POLSKI
Introduction
Dementia is considered a critical global health issue in ageing societies, as emphasized by the World Health Organization (WHO) [1]. In 2019, an estimated 55.2 million individuals were living with dementia, and this number is projected to rise to 65.7 million by 2030. Consequently, the annual costs associated with hospital care and long-term nursing are expected to increase substantially—from approximately US $1.3 trillion to US $2 trillion [1].
Dementia refers to a group of disorders characterized by progressive impairments in memory, cognitive functions, and behavior that interfere significantly with a person’s ability to maintain their activities of daily living. While advancing age is the most prominent risk factor associated with dementia, the condition should not be considered an inevitable consequence of the ageing process [2].
Dementia results from diverse pathological mechanisms and neurological injuries that disrupt brain function through direct or indirect pathways. Alzheimer’s disease is the most common form, responsible for an estimated 60–70% of all cases. Other significant subtypes include vascular dementia, dementia with Lewy bodies—defined by the presence of abnormal intracellular accumulations of alpha-synuclein—and a range of conditions contributing to frontotemporal dementia, which is associated with progressive degeneration of the frontal and temporal brain lobes [3].
Currently, there is no curative therapy available for dementia; however, accumulating evidence suggests that lifestyle-related factors may contribute significantly to its prevention [4].
As noted above, evidence from epidemiological studies suggests that individuals can lower their risk of cognitive decline and dementia through modifiable lifestyle behaviors, such as engaging in regular physical activity, abstaining from smoking, limiting alcohol consumption, maintaining a healthy body weight, adhering to a balanced diet, and regulating blood pressure, lipid profiles, and glucose levels. Additional factors that contribute to dementia risk include depression, limited social interaction, lower levels of education, reduced cognitive engagement, and exposure to air pollution [3, 5].
This review aims to synthesize current evidence on modifiable risk factors associated with dementia, with particular emphasis on the preventive potential of physical activity, and to provide a comprehensive overview of the pathophysiological mechanisms underlying the onset and progression of distinct dementia subtypes.
Methods
A systematic review of scientific articles was conducted using PubMed, Google Scholar and ResearchGate, focusing on key search terms including: Dementia, prevention, lifestyle interventions, physical activity, cognitive decline, Alzheimer’s disease.
Types and Mechanisms of Dementia
Alzheimer’s disease
Alzheimer’s disease is the most prevalent type of dementia, responsible for approximately 60–70% of all diagnosed cases, followed successively by vascular dementia, dementia with
Lewy bodies, Parkinson’s disease dementia, and Frontotemporal dementia [6].
As noted above, Alzheimer’s disease accounts for the vast majority of dementia cases and is primarily characterized by symptoms such as memory loss, behavioral disturbances, and judgmental disorders. The key neuropathological features of Alzheimer’s disease include extracellular neuritic plaques composed of β-amyloid (Aβ) and intracellular neurofibrillary tangles (NFTs) formed by hyperphosphorylated tau protein. Recent studies have increasingly demonstrated that in Alzheimer’s disease and other tauopathies, tau pathology propagates in a stereotypical, anatomically structured pattern across functionally connected brain regions, resembling a prion-like transmission mechanism [7].
Vascular dementia
Vascular dementia refers to a group of neurocognitive disorders primarily associated with underlying cerebrovascular pathology. It is characterized by a progressive decline in cognitive function resulting from impaired cerebral perfusion, often due to major ischemic events such as stroke or an accumulation of smaller, subclinical infarcts. These vascular insults lead to neuronal injury and structural brain changes that underlie the cognitive deficits observed in Vascular dementia [8, 9].
Vascular dementia is acknowledged as the second most common form of dementia following Alzheimer’s disease, accounting for approximately 20% of all diagnosed cases. Closely associated with advancing age, this condition significantly impacts the health and quality of life of older adults, contributing to substantial individual and societal burden.
A wide range of risk factors have been implicated in the development of vascular dementia, most of which are vascular or lifestyle-related in origin. These include a poor diet, obesity, hypertension, hypercholesterolaemia, sustained heavy alcohol intake, diabetes, smoking, physical inactivity, and air pollution [8].
In addition, key vascular comorbidities such as atrial fibrillation and a history of cerebrovascular events, particularly stroke, are strongly associated with an increased risk of vascular dementia.
Modifiable risk factors—most notably obesity and hypertension—have been shown to exert a particularly negative impact on brain health in middle age and beyond [9].
Vascular pathological changes become increasingly prevalent with advancing age and commonly co-occur with other forms of brain pathology. Most notably, they are frequently observed alongside Alzheimer’s disease-related changes, as well as with other neurodegenerative alterations. This overlap is referred to as mixed pathologies or multiple coexisting pathologies [10, 11].
Dementia with Lewy bodies
Lewy body dementia encompasses two closely related neurodegenerative conditions: dementia with Lewy bodies and Parkinson’s disease dementia. Together, they represent the second most common form of neurodegenerative dementia after Alzheimer’s disease. Dementia with Lewy bodies accounts for approximately 4–8% of dementia cases in clinic-based populations, while dementia develops in up to 80% of individuals with Parkinson’s disease over the course of illness [12].
The neuropathological hallmark of Lewy body dementia is the abnormal accumulation of Lewy bodies, which are intracellular inclusions primarily composed of alpha-synuclein. These pathological aggregates are found in key brain regions—including the brainstem, limbic structures, and neocortex— and are central to the disease’s clinical manifestations. Their presence disrupts normal neurotransmission, particularly in dopaminergic, cholinergic, and other neurotransmitter systems, thereby contributing to the characteristic combination of cognitive deficits and parkinsonian motor symptoms observed in Lewy body dementia. In addition, chronic neuroinflammation is believed to exacerbate disease progression by further impairing neuronal function and network connectivity [13].
Frontotemporal Dementia
Frontotemporal dementia is one of the more prevalent forms of dementia, especially among individuals under the age of 65. Due to its marked behavioral manifestations, it often imitates primary psychiatric conditions, which can complicate diagnosis. Despite clinical similarities, Frontotemporal dementia arises from a range of distinct neuropathological processes, all of which involve selective degeneration of the frontal and temporal cortices [14].
The term currently refers to a spectrum of disorders characterized by impairments in behavior, language, and executive functioning, frequently accompanied by motor abnormalities [15].
Additionally, genetic predisposition plays a significant role in the pathogenesis of the disorder [14].
Shared Mechanisms in Dementia
Various forms of dementia share several contributing pathophysiological mechanisms beyond their primary etiologies. Among these are oxidative stress, mitochondrial abnormalities, calcium signaling imbalances, and deficient glymphatic elimination of toxic proteins. Additionally, neuroinflammation, primarily mediated by the activation of microglia and astrocytes, significantly contributes to ongoing neuronal injury and compromises synaptic plasticity.
These intricate neurobiological disruptions give rise to a spectrum of clinical manifestations, including deficits in memory, language disturbances, impaired executive function, alterations in personality, and a progressive loss of the ability to function independently [16, 10].
Comprehensive insight into the unique clinical presentations, underlying pathology, and molecular mechanisms of individual dementia subtypes is crucial for the development of effective, tailored approaches to prevention and therapy [17].
Risk Factors for Dementia
Non-modifiable risk factors such as age, genetics, and biological sex are foundational determinants in the risk of developing dementia.
Advancing age is the most significant risk factor for Alzheimer’s disease and other forms of dementia. However, despite the strong correlation, dementia should not be regarded as an inevitable consequence of the ageing process [18].
Moreover, dementia is not limited to the elderly population; cases of young-onset dementia, characterized by symptom emergence before the age of 65, represent as much as 9% of all diagnoses [3].
Current evidence indicates that over 20 genes are associated with an altered risk of developing dementia. Among them, the APOE gene—particularly the ε4 allele—was the first to be identified as significantly increasing susceptibility to Alzheimer’s disease, and remains the most potent genetic risk factor to date. In addition, there are rare deterministic gene mutations that directly cause dementia; however, these account for fewer than 1% of all cases. Such mutations are typically linked to early-onset forms of the disease, where clinical symptoms manifest before the age of 60 [18].
Even after adjusting for women’s longer average lifespan, Alzheimer’s disease occurs more frequently in women than in men. While the overall risk of developing dementia is comparable between sexes, epidemiological data suggest that women aged over 80 exhibit a modestly elevated risk compared to men of the same age group. The underlying causes of this sex-based disparity remain incompletely understood [18, 19].
Modifiable risk factors
Research indicates that the risk of cognitive decline and dementia can be significantly lowered through the adoption of healthy lifestyle behaviors, such as engaging in regular physical activity, not smoking, avoiding harmful alcohol consumption, maintaining a healthy body weight, following a nutrient-rich diet, and effectively managing blood pressure, cholesterol, and glucose levels. Additional contributing factors to dementia risk include depression, social isolation, low levels of formal education, cognitive inactivity, and exposure to air pollutants [3].
Physical Activity
Given the absence of a definitive cure or disease-modifying treatment for dementia, growing attention has been directed toward preventive strategies aimed at mitigating cognitive decline and slowing disease progression. Among lifestyle interventions, physical activity—especially aerobic training combined with resistance exercises—has emerged as one of the most extensively studied and advocated approaches for enhancing overall health and promoting healthy aging [20].
Physical activity has been widely recognized for its neuroprotective properties and its positive effects on cognitive functions, particularly those associated with memory and learning [21].
Interestingly, research indicates that Dance Movement Therapy and yoga interventions enhance cognitive function and brain connectivity in older adults with mild cognitive impairment (MCI), providing effective non-pharmacological approaches to cognitive support [22, 23].
Moreover, regular physical exercise has been shown to lower risk of heart disease, stroke, hypertension, and type II diabetes mellitus, all of which are modifiable risk factors for dementia [20].
Recent evidence consistently highlights the protective role of physical activity in relation to dementia risk. Engaging in regular physical activity has been shown to reduce the likelihood of developing all-cause dementia, Alzheimer’s disease, and vascular dementia, independent of baseline age. The most pronounced cognitive benefit is observed when individuals transition from complete physical inactivity to even modest levels of activity, underscoring the preventive value of movement across the lifespan [5, 24].
Sustained engagement in physical activity throughout adulthood has been consistently associated with improved cognitive outcomes in later life. Evidence suggests that maintaining or increasing physical activity levels during midlife significantly reduces the risk of developing dementia, whereas persistent inactivity is linked to elevated risk. Notably, among men, regular participation in moderate-to high-intensity exercise has been shown to lower the likelihood of mild cognitive impairment (MCI). Importantly, the cognitive benefits derived from physical activity appear to be influenced by the specific characteristics of the activity—namely, its type, intensity, and duration. Additionally, a decline in cardiorespiratory fitness, as reflected by reduced maximal oxygen uptake (VO2max), may further contribute to cognitive deterioration, emphasizing the importance of preserving aerobic capacity as part of dementia prevention strategies [5].
Regular physical activity raises cerebral blood flow by increasing cardiac output, which in turn supports neural functioning and contributes to the attenuation of oxidative stress. Furthermore, exercise stimulates the upregulation of key neurotrophic and growth factors, such as brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and insulin-like growth factor 1 (IGF-1), thereby promoting neuroplasticity and angiogenic processes within the brain [20].
These processes not only counteract the pathological hallmarks of Alzheimer’s disease, but also support neuronal growth and survival by inhibiting sustained neuroinflammatory responses [6]. Evidence from mouse models also suggests that irisin, a myokine released during exercise, might be neuroprotective [5]. 8
Although numerous studies have emphasized the protective role of physical activity in maintaining cognitive health, not all research consistently supports a direct causal link between physical activity and reduced dementia risk.
Recent evidence suggests that physical inactivity, when considered in isolation, may not constitute a direct risk factor for dementia or Alzheimer’s disease. Although inactivity is associated with cardiometabolic conditions, such as diabetes and cardiovascular disease, which are established dementia risk factors, its independent effect appears limited. Notably, an increased dementia risk was observed among individuals who were both physically inactive and developed cardiometabolic disease, indicating a possible interaction effect. The study further highlights methodological constraints, particularly the reliance on self-reported activity levels, which may limit the accuracy of findings. For more robust conclusions, future investigations should incorporate objective monitoring tools and extended longitudinal follow-up. Overall, while promoting physical activity remains essential for general health, its role in dementia prevention may depend on broader lifestyle and metabolic factors [25].
From a public health perspective, strategies that promote physical activity at the population level are essential. In this context, the World Health Organization recommends structural interventions—such as urban planning and access to green spaces—as effective measures to reduce physical inactivity and mitigate dementia risk across communities [5].
Lifestyle Interventions
In addition to physical activity, various lifestyle factors have been identified as influential in modulating the risk of cognitive decline and dementia.
Diet
Dietary habits have been identified as important modifiable determinants influencing the risk of cognitive decline and dementia [26].
Several nutritional components, including antioxidants, certain vitamins, polyphenols, and fish, have been associated with a reduced risk of developing Alzheimer’s disease, whereas diets high in saturated fats, excessive caloric intake, and elevated alcohol consumption have been linked to an increased risk [27]. Eggs also appear to support cognitive health, primarily due to its rich content of choline and essential nutrients that contribute to neuronal membrane integrity, neurotransmitter synthesis, and neuroplasticity [28].
In addition, lifestyle factors such as tobacco smoking and alcohol consumption further exacerbate neurodegenerative risk. Smoking is associated with an elevated risk of developing dementia. However, individuals who quit smoking may lower their risk to a level comparable with that of those who have never smoked [29].
A large-scale retrospective cohort study of over 30 million French hospital patients found that alcohol use disorders were strongly associated with all major forms of dementia, particularly early-onset cases. Reducing harmful alcohol use may therefore represent an effective dementia prevention strategy [30].
Available data indicate that whole dietary patterns, particularly the Mediterranean diet, may offer modest protective effects against cognitive decline, especially in individuals with cardiovascular risk factors [5, 31]. The Mediterranean diet is characterized by a high intake of whole grains, fruits, vegetables, legumes, and olive oil, moderate consumption of fish and dairy products such as cheese, and a low intake of red and processed meats, sweets, and alcohol [32].
In addition to the Mediterranean diet, other dietary patterns have also demonstrated beneficial effects on cognitive health. One such example is the Dietary Approaches to Stop Hypertension (DASH) diet, which was originally developed to manage high blood pressure but is now also being investigated for its potential to lower the risk of Alzheimer’s disease [33]. Specifically, the DASH diet encourages the consumption of whole grains, fruits, vegetables, low-fat dairy products, lean meats such as fish and poultry, as well as nuts, seeds, and legumes, while allowing moderate amounts of healthy fats and oils [34]. Furthermore, it focuses on limited intakes of salt and added sugar [33]. Hypertension is a known risk factor for cognitive decline due to its negative impact on cerebral blood flow, particularly in regions vulnerable to aging and Alzheimer’s disease. Individuals carrying the APOE4 allele are especially susceptible to such vascular changes. By targeting this modifiable risk factor, the DASH diet may help preserve cognitive function [34].
In contrast, individual nutrient supplements, such as vitamins B, E, and omega-3 fatty acids, have not shown consistent benefits in preventing dementia. As a result, the World Health Organization (WHO) recommends the Mediterranean diet for dementia risk reduction but does not support the use of multinutrient supplementation for cognitive health [5, 31].
Although vitamin D is primarily recognized for its essential role in maintaining bone health and preventing osteoporosis, emerging evidence indicates that it also contributes to the pathogenesis of chronic conditions, including Alzheimer’s disease and other dementias in older adults. Notably, vitamin D supplementation has been significantly associated with a reduced incidence of dementia across diverse populations [35].
Individuals without dementia at baseline who received vitamin D were shown to have a 40% lower risk of developing the condition over a 10-year follow-up, with the effect especially pronounced among women, individuals with preserved baseline cognitive function, and non-carriers of the APOE ε4 allele. These findings support a potential neuroprotective role of vitamin D, possibly mediated through anti-inflammatory, neurotrophic, and amyloid-clearing mechanisms [36]. Given its additional involvement in neurotrophic signaling, neurotransmission, and synaptic plasticity, vitamin D deficiency may be a contributing factor in the progression of Alzheimer’s disease and related dementias [37].
Additionally, growing evidence highlights the gut microbiota as another important factor in the development of Alzheimer’s disease. A recent study demonstrated that transplantation of gut microbiota from Alzheimer’s patients into healthy animals induced memory impairments and reduced hippocampal neurogenesis, suggesting a causal role of microbial composition in disease pathology [38].
Sleep hygiene
Sleep disturbances are hypothesized to promote inflammation, which in turn increases β-amyloid accumulation, potentially contributing to the onset of Alzheimer’s disease and worsening sleep disruptions [5, 31].
Recent research indicates that even a single night of sleep deprivation can significantly elevate β-amyloid accumulation in brain regions vulnerable to Alzheimer’s disease, such as the hippocampus and thalamus, highlighting the essential role of sleep in maintaining brain clearance mechanisms and potentially reducing neurodegenerative risk [39].
Moreover, impaired sleep architecture, characterized by reduced slow-wave and REM sleep, has been associated with brain atrophy in regions vulnerable to Alzheimer’s disease, as well as with the presence of cerebral microbleeds indicative of small vessel pathology. These associations are more pronounced in individuals carrying the APOE4 allele, suggesting that poor sleep may interact with genetic vulnerability to accelerate neurodegenerative processes [40].
In this context, preclinical and clinical evidence suggests that omega-3 supplementation may help improve sleep quality, reduce neuroinflammation, support brain function, and decrease amyloid-β aggregation. Due to their neuroprotective properties and safety profile, omega-3 fatty acids represent a promising strategy for managing sleep disturbances and potentially slowing the progression of Alzheimer’s disease [41].
Technology use
Excessive use of digital technology has been linked to cognitive decline, often described as digital dementia or brain rot. Studies show that high screen time can cause attention deficits, reduced emotional and social skills, poor sleep, and technology addiction, all factors that may increase dementia risk [42, 43]
“Brain rot,” in particular, affects young people exposed to low-quality digital content, leading to mental exhaustion and impaired executive function [44, 45].
However, not all digital use is harmful. Tools like cognitive training apps and purposeful internet searching can stimulate brain areas involved in memory and decision-making, potentially protecting cognition [46].
Balanced use of technology, including limiting screen time, promoting digital literacy and engaging in offline activities, may reduce dementia risk while preserving the cognitive benefits of digital tools.
Cognitive Engagement and Social Interaction
Social engagement is a protective factor against cognitive decline.
Cognitively engaging leisure activities have been increasingly recognized as effective, nonpharmacological strategies for preserving cognitive function in older adults. Engaging in traditional board games may protect against cognitive decline in older adults. These games, such as Go, Mahjong, and chess, have been shown to improve cognitive performance, enhance executive functions, increase brain-derived neurotrophic factor (BDNF) levels, and improve quality of life and mood. Incorporating these activities into daily routines may be an effective strategy to support cognitive health and well-being in the elderly [47].
Growing evidence suggests that cognitively stimulating activities, especially those engaging higher-order executive and visuospatial functions, may play a protective role in mitigating the risk of neurodegeneration. Occupational engagement in complex visuospatial and navigational tasks, as exemplified by taxi and ambulance drivers, appears to be associated with a reduced mortality risk from Alzheimer’s disease. These findings support the hypothesis that sustained cognitive activity, particularly in spatial and executive domains, may confer protective effects against neurodegenerative decline. Promoting cognitively demanding activities throughout adulthood may thus represent a viable strategy for Alzheimer’s disease prevention [48].
Findings from a 2020 longitudinal study revealed that frequent feelings of loneliness were significantly associated with an increased risk of all-cause dementia and Alzheimer’s disease, but not Vascular dementia. These associations remained even after adjusting for confounders and excluding early dementia cases, suggesting that loneliness may be an independent and modifiable risk factor for dementia, particularly Alzheimer’s disease [49].
