Type of dementia
Percentage of all dementia types (approximate) (%)
Causes
Alzheimer’s disease
60
Degenerative disease causing “plaques and tangles” to build up in the brain tissues that kill and shrinks the brain
Lewy body dementia
15
Degenerative disease associated with an accumulation of “Lewy Bodies” in the brain causing impairment in cognitive function
Mixed dementia
10
Combination of degenerative disease and other type of dementia
Vascular dementia (multi-infarct or mini-strokes)
5
Circulatory disease of heart and blood vessels resulting in stroke or mini-stroke that damage areas of the brain
Other dementias
10
1. Frontal lobe dementia and Picks disease
1. Affects frontal lobe, behavior problems
2. Creutzfeldt-Jakob disease
2. Viral disease
3. Multiple sclerosis, Parkinson’s disease, Huntington’s chorea
3. Diseases of the nervous system
4. Brain damage alcohol abuse, toxins
4. Brain trauma, damage may improve if toxins are removed
Risk Factors
Many factors can eventually lead to dementia. Some can’t be changed while other can be addressed to reduce the risk.
Non-modifiable Risk Factors
Age. The risk of Alzheimer’s disease, vascular dementia and several other dementias increases significantly with age [1]. However, dementia isn’t a normal part of aging.
Family history. People with a family history of dementia are at greater risk of developing it. However, many people with a family history never develop symptoms, and many people without a family history do. If they have specific genetic mutations, they are at significantly greater risk of developing certain types of dementia [2].
Down syndrome. By the time they reach middle age, most people with Down syndrome develop the plaques and tangles characteristic of Alzheimer’s disease, according to studies [3]. Many, but not all, also develop dementia.
Modifiable Risk Factors
The following factors can be controlled to reduce the risk of dementia:
Alcohol use. Alcohol consumption is one possible risk factor for Alzheimer’s Dementia, AD. Alcoholism is associated with extensive cognitive problems [4], including alcoholic dementia [5]. The effects of alcohol on cognition, brain disorders, and brain chemistry are somewhat similar to AD’s effects on these three areas, it possible that alcohol use might increase the risk of developing AD [6].
Atherosclerosis. This buildup of plaques is a significant risk factor for vascular dementia as it may lead to stroke. Studies have also shown a possible link between atherosclerosis and Alzheimer’s disease [7]
Blood pressure. Uncontrolled hypertension is a risk of developing Alzheimer’s disease and vascular dementia. Cumulative evidence implicates hypertension in the pathogenesis of AD [8, 9]
Cholesterol. High levels of low-density lipoprotein (LDL) cholesterol can significantly increase the risk of developing vascular dementia [10]. Some research has also linked high cholesterol levels in middle age each increase the risk of going on to develop AD in later life [11].
Depression. Late-life depression, especially in men, may be an early indication for the development of Alzheimer’s-related dementia [12].
Diabetes. People with Type 2 diabetes have an increased risk of developing both Alzheimer’s disease and vascular dementia [13].
High estrogen levels. High levels of total estrogen in women have been associated with greater risk of developing dementia [14–16].
Homocysteine blood levels. Elevated blood levels of homocysteine – a type of amino acid produced in the body – may increase the risk of developing Alzheimer’s disease and vascular dementia [17].
Environmental Toxins and Dementia
Dementia may originate from environmental toxic substances, namely exposure to heavy metals such as lead, mercury and aluminum; as well as to carbon monoxide, solvents, pesticides and electromagnetic fields [20]. This tends to affect exposed individuals at a relatively young age and the optimal preventative strategies include avoidance of the toxic substances.
Toxic encephalopathy is a general term used to describe any sort of cerebral damage that comes from the use of or exposure to toxic compounds, chemicals or metals [21]. This damage is sometimes reparable, but in cases in which the damage persists, the risk for development of degenerative dementia increases.
Exposure to any kind of toxic substance with a negative effect on the brain can cause toxic encephalopathy, and ultimately, the onset of dementia. Some of the most common environmental toxic substances that can cause this damage are:
Heavy metals: Mercury, lead, aluminum, arsenic, lead, toluene and lithium, even in small doses, can have a long-term damaging effect on the brain [22] leading to both encephalopathy and dementia (Table 6.2).
Table 6.2
Effects of environmental toxins on human health
Metal
Organic diseases
Neurologic and psychiatric effects [23]
Aluminum
Joint pain, bone calcium loss aneamia [24]
Dementia, Alzheimers, Parkinsons, Encephalopathy with loss of memory, concentration and mobility
Arsenic
Type 2 diabetes [25]
Damage to the nervous system leading to weakness, deafness, paresthesia, organic psychosis with drowsiness, agitation, stupor, delirium, schizophrenia
Cadmium
Damage to kidney and lungs, fragile bones, aneamia, increased risk of cancer if inhaled [26]
No reference found at this stage
Mercury
Diminished intelligence, speech disorders, restlessness, aggressiveness, visual and hearing disorders, polyneuropathy, myasthenia gravis, Alzheimers
Nickel
Allergies, dermatitis, Eczema [29]
Headache, dizziness, lack of sleep
Lead
Depression that may lead to suicide, lack of attention, damage to visual intelligence and motor function, memory disorder, learning difficulties, fatigue, agitation, aggressivess, psychoses, hallucinations, peripheral polyneuropathy, encephalopathy, saturnism (lead poisoning)
Organic zinc
Stomach cramps, nausea, vomiting, anaemia, damage to the pancreas
Cerebral edema with nausea, vomiting, dizziness, visual disorder, cramps, forgetfulness, fatigue, lack of interest, headaches, sleeping difficulties
Pesticides: Many families of pesticides are known to contain neurotoxic properties [31] that cause serious central nervous system damage e.g., carbamates, organophosphates, organochlorines, and bipyridyles [32]. Evidence consistently suggests that a higher risk of Parkinson’s Dementia (PD) is associated with pesticides and that a higher risk of AD is associated with pesticides [33].
Solvents: It is recognized that exposure to solvents can be neurotoxic [34]. However, an association between solvent exposure and neuro-degeneration, particularly AD, has yet to be established. Some studies have demonstrated a moderate-to-strong association between solvent exposure and AD, with a greater effect in men and more years of exposure [35].
Electromagnetic fields: Although no documented causal relationship between occupational electromagnetic field (EMF) exposure and AD has been found, a link between occupations involving exposure to electric and magnetic fields and the subsequent development of AD has been hypothesized. Some research findings [36] suggest that EMF exposure may contribute to an increased production of b-amyloid in the brain, which might eventually result in AD.
Carbon Monoxide: In patients with acute poisoning, 30 % or more may experience delayed onset of neuropsychiatric symptoms [37]. Symptoms include cognitive and personality changes, dementia, psychosis, Parkinsonism, amnesia, depression, and incontinence
Even small amounts of these toxic materials, especially over a long period of time, can cause gradual mental deterioration.
Association Between Toxic Environmental Exposures and Dementia
This section examines whether evidence from previous studies on association between toxin environmental exposures and dementia is of sufficient strength to warrant specific recommendations for behavioral, lifestyle, or pharmaceutical interventions/modifications targeted to these endpoints.
Williams et al. [38] identified a systematic review by Santibanez et al. [39], that examined occupational risk factors for Alzheimer’s disease (AD), focusing on the associations between AD and pesticides, solvents, electromagnetic fields, lead, and aluminum in the workplace. The review included 21 case-control studies and three cohort studies published between 1984 and 2003. Some studies examined multiple factors, and number of studies and subject counts are included for each exposure. Therefore, the study count in Table 6.3 exceeds the 22 studies identified. Case control studies were included in spite of the inherent weakness for establishing causality, due to paucity of data from cohort studies. Further, exposures to specific toxic substances are relatively uncommon and would require very large sample sizes to have sufficient power to detect an effect in general community samples.
Table 6.3
Toxic environmental factors and risk of developing AD – characteristics of studies reviewed by Santibanez et al. [39]
