Prevention of dementia

Last updated

The prevention of dementia involves reducing the number of risk factors for the development of dementia, and is a global health priority needing a global response. [1] [2] [3] [4] Initiatives include the establishment of the International Research Network on Dementia Prevention (IRNDP) [5] which aims to link researchers in this field globally, and the establishment of the Global Dementia Observatory [6] a web-based data knowledge and exchange platform, which will collate and disseminate key dementia data from members states. Although there is no cure for dementia, it is well established that modifiable risk factors influence both the likelihood of developing dementia and the age at which it is developed. [1] [7] Dementia can be prevented by reducing the risk factors for vascular disease [1] [7] [8] such as diabetes, high blood pressure, obesity, smoking, physical inactivity and depression. [7] [1] A study concluded that more than a third of dementia cases are theoretically preventable. Among older adults both an unfavorable lifestyle and high genetic risk are independently associated with higher dementia risk. [9] A favorable lifestyle is associated with a lower dementia risk, regardless of genetic risk. [9] In 2020, a study identified 12 modifiable lifestyle factors, and the early treatment of acquired hearing loss was estimated as the most significant of these factors, potentially preventing up to 9% of dementia cases. [1]

Contents

Lifestyle

Mental activity

"Use it or lose it" might be applied to the brain when it comes to dementia. Intellectual activities help keep the mind in shape in later years. Activities such as reading, learning a new language, playing cards and board games [10] [11] and playing a musical instrument can postpone the onset and slow the progression of both Alzheimer's and vascular dementia. [12] [13] The risk decrease is proportional to frequency of activity, [12] with slower cognitive decline being associated with both late-life and early-life increased cognitive activity. [14]

Apart from spare time activities, a mentally demanding job may prevent dementia, especially during the thirties, forties and fifties. [12]

Mental activity may help to prevent dementia by building up a "brain reserve": additional connections between neurons are created which are more resistant to the deterioration seen in dementia. [12]

Physical activity

Since vascular dementia is the second most common form of dementia (after Alzheimer's disease), reducing the risk of cerebrovascular disease also reduces the risk of dementia. [15] Thus, physical exercise, having good blood cholesterol, healthy body weight and blood pressure lowers the risk of developing dementia. [12] An active lifestyle can almost halve the risk compared to a sedentary one. [12]

Results of one meta-analysis, which investigated the relationship between physical activity and risk of cognitive decline in people without dementia, showed exercise had a significant and consistent protective effect against cognitive decline, with high levels of physical activity being most protective. [16] Another meta-analysis showed that not only did aerobic exercise reduce the risk of dementia but it may also slow cognitive decline in those with dementia. [17]

The effect of physical activity is not limited to vascular effects. Physical activity can give rise to new neurons in the brain, as well as releasing a substance that can protect them. [12] The protein known as brain-derived neurotrophic factor (BDNF) is known to be important in the development, survival and plasticity of neurons. Regular exercise can boost BDNF levels by 2–3 times. [18]

Diet

Obesity increases the risk of any dementia and Alzheimer's disease in particular. [12] The effect of alcohol on the risk of dementia is a J curve: [19] high alcohol consumption increases the risk of dementia [20] while low alcohol consumption may be protective. [19] [21] However, low alcohol consumption may not protect against vascular dementia and overall cognitive decline. [19] Moderate alcohol consumption can possibly reduce the risk of vascular disease and dementia because it can increase blood levels of HDL cholesterol and weakens blood-clotting agents such as fibrinogen, which offers some protection against heart attacks and small subclinical strokes that together can ultimately damage the brain. [22]

The effects of omega-3 fatty acid in the prevention of dementia is uncertain. [23] Vegetables and nuts may be of benefit, [12] because of their high content of polyunsaturated fats. Non-fish meat, on the other hand, increases the risk of Alzheimer's, [12] because of its high content of saturated fat. [ citation needed ][ original research? ]

Niacin (vitamin B3) is also believed to prevent dementia as research shows those who have the highest levels of niacin in their blood, are believed to have the lowest risk of developing dementia or having cognitive decline. Niacin is involved with DNA synthesis and repair and also neural cell signaling, it improves circulation and reduces cholesterol levels. In order for niacin to have a positive effect on the brain, it is recommended that patients have 100 to 300 mg per day. [22]

There is evidence for an association between cognitive decline, homocysteine (Hcy) status, and vitamin B status relating especially to B12 [24] and also to vitamins B6 and B9. [25] In particular, deficiency of vitamin B12 and/or of folate can cause an increase in Hcy plasma levels, which in turn leads to toxic effects on the vascular and nervous systems. [26]

Vitamin D deficiency correlates with cognitive impairment and dementia; however, the value of vitamin D substitution in cognitive impairment remains doubtful. [27] [28] [29]

Sleep pattern

More than nine hours of sleep per day (including daytime napping) may be associated with an increased risk of dementia. [30] Lack of sleep may also increase risk of dementia by increasing beta-amyloid deposition. [31]

Personality and mental health

Some personality traits such as being neurotic increases the risk of developing Alzheimer's, a type of dementia. [32] [33] [34] Neuroticism is associated with increased brain atrophy and cognitive impairment in life, while conscientiousness has a protective effect by preventing brain atrophy. [35] A meta-analysis found that the openness and agreeableness traits have also some protective effects. [36]

Based on the English Longitudinal Study of Ageing (ELSA), research found that loneliness increased the risk of dementia by one-third. Not having a partner (being single, divorced, or widowed) doubled the risk of dementia. However, having two or three closer relationships reduced the risk by three-fifths. [37] [38]

Depression

Depressive symptoms can be a part of the clinical presentation of dementia, leading to debate as to whether depression is a cause or a symptom of dementia. [39] The evidence remains unclear. However, Livingstone et al. (2014) [39] report that it is "biologically plausible" that depression increases the risk of dementia. There is some evidence that late-life depression increases the risk of dementia however [40] suggesting treating depression in mid-life might delay or prevent dementia.

Medication

Hypertension

Some studies say Alzheimer's and other dementias may be caused by high blood pressure, since it can cause blood vessel damage through constriction. [41] [42] The etiology of vascular dementia includes hypertension, and thus, lowering blood pressure with antihypertensives may have a positive effect in the prevention of dementia, just as physical activity.

However, one study failed to demonstrate a link between high blood pressure and developing dementia. The study, published in the Lancet Neurology journal of July 2008, found that blood pressure lowering medication did not reduce the incidence of dementia to a statistically significant degree. A prospective meta-analysis of the data from this study with other studies suggested that further research might be warranted. [43]

While the results of studies are somewhat inconsistent, it has been recommended that hypertension in mid-life (45–65 years) and older age (65+ years) should be actively treated to reduce the risk of dementia. [39]

Anti-diabetic drugs

Diabetes mellitus is a risk factor for vascular dementia, and is thus the risk is lowered with anti-diabetic drugs. [44]

Besides, Rosiglitazone (Avandia) improves memory and thinking ability for people with mild Alzheimer's disease. The mechanism of the effect may be the ability of the drug to reduce insulin resistance. [12] Thus, less insulin needs to be released to achieve its metabolic effects. Insulin in the bloodstream is a trigger of amyloid beta-production, [44] [45] so decreased insulin levels decrease the level of amyloid beta. This leads to less formation of amyloid plaques seen in Alzheimer's disease.

Steroid hormones

Estrogen may also help in the prevention of dementia but cannot help when dementia is already present and when cognitive function is already impaired. It increases cerebral blood flow and is an anti-inflammatory agent, enhancing activity at the neuronal synapses in the brain. It may also help to increase brain activation in regions that are affected by dementia which is mainly the hippocampus region.[ citation needed ] Recent evidence on the effects of estrogen do not allow for an unambiguous recommendation for estrogen supplementation and they indicate that the timing of estrogen supplementation may be important, with early postmenopausal use being preferable over its use later in life. [46] [47]

NSAIDs

Non-steroidal anti-inflammatory drugs (NSAIDs) can decrease the risk of developing Alzheimer's and Parkinson's diseases. [12] The length of time needed to prevent dementia varies, but in most studies it is usually between 2 and 10 years. [48] [49] [50] [51] [52] Research has also shown that it must be used in clinically relevant dosages and that so called "baby aspirin" doses are ineffective at treating dementia. [53]

Alzheimer's disease causes inflammation in the neurons by its deposits of amyloid beta peptides and neurofibrillary tangles. These deposits irritate the body by causing a release of e.g. cytokines and acute phase proteins, leading to inflammation. When these substances accumulate over years they contribute to the effects of Alzheimer's. [54] NSAIDs inhibit the formation of such inflammatory substances, and prevent the deteriorating effects. [55] [56] [57]

In 2020 a systematic review conducted by Cochrane of four randomized controlled trials with 23,187 participants concluded that the use of low-dose aspirin and NSAIDS of any type for the prevention of dementia was not supported and that there could be harm. [58]

Vaccine

There is as yet no vaccine against dementia. [12] It has been theorized that a vaccine could activate the body's own immune system to combat the beta amyloid plaques in Alzheimer's disease. One problem to overcome is overreaction from the immune system, leading to encephalitis. [12]

Anticholinergic medication use

Anticholinergic medications are often prescribed to treat health conditions commonly experienced by older people including overactive bladder and many commonly used medications have anticholinergic activity. There has been some observational research that has suggested a linkage between anticholinergic medication use and cognitive decline in older adults. [59] Suggestions to reduce the 'anticholinergic burden', try to modify a person's medications to reduce the use of medications that have anticholinergic activity in a safe way, are often made in dementia guidelines with the goal of improving cognition and/or reducing further decline. The evidence supporting this approach to preventing dementia is weak, however, if safe to do so, and in light of some weaker observational evidence suggesting that these medications may be related to adverse effects or poorer outcomes, it is clinically suggested to prescribe these medications with caution and if safe to do so reduce their use. [59]

See also

Related Research Articles

<span class="mw-page-title-main">Dementia</span> Long-term brain disorders causing impaired memory, thinking and behavior

Dementia is the general name for a decline in cognitive abilities that impacts a person's ability to perform everyday activities. This typically involves problems with memory, thinking, and behavior. Aside from memory impairment and a disruption in thought patterns, the most common symptoms include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, caregivers, and on social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than what is caused by normal aging.

Vascular dementia (VaD) is dementia caused by problems in the blood supply to the brain, resulting from a cerebrovascular disease. Restricted blood supply (ischemia) leads to cell and tissue death in the affected region, known as an infarct. The three types of vascular dementia are subcortical vascular dementia, multi-infarct dementia, and stroke related dementia. Subcortical vascular dementia is brought about by damage to the small blood vessels in the brain. Multi-infarct dementia is brought about by a series of mini-strokes where many regions have been affected. The third type is stroke related where more serious damage may result. Such damage leads to varying levels of cognitive decline. When caused by mini-strokes, the decline in cognition is gradual. When due to a stroke, the cognitive decline can be traced back to the event.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired, typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Cognitive reserve is the mind's and brain's resistance to damage of the brain. The mind's resilience is evaluated behaviorally, whereas the neuropathological damage is evaluated histologically, although damage may be estimated using blood-based markers and imaging methods. There are two models that can be used when exploring the concept of "reserve": brain reserve and cognitive reserve. These terms, albeit often used interchangeably in the literature, provide a useful way of discussing the models. Using a computer analogy, brain reserve can be seen as hardware and cognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve is commonly used to refer to both brain and cognitive reserves in the literature.

The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy: a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain. Amyloid beta is a short peptide that is an abnormal proteolytic byproduct of the transmembrane protein amyloid-beta precursor protein (APP), whose function is unclear but thought to be involved in neuronal development. The presenilins are components of proteolytic complex involved in APP processing and degradation.

Mild cognitive impairment (MCI) is a neurocognitive disorder which involves cognitive impairments beyond those expected based on an individual's age and education but which are not significant enough to interfere with instrumental activities of daily living. MCI may occur as a transitional stage between normal aging and dementia, especially Alzheimer's disease. It includes both memory and non-memory impairments. The cause of the disorder remains unclear, as well as both its prevention and treatment, with some 50 percent of people diagnosed with it going on to develop Alzheimer's disease within five years. The diagnosis can also serve as an early indicator for other types of dementia, although MCI may remain stable or even remit.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens, and is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the typical life expectancy following diagnosis is three to nine years.

<span class="mw-page-title-main">Hyperintensity</span> High intensity on MRI brain scans

A hyperintensity or T2 hyperintensity is an area of high intensity on types of magnetic resonance imaging (MRI) scans of the brain of a human or of another mammal that reflect lesions produced largely by demyelination and axonal loss. These small regions of high intensity are observed on T2 weighted MRI images within cerebral white matter or subcortical gray matter. The volume and frequency is strongly associated with increasing age. They are also seen in a number of neurological disorders and psychiatric illnesses. For example, deep white matter hyperintensities are 2.5 to 3 times more likely to occur in bipolar disorder and major depressive disorder than control subjects. WMH volume, calculated as a potential diagnostic measure, has been shown to correlate to certain cognitive factors. Hyperintensities appear as "bright signals" on an MRI image and the term "bright signal" is occasionally used as a synonym for a hyperintensity.

<span class="mw-page-title-main">Type 3 diabetes</span> Medical condition

Type 3 diabetes is a proposed pathological linkage between Alzheimer's disease and certain features of type 1 and type 2 diabetes. Specifically, the term refers to a set of common biochemical and metabolic features seen in the brain in Alzheimer's disease, and in other tissues in diabetes; it may thus be considered a "brain-specific type of diabetes." It was recognized at least as early as 2005 that some features of brain function in Alzheimer's disease mimic those that underlie diabetes. However, the concept of type 3 diabetes is controversial, and as of 2021 it was not an officially recognized diagnosis.

<span class="mw-page-title-main">Nutritional neuroscience</span> Scientific discipline

Nutritional neuroscience is the scientific discipline that studies the effects various components of the diet such as minerals, vitamins, protein, carbohydrates, fats, dietary supplements, synthetic hormones, and food additives have on neurochemistry, neurobiology, behavior, and cognition.

Alzheimer's Disease Neuroimaging Initiative (ADNI) is a multisite study that aims to improve clinical trials for the prevention and treatment of Alzheimer's disease (AD). This cooperative study combines expertise and funding from the private and public sector to study subjects with AD, as well as those who may develop AD and controls with no signs of cognitive impairment. Researchers at 63 sites in the US and Canada track the progression of AD in the human brain with neuroimaging, biochemical, and genetic biological markers. This knowledge helps to find better clinical trials for the prevention and treatment of AD. ADNI has made a global impact, firstly by developing a set of standardized protocols to allow the comparison of results from multiple centers, and secondly by its data-sharing policy which makes available all at the data without embargo to qualified researchers worldwide. To date, over 1000 scientific publications have used ADNI data. A number of other initiatives related to AD and other diseases have been designed and implemented using ADNI as a model. ADNI has been running since 2004 and is currently funded until 2021.

<span class="mw-page-title-main">Cerebral atherosclerosis</span> Medical condition

Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some of the main components of the plaques are connective tissue, extracellular matrix, including collagen, proteoglycans, fibronectin, and elastic fibers; crystalline cholesterol, cholesteryl esters, and phospholipids; cells such as monocyte derived macrophages, T-lymphocytes, and smooth muscle cells. The plaque that builds up can lead to further complications such as stroke, as the plaque disrupts blood flow within the intracranial arterioles. This causes the downstream sections of the brain that would normally be supplied by the blocked artery to suffer from ischemia. Diagnosis of the disease is normally done through imaging technology such as angiograms or magnetic resonance imaging. The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are numerous factors that can be controlled in attempt to lessen risk.

<span class="mw-page-title-main">Vladimir Hachinski</span> Canadian clinical neuroscientist

Vladimir Hachinski is a Canadian clinical neuroscientist and researcher based at the Schulich School of Medicine and Dentistry at Western University. He is also a Senior Scientist at London's Robarts Research Institute. His research pertains in the greatest part to stroke and dementia, the interactions between them and their joint prevention. He and John W. Norris helped to establish the world's first successful stroke unit at Sunnybrook Hospital in Toronto, and, by extension, helped cement stroke units as the standard of care for stroke patients everywhere. He discovered that the control of the heart by the brain is asymmetric, the fight/flight (sympathetic) response being controlled by the right hemisphere and the rest and digest (parasympathetic) response being controlled by the left hemisphere and damage to one key component can lead to heart irregularities and sudden death. This discovery has added fundamental knowledge to how the brain controls the heart and blood pressure and lays the foundation for helping prevent sudden death.

The neuroscience of aging is the study of the changes in the nervous system that occur with ageing. Aging is associated with many changes in the central nervous system, such as mild atrophy of the cortex that is considered non-pathological. Aging is also associated with many neurological and neurodegenerative disease such as amyotrophic lateral sclerosis, dementia, mild cognitive impairment, Parkinson's disease, and Creutzfeldt–Jakob disease.

<span class="mw-page-title-main">Hypertension and the brain</span>

Hypertension is a condition characterized by an elevated blood pressure in which the long term consequences include cardiovascular disease, kidney disease, adrenal gland tumors, vision impairment, memory loss, metabolic syndrome, stroke and dementia. It affects nearly 1 in 2 Americans and remains as a contributing cause of death in the United States. There are many genetic and environmental factors involved with the development of hypertension including genetics, diet, and stress.

The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons. The NVU addresses the brain's unique dilemma of having high energy demands yet low energy storage capacity. In order to function properly, the brain must receive substrates for energy metabolism–mainly glucose–in specific areas, quantities, and times. Neurons do not have the same ability as, for example, muscle cells, which can use up their energy reserves and refill them later; therefore, cerebral metabolism must be driven in the moment. The neurovascular unit facilitates this ad hoc delivery and, thus, ensures that neuronal activity can continue seamlessly.

Alzheimer's disease (AD) in African Americans is becoming a rising topic of interest in AD care, support, and scientific research, as African Americans are disproportionately affected by AD. Recent research on AD has shown that there are clear disparities in the disease among racial groups, with higher prevalence and incidence in African Americans than the overall average. Pathologies for Alzheimer’s also seem to manifest differently in African Americans, including with neuroinflammation markers, cognitive decline, and biomarkers. Although there are genetic risk factors for Alzheimer’s, these account for few cases in all racial groups.

Alzheimer's disease (AD) is a complex neurodegenerative disease that affects millions of people across the globe. It is also a topic of interest in the East Asian population, especially as the burden of disease increases due to aging and population growth. The pathogenesis of AD between ethnic groups is different. However, prior studies in AD pathology have focused primarily on populations of European ancestry and may not give adequate insight on the genetic, clinical, and biological differences found in East Asians with AD. Gaps in knowledge regarding Alzheimer's disease in the East Asian population introduce serious barriers to screening, early prevention, diagnosis, treatment, and timely intervention.

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