Prevention of Alzheimer’s Disease in Daily Life

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1		Agnieszka Ochocińska	--	4480	2022-04-26 13:02:32	\|
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This entry is adapted from the peer-reviewed paper 10.3390/nu14081534

The ageing of the population is resulting in neurodegenerative diseases, including Alzheimer’s disease (AD), which are an increasing social, economic and medical problem. Diet and physical activity are now considered as important modifiable factors that help prevent or delay the development of AD and other dementia-related diseases. The pyramid of healthy nutrition and lifestyle is a way of presenting the principles, the implementation of which gives a chance for proper development and a long healthy life.

Alzheimer’s disease L-carnitine diet physical and mental activity

1. A Diet to Prevent Alzheimer’s Disease (AD)

The best effects of AD prevention occur when the dietary intervention takes place before the first prodromal symptoms appear, for example, when the number of synapses, nutritional status, cognitive level and neuropathological changes in the central nervous system are compensated. Research shows that first prodromal AD symptoms occur at around the age of 50 years. However, it seems more realistic to take action against AD when the first symptoms appear, for example, around the age of 60–65 years. In turn, the ideal age for assessing the results of AD prevention is the age of 70 years. Researchers carrying out preventive research propose to include, in AD prevention, a population of people between the ages of 50 and 70 without signs of cognitive impairment but with risk factors such as hypertension, hypercholesterolemia and obesity. Interventions would be multidirectional, both pharmacological and non-pharmacological, and the real time of their implementation should be at least 4–8 years ^[1].

In the prevention of neurodegenerative diseases, one of the main goals is the implementation of an appropriate diet, and properly balanced nutrition can prevent AD and support the pharmacological treatment of elderly people. Changes in daily habits that can protect against dementia, including AD, are primarily not smoking, maintaining proper blood pressure, optimal cholesterol, glucose, homocysteine levels, preventing overweight and obesity, reducing stress, mental gymnastics and physical training—these are important elements in the prevention of AD. Another element of prophylaxis against neurodegenerative diseases is the introduction of certain nutrients into the diet or eating according to a given nutritional model, which may be helpful in neurodegenerative disease prevention and may support the basic treatment of people with AD. It is believed that including omega-3 fatty acids, antioxidant vitamins, B vitamins, folic acid, plant polyphenols, fish and vegetables in the diet, and limiting the amount of fried meat, may reduce the risk of developing AD ^[2]. Meals prepared with heated, fried or irradiated food products involve reactions of the aldehydes and amino group (Maillard reaction), thereby substantially speeding up the occurrence of AD ^[3].

1.1. Mediterranean Diet

Increased risk of AD and dementia is associated with dietary patterns high in saturated fat and simple carbohydrates, while diets high in mono- and poly-unsaturated fats, vegetables, fruits and lean proteins are associated with reduced risk. With overall health and well-being in mind, switching to a Mediterranean-style diet is not only a prudent lifestyle choice, but is also a scientifically proven issue that can benefit the prevention and treatment of many diseases. An association between the consumption of a Mediterranean diet and a reduction in the incidence of Alzheimer’s disease has been demonstrated, raising the prospect that the Mediterranean diet may be used as a modifiable risk factor for protection against AD ^[4]. Researchers indicate that the Mediterranean diet, i.e., eating fruits with a low glycaemic index, vegetables with low starch content, whole grains, nuts, pulses, fishes (especially sea fishes: halibut, herring, mackerel, sardines), plant oils (olive, colza, linen, sunflower) and limited consumption of red meat but regular low to moderate alcohol consumption (mainly wine with meals) may delay the development of AD ^[4]. In contrast, it limits and recommends the consumption of low or average consumption of dairy products and poultry ^[5]. The Mediterranean diet is a way of eating and lifestyle at the same time and is considered as one of the healthiest. It is well known that following the Mediterranean diet can prevent many diseases: obesity and diabetes, cardiovascular diseases, cancer and neurodegenerative diseases. Research by Abbatecola et al. ^[6] showed that in people on the Mediterranean diet, the risk of mild cognitive impairment (MCI) was reduced by 28% and the risk of developing AD decreased by 48% compared to people who did not use this diet. A new model of nutrition has been developed, which is the MIND diet (Mediterranean-DASH Intervention for Neurodegenerative Delay) composed of the DASH (Dietary Approaches to Stop Hypertension) diet and the Mediterranean diet. The MIND diet aims to improve the functioning of the nervous system and the work of the brain. It is used in the prevention of AD and neurodegenerative brain diseases. A growing body of evidence supports a multicomponent intervention to alleviate cognitive impairment. Adherence to the MIND diet and increased physical activity have been shown to be associated with a reduced risk of dementia ^[7]. Fish, cheese and yogurt should be moderately consumed, while meat should be rarely consumed as a part of complex dishes. Wine and beer (non-alcoholic beer) during main meals are also some of the components of the Mediterranean diet. Beer consumption, and its content of bioavailable silicon, reduces the accumulation of aluminium in the body and brain tissue and lipid peroxidation and protects the brain against neurotoxic effects through the regulation of antioxidant enzymes ^[8]. The MIND diet emphasises the consumption of 15 groups of products, 10 of which are recommended to be eaten as often as possible. These are: vegetables, nuts, berries, legumes, whole grains, poultry, seafood and fish and mainly olive oil as well as wine/beer. The other five groups of products should be very limited: red meat, fatty cheeses, margarine and butter, sweets and cakes as well as fried and fast-food products ^[9].

The Mediterranean and Asian diets are very similar to each other and are considered the healthiest. The traditional Asian diet is characterised by a significant predominance of plant products over animal products ^[10]. The products commonly eaten in Asia include, first of all, rice and other cereal grains, as well as potatoes (including sweet potatoes), pasta, fruits and vegetables, legumes, soybeans (tofu, soy noodles, soy sauce), vegetable oils (sesame, soy), seeds, spices and tea. The consumption of fat, mainly animal fat and dairy products, is low. The proportion of fish is generally low to moderate, with the exception of those living in coastal regions. A healthy and balanced meal of plant-based foods and drinks such as green tea, vegetable oils, red wine, fruit and herbal spices has a beneficial effect on the prevention of amyloid diseases such as Parkinson’s, prion and Alzheimer’s diseases ^[10]. Actually, some foods or food groups traditionally considered harmful such as eggs and red meat have been partially rehabilitated, but there is still a negative correlation of cognitive functions with saturated fatty acids. A protective effect of elevated fish consumption and a high intake of monounsaturated fatty acids and polyunsaturated fatty acids (PUFA), particularly n-3 PUFA, against cognitive decline has been confirmed ^[6]. Martinez et al. evaluated the effects of a Mediterranean diet on cognitive function in men at high vascular risk. This multicentre, randomized showed that following a Mediterranean diet supplemented with additional extra-virgin olive oil or mixed nuts significantly improved cognitive function compared with a low-fat diet in the control group ^[11].

2. Food Products with Beneficial/Adverse Effects on Health

2.1. Advanced Glycation End Products (AGEs)

AGEs are a group of complex and heterogeneous compounds that are divided into colourless, non-fluorescent pre-melanoidins and colourful, fluorescent melanoidins. The former group includes glyoxal, methylglyoxal, 3-deoxyglucosone and carboxymethyl-lysine, while the latter one includes pentosidine. They are naturally present in unprocessed raw animal products, and heat treatment initiates the formation of new AGEs in these products. Grilling, baking and frying, in particular, are responsible for the formation of advanced glycation end products. The pathological effects of AGEs are related to their ability to promote oxidative stress and inflammation by binding to receptors on the cell surface, altering their structure and function. The accumulation of advanced glycation end products has been shown to play a role in the development and progression of age-related diseases ^[12]. AGEs, and especially AGE-2 derived from glyceraldehyde, show significant toxicity in cortical neuronal cells, the presence of which has been demonstrated in AD patients. AGE-2 may be involved in the development of dementia caused by the loss of cerebral pericytes in vascular dementia and neuronal cell apoptosis in AD ^[13].

A high concentration of AGEs is contained in products containing sugar, processed meat and processed dairy products; food containing trans fats (margarines, creams, mayonnaise); and highly fried products (fried potatoes, crisped cakes, pizza, etc.). The least concentration of AGEs is contained in natural products as well as in raw and unprocessed food, i.e., fresh fruits (strawberries, raspberries, blueberries, blackberries, cherries, currants and avocado); vegetables (cabbage, tomatoes, carrots, spinach, broccoli and kale); seafood (fatty fish, shrimps, clams, lobsters and squid), and briefly heat-treated products: slow-boiled, steamed and processed at lower temperatures ^[9]. Appropriate dietary supplementation, i.e., lipoic acid, glucagon-like peptide-1 (GLP-1), and physical exercise may be an effective method to reduce protein glycation and oxidative damage to cells and tissues. It has been suggested that the blockade of RAGE (receptor for advanced glycation end-products) may also limit the consequences of protein glycation ^[14].

2.2. Fatty Acids

A correctly composed diet rich in polyunsaturated fatty acids from families of omega-3 and omega-6 and monounsaturated fatty acids (MUFA), as well as antioxidative vitamins, reduce the risk of AD development. Epidemiological ones indicate that increased consumption of foods containing polyunsaturated omega-3 (α-linolenic—ALA; stearidonic—SDA; docosapentaenoic—DPA; docosahexaenoic—DHA; eicosapentaenoic—EPA acids) and omega-6 (gamma linolenic—GLA; linoleic—LA; and arachidonic—AA acids) as well as MUFA (oleic-, palmitoleic-, erucic acids) and antioxidant vitamins (A and its isomer β-carotene, E, C) has the ability to prevent the adverse effects of free oxygen radicals and may also reduce the risk of developing AD ^[15]. Many epidemiological ones have been conducted on the myriad health benefits of omega-3 polyunsaturated fatty acids. Vegetable oils, nuts and seeds are a rich source of omega-3 fatty acids, especially alpha-linolenic acid. In turn, EPA and DHA are found in fatty marine fish such as herring, mackerel, halibut, salmon, menhaden and seafood, algae and the blubber of marine mammals such as seals and whales. Recently, oils derived from algae, mushrooms and unicells have become popular as sources of long-chain omega-3 fatty acids. As a result of the ageing of the organism, the activity of the ∆-6-desaturase enzyme decreases with age, leading to the inhibition of the synthesis of DHA and an increased risk of disturbances in the functioning of the central nervous system in the elderly. Therefore, an adequate intake of omega-3 fatty acids or supplementation, especially DHA, is important in the elderly ^[16]. To achieve a proper balance in the body, you should limit the intake of foods rich in omega-6, such as processed meat and dairy products, as well as fast food and ready meals. The ideal ratio between omega-6 and omega-3 should be from 1:1 to a maximum of 2.5:1. The contemporary diet is rich in omega-6 fatty acids, and the ratio to omega-3 is as high as 15:1. As a result, the excess omega-6 has a pro-inflammatory effect and is considered as one of the main causes of civilisation diseases. It is recommended to consume natural fish or algae oil as often as possible, and at least 1–2 fish meals per week to ensure an adequate supply of omega-3 fatty acids ^[9].

2.3. Milk and Dairy Products

Regarding the risk of cognitive decline/cognitive disorders in adults and the consumption of milk and dairy products, the relationship cannot be clearly established. The evidence is too weak to draw firm conclusions. Poorer cognitive function and an increased risk of vascular dementia have been found to be associated with the lower intake of milk or dairy products, which are valuable sources of complete protein, calcium, potassium, phosphorus, vitamin A, some B vitamins and probiotics in fermented products. In addition, the consumption of full-fat dairy products, and/or dairy fats, may also be associated with worsening cognitive function in older adults. On the other hand, others have found adverse effects of full-fat dairy products (whole milk, dairy desserts and ice cream) on cognitive function in older adults ^[17]^[18]. It has been suggested that the consumption of milk > 1 glass/day at midlife may be associated with a greater rate of cognitive decline over a 20-year period. A significant inverse relationship has been observed between higher milk and dairy intake and reduced the risk of AD, but are limited to the Japanese population only ^[19]. For the relation between dairy products and cognitive decline are contradictory, and it probably depends on the type of dairy product and the quantity ingested. There are also positive effects of dairy product intake, e.g., in the prevention of sarcopenia, especially with a high consumption of low-fat milk and yogurt. In conclusion, the available scientific evidence is insufficient to clearly assess the positive or negative impact of milk or dairy intake on cognitive decline and Alzheimer’s disease risk. Therefore, in the opinion, low-fat milk and dairy products such as low-fat yogurt and skimmed cottage cheese should be consumed because the consumption of full-fat dairy products may impair cognitive function in the elderly.

2.4. Alcohol

The relationship between AD, dementia and alcohol use/abuse has been the subject of many with varying and conflicting results. It is still unclear whether light to moderate alcohol consumption can lead to dementia or whether alcohol consumption can reduce the risk of developing AD ^[20]. Numerous published data confirm that low to moderate alcohol consumption, including wine (part of the Mediterranean diet), which contains numerous polyphenols which have protective effects, including minimising the effects of oxidative stress, inhibiting β-amyloid deposition, significantly reduces the risk of dementia and the risk of AD ^[21]. However, excessive amounts of ethanol increase the accumulation of Aβ and tau protein phosphorylation, contributing to the development of Alzheimer’s disease. Observational ones were indicated that high alcohol consumption leads to a deterioration of cognitive and executive functions and leads to alcoholic dementia. The link between alcohol consumption and cognitive decline is believed to be “J” or “U” shaped ^[22]. In contrast, light/moderate alcohol consumption is associated with a reduced risk of dementia in individuals aged 55 years or older ^[23]. Regarding the type of alcoholic beverage, the Ritinberg were ^[23] found no difference between wine, beer or liquor. It is believed that beer (which is a component of the Mediterranean diet) and its ingredients (carbohydrates, protein/amino acids, minerals, vitamins and other compounds, such as polyphenols) exert a beneficial effect in the prevention of Alzheimer’s disease. Regular consumption of beer, or low-alcohol or non-alcoholic beer, can prevent AD and other neurodegenerative diseases as it effectively reduces the accumulation of aluminium in the body and also alleviates the mineral imbalance in the body and the brain and the pro-oxidative and pro-inflammatory effects caused by aluminium ^[8]. While the Luchsinger ^[24] found that only wine (particularly red) has the strongest protective effect because resveratrol, a sirtuin 1 activator and other polyphenols present in the grapes of red wine reduce Aβ plaque burden and improve cognitive function. It has been noted that resveratrol actually reduces the levels of Aβ40 and Aβ42 in cerebrospinal fluid, but at the same time, it accelerated brain atrophy ^[25]; further are needed to confirm these results. Surprisingly, heavy drinking in late life has no effect on dementia risk compared to non-drinkers ^[23]^[26], but heavy drinking in adolescence is associated with damage to the prefrontal cortex and the hippocampus, and with neurocognitive dysfunction, it increases the risk of alcoholic dementia, similar to AD ^[20]. Importantly, alcohol misuse is also associated with a number of other disorders. Many publications state that ethanol and its metabolites not only have neurotoxic effects but directly exert toxic effects on the mucous membranes of the mouth (including periodontium), oral cavity, throat, oesophagus, liver, stomach, pancreas, kidney and can cause lung cancer (especially in cigarette smokers) and that regular drinking (even in small amounts) can lead to alcohol dependence ^[27]^[28].

Many support the benefits of low to moderate alcohol consumption in preventing AD ^[23]. However, these results should be considered insufficient to suggest that long-term abstinence should consider alcohol consumption in their diet to prevent AD risk. In addition, other risk factors (in addition to binge drinking), such as smoking or abusing other substances, can play an important role in the development and progression of many diseases, including neurodegenerative diseases. It was believed that light to moderate alcohol consumption may be important in preventing AD.

3. Lifestyle, Physical Exercise and Mental Activity in the Prevention of AD

There is growing evidence that three lifestyle components: social, mental and physical are inversely correlated with risk of dementia and Alzheimer’s disease. Cognitive disability associated with neurodegenerative diseases, in particular, AD, is becoming an increasingly serious cause of concern due to the dramatic increase in its incidence. Therefore, maintaining high physical, mental and social activity is one of the factors contributing to improving the quality and expectancy of life of elderly people, thereby reducing the risk of dementia and cognitive impairment in AD ^[29]. The use of various strategy programmes to prevent dementia, including the simplest, as for example, performing basic tasks related to memory stimulation, such as creating and realising a weekly plan or a schedule of activities during the day (practising simple physical exercises, reading newspapers, cooking, cleaning, meeting other people), counteract dementia and thus lead to a slowdown in cognitive decline ^[30]. It was reported that multi-domain programmes including diet, exercise, cognitive training and social activities give better results in slowing down disease progression than single-domain programmes ^[31]. Therefore, activating seniors to undertake education (Third Age Universities, computer courses), promoting volunteer initiatives (in hospitals, hospices, shelters), participation in social life, maintaining close relationships as well as promoting a healthy lifestyle delay dementia in neurodegenerative diseases and also improve cognitive function in people with AD ^[30]. In contrast, loneliness, as well as a lack of mental well-being and life satisfaction, are reflected as a worse quality of life in people with AD ^[32]. A great deal of evidence from numerous observations has shown that one third of AD cases worldwide are associated with seven common modifiable risk factors, i.e., diabetes, middle-aged hypertension, middle-age obesity, physical inactivity, depression, smoking and a low level of education ^[33]. Therefore, to reduce the likelihood of cognitive disability late in life, a high quality of life should be introduced at an early stage of life.

3.1. Physical Activity

Physical activity is an important factor in preventing pathological changes in dementia diseases, including AD. It is believed that physical exercises (morning gymnastics, walking, swimming, gardening, walking up the stairs and housework) intensify the formation of neurotrophic factors that are involved in maintaining homeostasis of the central nervous system and the regeneration of damaged brain tissue, thereby preventing destructive changes in the brain. In addition, physical exercise triggers the production of neurotrophins in the brain, which promote brain neuroplasticity and improve the functioning of neurons, also in those parts of the brain that are responsible for memory and other cognitive functions. Moreover, physical exercises stimulate the release of hormonal factors affecting neurons, such as brain-derived neurotrophic factor (BDNF) and epinephrine ^[34]. In addition to BDNF, insulin-like growth factor 1 (IGF-1) and vascular endothelial growth factor (VEGF) are also involved in the mechanisms by which exercise supports learning (regulated by IGF-1 and BDNF), but likewise, it supports normal neurogenesis and angiogenesis in the hippocampus—it appears to be regulated by IGF-1 and VEGF. These factors, produced in the periphery, penetrate the blood–brain barrier and lead to increased neuronal proliferation and differentiation ^[35]. Physical activity helps maintain optimal cardiovascular function, improves local blood flow and stops stroke and small blood vessel diseases. A comparative analysis of people exercising intensively with people who did not regularly do sports showed that those who exercised had a significantly lower risk of developing symptoms of AD disease within five years compared to people who did not do sports ^[36]. Another by Paillard-Borg et al. ^[37] showed a 17-month difference in the occurrence of dementia between an inactive group and the most active group. The highest risk of cognitive impairment was observed in people without physical, mental or social activity. Therefore, it is believed that physical activity protects against cognitive impairment in the elderly and slows down the course of AD disease, thus delaying the onset of dementia ^[38]. In another cohort reported by Law et al. ^[39], it has been shown that in middle-aged adults at risk of cognitive disease, moderate physical activity (but not light or intensive) has a beneficial effect on CSF biomarkers (higher Aβ42, lower total tau/Aβ42 and lower phosphorylated tau/Aβ42). In contrast, a sedentary lifestyle was associated with reduced Aβ42 in the CSF of the group. It is, therefore, believed that physical exercise and cognitive training prevent cognitive memory deficits associated with β-amyloid neurotoxicity ^[40]^[41]. Aerobic exercise, including morning gymnastics, cycling, swimming, walking, running, rollerblading, skipping or cross-country skiing, as well as cognitive training (aerobic fitness) improve blood supply and thus brain oxygenation. Thanks to the combination of aerobic exercises and aerobic fitness a synergistic effect on increasing cognitive functions, by improving the structure of the brain and its functioning, may be achieved ^[42].

Although the general pathogenesis of AD is being clarified, the exact mechanisms of AD’s pathogenesis are still unclear. In recent years, it has been reported that impaired autophagy (or autophagocytosis) associated with microRNA (miRNA) dysfunction is involved in ageing and neurodegenerative diseases. Therefore, the regulation of autophagocytosis via miRNA can become one of the strong AD intervention strategies. In addition, autophagy is tightly regulated by the signalling pathway of mTOR (mechanistic target of rapamycin, mammalian target of rapamycin), which is a serine-threonine kinase that regulates the rate of some intracellular processes in response to extracellular signals. mTOR in the central nervous system plays multiple roles: regulates cell viability, differentiation, transcription, translation, protein degradation, ribosome biogenesis, actin cytoskeletal organisation and autophagy, as well as the development of axonal and dendritic trees, synaptogenesis, synaptic plasticity and learning and memory. Dysregulation of the mTOR kinases pathway can be one of the causes of numerous neuropathologies and neurodegenerative diseases, including Alzheimer’s, Parkinson’s and Huntington’s diseases. Recently it has shown that physical activity helps to regulate the state of autophagy via the mTOR signalling pathway, which can prevent and be helpful in treating AD ^[43]. In addition, physical activity and physical fitness improve cerebral blood flow (CBF) in the lower temporal gyrus, angular veins and posterior gyrus (reduced CBF is a hallmark of ageing and AD disease), which has been proven to be the predictor preceding cognitive impairment in the elderly ^[44].

3.2. Mental Activity

Dementia is a syndrome characterised by cognitive disorders such as the impairment of memory, abstract thinking, orientation, understanding, counting, learning ability, language functions and the ability to compare, evaluate and make choices. As a result of the above-presented developing disorders, intellectual performance is reduced, and efficient functioning in everyday life is impaired. Alzheimer’s disease and/or damage to the cerebral vessels with impaired blood flow are the most common causes of dementia, where many patients acquire it simultaneously. There is scientific evidence that the factors associated with a healthy lifestyle, such as regular exercise, high mental activity, a healthy diet, non-smoking, maintaining normal blood pressure and cholesterol, avoiding depression and middle-aged overweight/obesity and proper control of diabetes (if present), help reduce the risk of dementia ^[45]^[46].

Preventive measures against the onset of neurodegenerative diseases (including AD) should start early, before the occurrence of pronounced structural changes in the brain, and not in old age. In a Finnish multimodal intervention one consisting of diet, exercise, cognitive training and social activity, vascular risk monitoring concerned the prevention of cognitive impairment and disability (FINGER—Finnish Geriatric Intervention one to Prevent Cognitive Impairment and Disability—it is a multicentre, randomized, rigorously controlled trial) in people aged 60–77 years with an increased risk of dementia (but without dementia/significant cognitive impairment) after 2 years of experiments between the control group (general health advice). The group was included in a balanced diet and exercise intervention. The cognitive training included group activities and individual sessions. Individual sessions consisted of computer-based training. The cognitive training included executive processes, for example, updating spatial, updating letter, updating number and mental set shifting tasks; working memory, for example, maintenance tasks; episodic memory, for example, relational and spatial tasks; and mental speed, for example, shape match task. Social activities were stimulated through the group meetings. Observational outcomes of cognitive function were measured by the modified Neuropsychological Test Battery, Stroop test and Trail Making Test ^[47]. This was noted significant intervention effects on the overall cognition and executive functioning and processing speed and other outcomes, i.e., BMI, dietary habits and physical activity. No significant effect was noted on memory, but post-hoc analyses showed an effect on more complex memory tasks and also beneficial effects on lower risk of cognitive decline ^[47]. This supports the efficacy of multidomain prevention approaches. Other are in the FINGER ^[48] investigated the relationship between change in CAIDE (Cardiovascular Risk Factors, Aging and Dementia) score and change in neuroimaging biomarkers—MRI (Magnetic Resonance Imaging) and Pittsburgh Compound B-positron emission tomography (PiB-PET). The participants had brain measurements (hippocampal, total grey matter and white matter lesion volumes and Alzheimer’s disease signature cortical thickness). A reduction in the CAIDE score was observed in 30% participants in the intervention and 21% in the control group. In this neuroimaging one, a reduction in the CAIDE score (indicating lower dementia risk) during the intervention was associated with lesser decline in hippocampal volume. It is suggested that preventive strategies may be more effective if started early, before the more pronounced structural changes in the brain that characterise Alzeimer’s disease develop. According to them, it is important to develop dementia risk assessment tools that will be even more sensitive to lifestyle changes and their potential effects on brain structure ^[40]^[47]^[48]. The large-scale online programmes on healthy lifestyles and brain health enable the implementation of preventive measures in a healthy adult population. Implementing these programmes can help prevent dementia in old age ^[49]. Primary prevention of dementia aims to reduce the risk factors by focusing efforts on improving the lifestyle of middle-aged people before or in the earliest stages of neuropathological changes that characterise AD and other types of dementia. An alternative strategy is secondary prevention, which is to minimise the symptoms of progressive disease, characterised by subjective cognitive decline and mild cognitive impairment ^[50]. All forms of memory training activities by seniors, such as solving crosswords, reading books and magazines; arranging puzzles; playing cards, checkers, chess and board games; and participation in musical classes, are a way to maintain intellectual activity and mental fitness. Participation in special programmes of cognitive activity, organised by various Memory Disorders Therapy Centres, which help improve attention, concentration, perceptiveness, logical thinking, learning ability and visual memory, i.e., cognitive functions, is necessary for the proper functioning of the elderly ^[51]^[52].

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