Drugs developed to reduce levels of a protein found at high levels in Alzheimer’s patients could lead to treatments aimed at curbing the disease before symptoms show up, a new study suggests.
A growing body of studies suggests that many people may start living with Alzheimer’s years before they even spot signs of the disease. They start to experience erasure of memories, language and thoughts without even realising, and once they do spot the symptoms, it may be too late to reverse or stop the degenerative disease.
Researchers assessed one of the earliest signs of the condition and found that targeting a brain protein could be a promising way to thwart chronic, damaging inflammation and curb the progression of Alzheimer’s.
The brain protein TSPO, or Translocator protein 18 kDA, is detectable even before memory loss or cognitive decline are evident, and influences the onset of Alzheimer’s, according to the study, published in the journal Acta Neuropathologica.
“If we can use TSPO to detect it early, right at the beginning stages of the disease, it could mean slowing progression or delaying symptoms by five or six years,” said Dr Tomas R Guilarte, one of the authors of the study, from Florida International University.
“That’s five or six years where someone has a better quality of life,” Dr Guilarte said.
TSPO levels are normally very low in the brain, but when inflammation is present, they tend to keep increasing, scientists say.
The latest study narrowed down where and when TSPO initially appears in the brain.
Researchers found that its appearance coincides with small scatterings of amyloid plaques, known to be a “smoking gun” sign of Alzheimer’s.
Probing further, scientists found that TSPO signals were given off by specific brain cells – microglia and astrocytes – which are responsible for protecting neurons. Microglia cells in the closest proximity to amyloid plaques appeared to have the highest concentration of TSPO, the study found.
TSPO signals could be seen in one-and-a-half-month-old mice – the equivalent of an 18- to 20-year-old human, researchers say.
“What we believe is happening is that something goes wrong with the microglia. They stop doing their job in removing the plaques and just keep sending out TSPO signals,” Dr Guilarte said. “This constant signal of neuroinflammation is like adding wood to a fire,” he explained.
Scientists found the same pattern in human brain samples donated by patients from Colombia with a rare form of Alzheimer’s disease, who showed symptoms as early as their thirties and forties, and died in their fifties.
“One of the biggest problems with Alzheimer’s is people see it as a disease of ageing, and that impacts when people get diagnosed,” said Dr Daniel Martinez-Perez, another author of the study. “But the reality is that the disease starts decades before diagnosis, and the more biomarkers and therapeutic targets our global community of scientists are finding, the closer we all get to physicians having a whole panel of diagnostics to be able to deliver more personalised, tailored treatments.”
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