking of A.G.E.s are part of the normal aging process and are accelerated in diabetes, where higher sugar levels are present.

Research has shown that A.G.E.s are a factor in many complications of aging and diabetes, including heart, kidney and eye diseases.

The ability to inhibit A.G.E.s and their chemical crosslinks may impact these diseases, according to the study published in Free Radical Biology & Medicine.

Researchers examined postmortem human tissue samples in 27 persons known to have had Alzheimer's disease. Their results show that A.G.E.s may produce harmful biochemical consequences and are a factor in the accumulation of neurofibrillary tangles found in Alzheimer's.

Their study also confirms that active glycation is still occurring in Alzheimer's 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, Ph.D., Professor at Case Western Reserve University.

Other sources: Case Western Reserve, Alteon