Researchers at the University of California, Irvine, Wisconsin-Madison and Wake Forest University found that age-related brain inflammation can link Alzheimer’s risk to sleep disturbances.
“Our findings indicate that age-associated increases in brain inflammation have a cascade effect on Alzheimer’s disease-related Tau proteins and synapse integrity. [pontos de contato pelos quais as células nervosas emitem sinais umas às outras]”, said the study’s lead author, Bryce Mander, in a statement.
“This results in deficits in the brain’s ability to generate fast sleep spindles, which contribute to age-related memory impairment in older adults,” Mander added.
Sleep spindles are one of the stages of sleep. They are characterized as rapid electrical discharges in the brain that happen several times during the sleep period. Studies indicate that time zones are important for older memories and for developing the ability to solve problems, use logic and identify patterns in new situations that people experience.
The research revealed that, with age, the chronic activation of immune cells in the brain (responsible for inflammation), known as “glial cells”, increases the production of beta-amyloid and tau proteins, two markers of Alzheimer’s disease.
It is worth noting that Tau proteins appear in abundance in neurons of the central nervous system. When affected or in excess, they interfere with biological and morphological functions in neurons, causing dementia.
The accumulation of beta-amyloid proteins leads to the formation of solid protein plaques that accumulate between neurons, disrupting neural activities.
Sleep disorders have already been linked to Alzheimer’s, but this study showed that they are also linked to inflammation.
about the study
The research investigated the brain activities of 58 adults, aged between 50 and 60, cognitively intact, that is, with a parental history of Alzheimer’s or with genetic risk factors, but without beta-amyloid plaques or excess tau protein.
Scientists analyzed the patients’ sleep during the night using a high-intensity electroencephalogram and mapped their brain waves during sleep, as well as memory retention.
Volunteers also underwent a lumbar puncture for detailed analyzes of neuronal integrity and beta-amyloid and tau proteins.
The results showed that the activation of two types of glial cells (which trigger brain inflammation), microglia and astrocytes, were associated with sleep disorders. This relationship in people without signs of Alzheimer’s indicates that the disorders and inflammation may be the first warning signs for the disease.
“We don’t yet know whether anyone in this study will develop Alzheimer’s dementia, but one of the reasons our studies involve middle-aged participants is so we can detect problems before people develop symptoms of the disease,” said the statement. co-author Barbara Bendlin in a statement.
“These findings show that the effects of brain inflammation on sleep spindles and memory occur through its effects on neuronal activity and proteins related to Alzheimer’s disease and are apparent even before the onset of the disease,” said senior researcher and co-correspondent of the Ruth Benca study.
The study facilitates early detection of Alzheimer’s disease, which may help identify new treatments at pre-clinical stages.
What’s more, it provides a promising therapeutic target for halting cognitive decline associated with aging and disease.
“Discovering these mechanisms is an important step towards identifying at-risk individuals as early as possible and developing targeted interventions,” Mander concluded.
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According to the WHO (World Health Organization), currently 55 million people live with dementia worldwide, of which between 60% and 70% have Alzheimer’s.
With the aging population, it is estimated that dementia could affect 78 million people eight years from now and 139 million by 2050.
According to the non-profit Alzheimer’s Association, age is the biggest risk factor for the development of the disease in people over 65, although the WHO says that it “is not an inevitable consequence of biological aging”.
It is also estimated that about 25% of Alzheimer’s cases have a genetic influence, more specifically the APOE-e4 gene. Having parents who have suffered from Alzheimer’s also increases the risk, according to studies.
There are risk factors for Alzheimer’s that can be managed, such as those related to the health of the heart and blood vessels that supply the brain.