15 Alzheimer’s breakthroughs that give hope for the future

Late last year, scientists reported in the Journal of Nuclear Medicine that they had identified a new PET (positron emission tomography) tracer for tau tangles in the brain. The protein tau collects and builds up in the brains of people with Alzheimer’s. The tracer – called Flortaucipir – has been used in research since 2013 and is now awaiting regulatory approval for more widespread use. Identifying tau tangles in the brain can help diagnose Alzheimer’s. Drug developers are also hoping to target these tangles with new drugs.

At the moment, positron emission tomography imaging (PET scans) or invasive tests like sampling your cerebrospinal fluid are the only ways to catch Alzheimer’s in its early stages. But researchers have been developing blood tests that can detect amyloid beta, a toxic protein that forms the brain plaque associated with Alzheimer’s disease.

Scientists from Germany and Sweden analysed archived blood that was collected between July 2000 and December 2002 in a study of adults aged 50 to 75. The researchers then compared the samples from adults who were later diagnosed with Alzheimer’s with those from people who didn’t develop the disease. The new test correctly identified those with Alzheimer’s in almost 70 per cent of cases. Even better, this test could have spotted the disease up to eight years earlier. Another study produced a blood test that could spot Alzheimer’s even sooner – up to 20 years before diagnosis.

Even though a blood test won’t cure Alzheimer’s, it could help researchers develop treatments designed to slow the progress of the disease by identifying at-risk patients before too much damage has occurred. More work needs to be done to advance the treatment, but some researchers are hopeful that the blood test will be readily available to the public within a few years.

Even in the age of modern medicine, most new drugs and treatments for Alzheimer’s fail. Which is why experts are cautiously optimistic about something called BAN2401: not only does this antibody reduce amyloid brain plaques, but it also slows cognitive decline. In the study, reports the New York Times, researchers gave 856 patients from the United States, Japan and Europe injections of BAN2401. Doctors had previously diagnosed the patients with either mild cognitive impairment or mild Alzheimer’s dementia; they all had large amounts of amyloid beta in their brains. Only 161 patients were injected with the highest of the five doses of BAN2401 – every two weeks for 18 months. In the highest-dose group, 81 per cent showed significant drops in their amyloid levels. While their cognitive skills still declined, they did so at a rate that was 30 per cent slower than the placebo group’s rate of decline.

More trials are needed to truly determine the drug’s effectiveness and safety before the FDA gives its stamp of approval for Alzheimer’s patients.

Tau is a protein in the brain that can twist into microscopic fibres called tangles. When this happens, cells die because nutrients can no longer move through them; the brain’s transport systems eventually disintegrate. “Tau tangles are not unique to Alzheimer’s disease,” says  Dr Heather Snyder, senior director of medical and scientific operations at the Alzheimer’s Association. “Tau clumps in other brain diseases, like Parkinson’s disease dementia, so it’s being researched in other communities as well.”

Fortunately, scientists from the University of Texas Southwestern’s O’Donnell Brain Institute have just discovered how and when a healthy tau protein becomes toxic – what the study authors call the “Big Bang” of Alzheimer’s disease. The researchers found that a tiny portion of the toxic tau protein that is normally folded inside actually sticks out, and that causes it to connect and tangle with other tau proteins. “The hunt is on to build on this finding and make a treatment that blocks the neurodegeneration process where it begins,” says director of the centre for Alzheimer’s and neurodegenerative diseases, Dr Marc Diamond.

Scientists have also been looking into a possible genetic component behind Alzheimer’s disease – it does tend to run in families, after all. In one study, researchers from Boston University and the Alzheimer’s Disease Sequencing Project analysed entire genetic sequences in nearly 6000 people with Alzheimer’s disease, which they compared with the genes of 5000 healthy older adults. The result? They found several rare gene variations that they believe could be linked to Alzheimer’s disease. The study authors believe that an inflammatory response in the body could trigger changes in the genes, and that could lead to brain degeneration. More research is necessary to get the whole genetic picture, but the research is promising.

Other research suggests that inheriting just one variant copy of the apolipoprotein E (APOE) gene can double your risk for Alzheimer’s disease, according to the Harvard Heart Letter. Researchers believe that the e4 variant interferes with body defences that would block the growth of amyloid beta plaques. The only issue: sixty per cent of people who suffer from Alzheimer’s don’t have the e4 variant. “Identifying rare variants could enhance our ability to find novel therapeutic targets and advance precision medicine approaches for Alzheimer’s disease,” said Dr Eliezer Masliah, director of the Division of Neuroscience at the National Institute on Ageing.

It’s possible that we already have drugs – approved to treat other conditions – that could block Alzheimer’s. One example: Yale University School of Medicine researchers found that an experimental cancer drug, saracatinib, restored memory loss and reversed brain problems in mice; they are now testing it in humans. “They are investigating a pathway that results in the activation of a protein called Fyn kinase,” says Snyder. This protein plays a major role in how clusters of beta-amyloid damage brain cells – and the cancer drug seems to block Fyn kinase. The research team recently finished collecting data on its safety, tolerability, and effectiveness in treating Alzheimer’s. A total of 159 participants received either saracatinib or a placebo for one year. The results have yet to be released.

Your brain may not be the only target of Alzheimer’s disease: researchers from Cedars-Sinai Medical Centre used eye-imaging technology to analyse the retinas of a small group of Alzheimer’s patients. In the study, the Alzheimer’s patients had 4.7 times more amyloid beta in their eyes than the people who did not have the disease.

Another study revealed that people with rosacea (a skin condition that causes facial redness) are seven per cent more likely to develop some form of dementia and 25 per cent more likely to develop Alzheimer’s disease. The inflammation of rosacea – and the proteins involved – may contribute to the development of Alzheimer’s, the study authors say.

It’s time to have your eyes checked if you notice any of these signs.

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Source: RD Canada