Young people who abuse heroin may suffer brain damage similar to what’s seen in the early stages of Alzheimer’s disease, according to UK researchers.

Comparing autopsied brain tissue from young heroin abusers and non-drug users, UK researchers found that before they died, the drug users had begun to develop damage in brain areas involved in learning, memory and emotion.

Specifically, they had heightened levels of two proteins that contribute to the “plaques” and “tangles” that build up in the brains of people with Alzheimer’s.

One of these proteins is called tau, and drug users in this study showed higher levels of an abnormal, insoluble form of tau that is seen the tangles that mark Alzheimer’s and other forms of dementia.

“Since abnormal tau is clearly linked to dementia in a number of other conditions,” said senior study author Dr. Jeanne E. Bell, “there is cause for worry about accelerated aging of the brain in people who start to abuse opiates at a young age.”

It’s unlikely that the protein levels seen in drug abusers’ brains had already caused problems with thinking, memory or behavior, according to Bell, a professor of neuropathology at the University of Edinburgh.

“However,” she added, “our findings do relate to areas of the brain involved in memory and emotional control, and if the process were to continue at an accelerated pace in opiate abusers compared with non-abusers, it seems likely that symptoms would follow.”

The findings were published online this week by the journal Neuropathology and Applied Neurobiology.

For their study, Bell and her colleagues examined brain tissue from 34 intravenous drug users younger than 40 who had abused heroin or methadone. Most had died of a drug overdose; one committed suicide.

For comparison, the researchers also looked at tissue from 16 people in the same age range who had died suddenly and had no known history of drug abuse.

While none of the brain tissue contained Alzheimer’s-like “plaques” - deposits composed of a protein called beta-amyloid - drug abusers were much more likely to show evidence of beta-amyloid precursor protein in two brain areas. This protein, when broken up by specific enzymes, forms the beta-amyloids that mark Alzheimer’s plaques.

Drug abusers were also far more likely than the comparison group to have brain tangles composed of abnormal tau.

More than twice as many opiate users - 44 percent versus 19 percent - showed such protein deposits. And while the tangles were limited to one brain area in non-drug users, they were more widespread in drug abusers’ brains.

The findings, Bell said, show only an association between drug abuse and abnormal protein deposits in the brain, and so cannot establish heroin or other opiates as the cause.

That means it’s also impossible to say whether the brain damage could be reversed if the drug abuse were to stop, according to the researcher.

It will be important, Bell noted, to find out whether opiates in fact cause the abnormal protein deposits, and if they do, the mechanisms at work. Doing so, she said, could also yield clues to the early development of Alzheimer’s and other forms of dementia.

SOURCE: Neuropathology and Applied Neurobiology, online June 21, 2005.