Washington, March 15 (IANS) Curbing excess production of a peptide associated with Alzheimer’s disease could potentially show the way to a therapy where none currently exists, according to University of California researchers The study led by Vivian Y.H. Hook, findings of which have been published in the latest issue of the Journal of Biological Chemistry, demonstrated substantial memory improvement in an animal model of Alzheimer’s.

The disease is characterised by accumulation of amyloid plaque deposits, noticed during autopsy of the patient’s brain. The plaque is composed primarily of neurotoxic beta-amyloid (AB) peptide, believed to be a major factor in causing Alzheimer’s.

These peptides are ‘cut’ out from a larger protein called the amyloid precursor protein (APP) and bind together to form plaques in brain regions responsible for memory. One drug strategy to fight Alzheimer’s disease is to reduce production of AB.

“We discovered two chemical compounds that inhibit a new enzyme target, leading to reduced production of AB and improved memory in a mouse model of Alzheimer’s disease. After drug treatment, using water maze memory tests, we found that the mice exhibited great improvement in their memory, as well as reduced brain levels of beta amyloid.

“These results are consistent with previous research indicating that a different protease, called Cathepsin B (CatB), is elevated in brains of Alzheimer patients,” said Hook.

She added that a drug that duplicates this reduction by targeting CatB in humans could be an effective treatment for Alzheimer’s disease in the more than 99 percent people with the normal beta-secretase site.

“By disabling the enzyme’s ability to cut the ‘beta’ end of the amino acid sequence, researchers may discover a way to limit production of neurotoxic AB and reduce amyloid plaques in the brain.”