2023-09-10 06:10:00
The many risk factors involved in cognitive aging and Alzheimer’s disease do not always overlap, but are often common. Since 2017, researchers from GIGA-CRC-In Vivo Imaging at the University of Liège have been carrying out a vast study on the subject. Called CoFitAge (Cognitive Fitness in Aging), it distinguishes between the factors of cognitive aging over which we have no control (sex, age, certain genetic characteristics) and those which we can influence.
Among these, the “cognitive reserve”, made up of different elements supposed to intervene in a crucial way: having a high educational level, having an active lifestyle, exercising a profession of a certain complexity, engaging in culturally enriching, exercising, having an extensive social network, speaking several languages… These ingredients would promote mental flexibility, thus offering alternative pathways when, under the weight of aging or illness, the brain pathways traditionally used previously fill less well or no longer fulfill their function. More prosaically, we might speak in terms of “spare parts”.
The key issue of sleep
“But the emotional state also plays a roleexplains Professor Fabienne Collette, co-director of GIGA-CRC-In Vivo Imaging. Depressive symptoms or very high anxiety are associated with increased risk, including Alzheimer’s disease.” She also emphasizes what is commonly called “allostatic load”, a global biological wear and tear resulting from the constant adaptation of our body to the environment. The price to pay can be heavy, in the form of hypertension, diabetes, excess cholesterol, chronic inflammation or even excessive functioning of the sympathetic nervous system, which prepares the body for action, notably by increasing blood pressure and accelerating cardiac and respiratory activity. “Our studies show that two of the markers of allostatic load – poor lipid metabolism and excessive sympathetic nervous system activity – are most closely associated with poorer cognition.”, reports Fabienne Collette. Not eating too much fat and relaxing would be a weapon once morest cognitive aging.
Another element is at the heart of the debate: sleep. A modifiable factor which occupies a prominent place in the CoFitAge study. Insufficient or of poor quality, it also goes hand in hand with an increased risk of cognitive decline and Alzheimer’s disease. A reality that scientific work has well documented today even if the mechanisms at play remain little understood. However, many people, including an increasing number of young people, consult for chronic insomnia. At the origin of adolescents’ complaints: behaviors described as “socio-electronic” linked to the use in the evening, or even at night, of smartphones, tablets, etc. Exposure to the light of screens at late hours disrupts biological sleep-wake rhythms, while activity on social networks and consultation of information on the Internet maintains wakefulness and risks making the bed – if the we can say – a form of dependence. By reducing their sleep, are younger generations accelerating the cognitive aging that will affect them sooner or later? The question needs to be asked.
Will younger generations, more exposed to screens, be affected more quickly by cognitive aging? © Adobe Stock
Brain Drain
The theory that most challenges researchers in the field of the links between sleep and Alzheimer’s disease is certainly the one that proposes the existence of a sleep function that remained in the shadows until recently. Called glymphatic, it would consist of the elimination during sleep, through the circulation of cerebrospinal fluid (which bathes our brain), of toxic substances accumulated in the central nervous system during wakefulness due to the cellular activity which is associated. These may include, among others, lactate, enolase, carbon dioxide, but also beta-amyloid proteins and tau proteins, whose involvement in Alzheimer’s disease is well known when they form aggregates in the brain.
Proposed in 2013 by the group of Lulu Xie, from the University of Rochester in the United States, the theory of glymphatic function of sleep has been confirmed and further developed by other laboratories. Xie and his team discovered that the space between neurons increases during sleep and under anesthesia, alongside a reduction in their volume. In other words, the “evacuation pathways” being more widely open during sleep, this is when the neurons “empty” themselves of their toxins. Therefore, insufficient or poor quality sleep would prevent the proper elimination of toxic proteins at the origin of the lesions characteristic of Alzheimer’s disease and would promote their occurrence.
Get old, but like a young person
According to Gilles Vandewalle, qualified researcher at the FNRS and also co-director of GIGA-CRC-In Vivo Imaging, the link between sleep and Alzheimer’s disease seems to go in both directions. In other words, the presence of amyloid and tau proteins in the brain disrupts sleep while disrupted sleep promotes the accumulation of toxic proteins. “A vicious circle”, he summarizes. In addition, epidemiological data tends to make insomnia a risk factor for Alzheimer’s disease. Sleep apnea would represent another. For what? Two explanations, undoubtedly complementary, are possible. Through the frequent micro-awakenings (and awakenings) that they induce, apneas are not only the cause of sleep fragmentation, but are also associated with reductions in the quantity of oxygen available in the blood, which which is potentially damaging to the brain.
Furthermore, ULiège researchers have shown that the closer the dynamics of the brain functioning of elderly people remains to that of young individuals, the better their cognitive abilities appear to be during aging and the lower the risk of progressing towards death. Alzheimer’s disease. “In young subjects, the brain becomes more and more reactive to stimulation as the day goes byexplains Gilles Vandewalle. And in the event of prolonged wakefulness, that is to say when we remain active during the night, this reactivity continues to increase, sometimes beyond the optimum. In the elderly, things are different. Indeed, we observe an increase in the excitability of the cortex in some of them, but a decrease in others. However, we see that the cognitive performance of the latter is less good.”
Lifestyle
Gilles Vandewalle nevertheless wants to be the bearer of good news. According to his team’s work, the way the brain reacts in an awake person is not solely dependent on the amount of clumps of amyloid proteins or tau proteins that have formed there. “Although the accumulation of such clusters which constitute the pathological signature of Alzheimer’s disease has a negative impact on sleep, our cognition may partly depend on elements on which we can act.” It is conceivable that lifestyle measures, such as practicing physical exercise, going to sleep at a fixed time or consuming less caffeine or other stimulants in the evening, would be likely to promote better quality sleep regardless of the presence of protein clusters in the brain. Such measures might then positively influence the dynamics of brain functioning when awake – a dynamic as close as possible to that observed in young subjects – and thus improve cognitive performance.
Another point, quite intriguing: according to studies coordinated by Christina Schmidt, a qualified FNRS researcher within GIGA-CRC-In Vivo Imaging, daytime naps practiced by elderly people might have deleterious effects on the cognitive level if they is relatively long and established as a life habit. This chronic intrusion of periods of sleep during wakefulness would harm the cognitive performance of seniors, particularly in terms of episodic memory, this component of memory which allows us to remember events that we have personally experienced, such as a dinner at a restaurant. with friends.
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