Brain-maiming protein may have spread via surgery

A dangerous protein that attacks the brain's blood vessels may have infected children via poorly sterilized surgical instruments decades before the onset of harmful bleeding, researchers reported recently.

Investigating a quartet of mysterious cases in Britain of brain lesions caused by amyloid beta deposits in young adult patients, they found that all four had undergone brain surgery as kids, suggesting a causal link.

"It is introduced into children, takes 30 years to develop, and then -- when they are in their 30s -- the blood vessels are completely loaded with amyloid beta, which destroys the vessels," a professor of Neurology and lead author of a study detailing the findings, told the media.

"This is a very well-known phenomenon in the elderly, but it is unknown in young people."

A large-scale review of medical registries -- already in the pipeline -- will be needed to confirm the deadly protein can be spread by dirty surgical instruments, he added.

Amyloid beta is one of the signature proteins of Alzheimer's, but there were no signs of the disease in the cases examined, according to the study published recently.

"We didn't find any significant amount of the pathological tau protein, which is the other hallmark protein of Alzheimer's," the lead author said.

Previous work with lab animals had shown that tiny amounts of amyloid beta can stick to steel wires and transmit the pathology into animals' brains.

In 2015, the researchers uncovered amyloid beta deposits in the brains of people who had been treated as children with growth hormones extracted from human cadavers, another indication the protein can jump from one person to another.

It has also long been known that the brain-wasting protein that causes Creutzfeldt-Jakob disease, the human variant of "mad cow" sickness, can be passed on via medical procedures, or by eating infected brain matter.

Hospitals sterilize surgical equipment with high-pressure steam and chemicals that kill viruses and bacteria, but the new findings suggest these methods may not always be adequate.

'Just sterile dirt'

"What we didn't know at the time is that proteins can still be transmitted," said the researcher, who worked as a neurosurgeon for several years in the early 1990s.

He recalled one surgeon at work holding up a stainless steel instrument that had residue from a previous operation.

"'Don't worry,' the nurse in charge of sterilisation said through her mask, 'it's just sterile dirt'."

Hygiene standards are more stringent now, but the capacity of brain-attacking proteins to withstand sterilization is still unknown.

The incidence of infection during surgery with amyloid beta may be far higher than suspected, the researcher said.

But if the protein is transmitted into an adult and doesn't show up until late in life, it then becomes impossible to know whether it comes from the brain operation or the natural ageing process.

Unlike Creutzfeldt-Jakob disease, which causes one death per million people each year, amyloid beta build-up is very common among the elderly, even when there are no signs of dementia.

"So that means that there might a lot more cases of contamination, but that we simply can't tell them apart," the researcher said.

Outside experts said the results were suggestive but needed to be backed up by more research.

"This study provides strong, if circumstantial, evidence for an association between neurosurgery in childhood and the development in late adult life of cerebral amyloid angiopathy (CAA)," said  a clinical psychiatrist, using the clinical name of the disease caused by the protein.

The chief scientific officer at Alzheimer's Research , made a similar assessment, adding: "Any potential link will need to be explored in much larger studies."
The researcher said he has already gotten a green light from ethics watchdogs to comb through neuropathology records.

"We plan to identify those brain biopsies of people 50 or younger who -- for any reason -- had a brain bleed caused by amyloid beta," he explained.

"Then we'll go to the clinical notes to check if they had a surgical procedure in their childhood."

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Bipolar Disorder Drugs May 'Tweak' Genes Affecting Brain

Medications taken by people with bipolar disorder may actually be nudging hundreds of genes that direct the brain to behave more normally, according to new research.

The study suggests that anti-psychotic drugs activate a wide range of genes, changing their function. 

"A gene's activity in any given cell will vary depending on what it's exposed to.

It's not often that scientists stumble upon something in research that they totally weren't expecting to see. "It was a major surprise to us that people treated with an antipsychotic [medication] had changes in the gene expression pattern.

The findings could help point the way to new gene-targeted and stem cell therapies, and provide valuable insight into what causes manic-depressive mood swings.

However, a genetics expert not connected to the study was more cautious about drawing implications from its findings.

Bipolar disorder, also known as manic-depressive illness, affects about 5.7 million American adults, or about 2.6 percent of the U.S. population aged 18 and older, according to the U.S. National Institute of Mental Health (NIMH). The brain disorder causes severe and unusual shifts in mood, energy, activity levels, and the ability to carry out routine daily tasks.

The new research, published in a recent issue of the journal Bipolar Disorders, involved examining 26 brains donated to a nonprofit brain bank. Fourteen of the brains were from people who had bipolar disorder. Of those, seven were from people who had been taking one or more antipsychotic medications -- such as clozapine, risperidone and haloperidol -- when they died. Twelve brains were from those with no mental health condition.

In comparing the brains, the scientists observed that the genes of those that had been exposed to anti-psychotics at the time of death or during their lifetime were similar to those from people who did not have bipolar disorder. This suggests that the drugs may normalize or suppress the kinds of brain pathology one would expect in bipolar disorder, according to the researchers.

The study also supports the idea that the ability of brain cells to effectively communicate with each other may be impaired in people with bipolar disorder. The researchers found that the brains of people who were taking anti-psychotics and those who did not have bipolar disorder showed striking similarities in how their brains relayed signals between cell gaps, or synapses, and on high-speed neuronal "freeways" called the nodes of Ranvier.

While anti-psychotic medications can often be effective in moderating the effects of bipolar disorder, the side effects are often difficult for people to deal with. These include metabolic syndrome -- a combination of symptoms that increase the risk of developing cardiovascular disease and diabetes -- as well as weight gain, increased blood sugar levels, and tremors.

"It's still not known if these changes just happen to occur or play a key role in the therapeutic effect," said a Dr. 

The researchers don't have data on what medications the brains were exposed to during their lifetimes. Patients [with bipolar disorder] are exposed to antidepressants, drugs of abuse, and other medications, and we don't have medication exposure data on the brains [of the people without bipolar disorder].

According to the study, the research represents a step toward a radical evolution in the design of drugs for psychiatric conditions by the pharmaceutical industry.

"A lot of these psychiatric illnesses fluctuate, but now we give medications at a constant rate, almost as if we were giving a diabetic the same amount of insulin no matter what the person's blood sugar is," a  researcher said. "Medications as we know them will change based on our understanding of the biological mechanisms behind disease."