The protein beta amyloid that accumulates in Alzheimer'sdisease prompts nerve tissue damage when it is depositeddirectly into the brain of rats, supporting the theory that theprotein is causative in the disease.

According to neurobiologist Bruce Yankner and colleagues,reporting this week in the Proceedings of the NationalAcademy of Sciences, beta amyloid damage was prevented bygiving the rats substance P, a peptide neurotransmitter.

Yankner and his colleagues at Children's Hospital andMassachusetts General Hospital in Boston and the University ofAlaska in Fairbanks had shown last year that the protein istoxic to neurons grown in the lab and that the effect could beblocked by substance P.

In the latest research, the neurotoxic effect of beta amyloidwas observed with intracerebral injection of an amount of theprotein equivalent to the content of a single senile plaque fromAlzheimer's patients. The intracerebral beta amyloid causedchanges in the rat brain that resemble the human pathology inthe disease, the researchers wrote.

The injection also prompted induction of the Alz-50 antigen.Alz-50 proteins form paired helical filamentsindistinguishable from neurofibrillary tangles, which are theother pathologic feature of Alzheimer's.

Substance P can cross into the brain from the bloodstream, andit is one of the neuropeptides depleted in the brains ofAlzheimer's patients, the scientists said. If neuronal death isindeed due to beta amyloid, the scientists wrote, thensubstance P could provide the basis for a neuro-protectivetherapy.

-- Roberta Friedman, Ph.D. Special to BioWorld

(c) 1997 American Health Consultants. All rights reserved.