by The amount of a protein related to the disease Alzheimer’sAmyloid deposits, in addition to age, may be key in determining who will benefit from new anti-amyloid therapies to slow the progression of Alzheimer’s disease.
It is explained by experts from the university of pittsburgh(USA) in a study published in ‘Neurology‘ showing that while it is true that the accumulation of toxic beta amyloid deposits that indicate the pathology of Alzheimer’s disease accelerates in old age, the initial amyloid load and overall brain health that occur during this acceleration are predictors more powerful in determining which patient is more likely to have the disease progress more rapidly.
“Understanding the complexity of increased amyloid accumulation, when individuals are cognitively normal, is essential to improve the implementation of treatments for dementia,” says Oscar López, author of the study.
The presence and overall quantity and distribution of clusters of beta amyloid, or beta A, in the brain are some of the most common neuropathologies associated with Alzheimer’s.
However, while people aged 80 years and older have the highest prevalence of Alzheimer’s-associated dementias, most studies measuring A-beta load in the brain using imaging techniques have focused on younger populations. As such, the Connection between A-beta and dementia in older people remains unclear.
López and his colleagues set out to change that by examining the relationship between A-beta deposition and new cases of dementia in 94 older people who had no cognitive problems when the study began. Participants were enrolled in the study with an average age of 85 years and were followed for 11 years or until death. The rate of amyloid deposition in the brains of these individuals was compared to that of a younger group in the study. Australian images, biomarkers and lifestyle (AIBL).
The researchers observed a steady increase in A-beta accumulation in all participants over time, regardless of their A-beta status at the beginning of the study. But this accumulation was significantly faster in patients aged 80 years and older compared to participants aged 60 years, explaining the higher prevalence of A-beta in older people.
Two years before
In the end, very few participants developed dementia without having A-beta deposits in the brain. Importantly, people whose brain scans tested positive for amyloid at the start of the study. developed dementia two years earlier than those who tested negative for amyloid.
The study also found that the short-term change in A-beta alone over a 1.8-year period could not predict future dementia risk. In contrast, the severity of baseline A-beta load, along with other markers of brain damage defined by the presence of white matter lesions (a marker of small vessel disease) and decreased gray matter thickness . in the cerebral cortex (a marker of neurodegeneration) were the strongest predictors of risk, indicating that an active pathological process was already underway when the study began.
