Alzheimer’s is a common degenerative neurological disease. This disease can be categorized into two subsets: early onset and late onset Alzheimer’s disease. Late onset Alzheimer’s disease makes up 95% of cases, and occurs at 65 years or older (Filley, 1986). Early onset is quite uncommon, and typically occurs in peoples 40s-50s (Lava, 2018). In addition, early-onset is associated with genetic mutation and down syndrome, whereas what determines who develops late-onset Alzheimer’s disease is not as clear (Lava, 2018). Dementia and Alzheimer’s are frequently used as interchangeable terms, but these are separate and distinct entities. Dementia is a term to describe a group of symptoms rather than an actual disease, simply referring to the loss of “memory, performance of daily activities, and communication abilities” (Legg, 2016). Alzheimer’s, on the other hand, is a neurodegenerative disease, and the most common cause of Dementia symptoms (Legg, 2016). PREVALENCE AND INCIDENCE Alzheimer’s disease is quite prevalent but is not considered to be part of a natural healthy aging process. As of 2012, there were over 747,000 Canadians were living with Alzheimer’s disease (Statistics Canada, 2017a). Currently the annual incidence rate for Alzheimer’s disease in Canada is approximately 25,000 new cases diagnosed every year (Alzheimer Society Canada, 2018a). There were an estimated 35.6 million people globally with dementia in 2010, and prevalence of Alzheimer’s is expected to double globally between 2010 and 2030 (Statistics Canada, 2017a). Globally the incidence rate is so high that one person develops Alzheimer’s every 3 seconds (Barbarino, 2018). The global prevalence increase is due to a decrease in premature death from infectious diseases allowing people to live long enough to develop noncommunicable diseases, such as Alzheimer’s. Canada has seen a steady increase in the prevalence within the population, with the highest prevalence in those 80 years and over age demographics (Statistics Canada, 2017a). In Canada Alzheimer’s is “ranked seventh among the leading causes of death [in the population]” (Statistics Canada, 2017b); ninth cause amongst men, and sixth among women (Statistics Canada, 2017b). PATHOPHYSIOLOGY Alzheimer’s disease has a drastic physiological effect. The disease causes brain cells, neurons, to waste away and die. This cell death breaks neural pathways, causing a progressive loss in cognitive function and eventually impacting physical functioning. There are two components of Alzheimer’s that disrupt cell communication and have been recognized. One clear cause is the development of plaques between neurons, disrupting cell to cell communication (Mayo Clinic, 2018). These plaques form due to a leftover fragment of a larger protein, and this fragment is called Beta-amyloid (National Institute on Aging, 2017b). These fragments cluster together and form plaques, and not only disrupt cell communication, but also appear to have a toxic effect on the neurons (Mayo Clinic, 2018). These plaques when larger can also include cellular debris (Mayo Clinic, 2018). The other recognized effect is when the tau proteins change “shape and organize themselves into structures called neurofibrillary tangles” (Mayo Clinic, 2018). When Tau proteins are functioning normally, they provide a transport system for nutrients and other essential materials and play a role in internal support to neurons (National Institute on Aging, 2017b). When they have malfunctioned and formed tangles, they no longer can functionally transport materials in turn disrupting the transport system, and further become toxic to cells, resulting in cell death (Mayo Clinic, 2018). Alzheimer’s has two secondary impacts on the brain. This is the vascular effects, and chronic inflammation. Alzheimer’s damages the vasculature of the brain. This occurs through the Beta-amyloid fragments of proteins becoming deposited in arteries (Bushak, 2017). These deposits can cause atherosclerosis, hardening of blood vessels, and mini strokes (Bushak, 2017). It also can cause deterioration of the blood brain barrier. This damage of the vasculature reduces the blood flow and oxygen delivered to brain cells, thus further causing damage to the brain (Bushak, 2017). The other impact secondary to neuron degeneration is chronic inflammation. Chronic inflammation occurs due to a buildup of glial cells, which normally function to remove cell debris from the brain (Bushak, 2017). When glial cells fail to clear waste proteins being to collect, including beta-amyloid plaques (Bushak, 2017). This results in chronic inflammation, and further decreases the health of the brain. DISEASE PROGRESSION Alzheimer’s disease does not progress through the brain simultaneously, it impacts different parts at different parts. The first part of the brain to be impacted by this disease is the entorhinal cortex and hippocampus, which damages memory (National Institute on Aging, 2017b). The disease then progresses to the cerebral cortex, and the damage here impacts an individual’s ability to use language, reasoning, and social behavior (National Institute on Aging, 2017b). Finally, the disease spreads to the remaining regions of the brain (National Institute on Aging, 2017b). As the rest of the brain degrades, an impact will be seen on fine and gross motor skills, an individual’s ability to function independently (BrightFocus Foundation, 2019). This digression in motor skills can lead to aspirating food and the development of pneumonia, fall accidents, immobility resulting in bed sores and infection, incontinence resulting in bladder infections, and potentially fatal comorbid conditions (Statistics Canada, 2017b). If fatal comorbid conditions do not occur first, the disease will eventually progress to the point of impacting involuntary nervous pathways, such as control of breathing, reflexes, and heart rate, which will lead to death (BrightFocus Foundation, 2019). DIAGNOSIS The diagnosis of Alzheimer’s disease is complex and requires a multistep process. The first screening usually involves looking at dementia symptoms, as Alzheimer’s is the most common cause of dementia. This screening first involves the physician testing basic functions such as reflexes, coordination, eye movement, sensation, muscle strength, and speech (Alzheimer’s Association, 2019b). If further testing is indicated, the patient will undergo a series of memory and cognitive tests (National Institute on Aging, 2017a). If these symptoms are present, then further screening will occur to rule out other causes. A physician then will use tests such as a CT scan, MRI scan or CAT scan to check for any abnormal loss of brain volume and density which would indicate the presence of Alzheimer’s (Alzheimer’s Association, 2019b). This loss of brain density seen on an MRI as a result of Alzheimer’s is shown in Appendix A. From here a conclusion on the presence of Alzheimer’s can be reached. The only definitive way of diagnosing the disease is through post-mortem brain autopsy which will clearly show a loss of brain volume, as shown in appendix b (National Institute On Aging, 2017a). TREATMENT There is currently no cure for Alzheimer’s disease, but it’s progression can be slowed, symptoms can be treated, and individuals with Alzheimer’s can be supported through disease progression (Mayo Clinic, 2018). There are currently two main medications on the market used to treat Alzheimer’s symptoms. The first class of drug are Cholinesterase inhibitors, which are sold under several brand names such as Aricept, Exelon, and Razadyne (National Institute on Aging, 2019). The second class of drugs is Memantine, which is sold under the name Namenda. These drugs are used to treat the cognitive symptoms: memory loss, confusion, and problems with thinking and reasoning (National Institute on Aging, 2019). These medications work through “regulating glutamate, an important brain chemical [which in] excessive amounts may result in cell death” (National Institute on Aging, 2019), in addition to treating symptoms. As the disease progresses further intervention than drugs will be needed such as at home care nurses, or assisted living facilities (National Institute on Aging, 2019). These interventions help prevent individuals with Alzheimer’s from getting injured or lost and provide the help they need. ECONOMIC DISEASE BURDEN Alzheimer’s disease presents a significant economic burden because of its high prevalence. According to the National Population Health Study of Neurological Conditions, in 2016 Alzheimer’s disease cost the Canadian healthcare system and the caregivers $10.4 billion (Chambers, 2019). This amount is predicted to increase to $16.6 billion by 2031 (Chambers, 2019). The Population Health Expert Panel reckoned that the long-term care costs per person with dementia amounted to approximately $14,000 per person per year (Chambers, 2019). The economic burden for patients with dementia appears to be 5.5 times more than patients not suffering from dementia (Chambers, 2019). Long-term care and home care and long-term put the highest weight on the direct costs (Chambers, 2019). In 2011, it was estimated that caregivers provided a 19.2 million worth of care (Chambers, 2019). The cost of Alzheimer’s is not one that is only burdened by the health care system, but also by families and patients. The diagnosis process can take up to several years, and many patients find that they must pay thousands for private health care to accelerate the diagnostic process (Kirson et al., 2016). Seeing a specialist at an earlier stage of disease progression allows fewer diagnostic tests to be required, and interventions to be implemented more rapidly. AT-RISK POPULATIONS Certain subgroups of the population have an above average risk of developing Alzheimer’s disease. The chances of developing Alzheimer’s are influenced by a mix of modifiable risk factors and genetics, but despite these variables some populations such as women, people with certain genes, the elderly, and individuals with Down Syndrome have consistently higher rates. The most important risk factor for Alzheimer’s is increasing age. As previously mentioned, most Alzheimer patients are 65 and older. After the age of 65, the risk of developing Alzheimer’s increases by 2% every year (Tyas, et al., 2001). Additionally, those over 85 compose almost one-third of all cases (Alzheimer’s Association, 2019a). There are several recognized genetic determinants, the first of which is biological sex. Women are more likely to develop Alzheimer’s disease than men are, partially due to a longer life expectancy (Lindsay, 2002). Another group with higher rates of Alzheimer’s are those with siblings or parents who have suffered from this disease. Having an immediate family member raises the existing risk of developing Alzheimer’s disease by about 30% (Harvard Health Publishing, 2019). The final recognized at risk group is those with certain genes. The presence of the TREM2 gene has been linked to the development of Alzheimer’s (Lindsay, 2002). This gene is responsible for microglia cells malfunctioning in clearing Beta-amyloid plaques in the brain, and therefore failing to prevent inflammation (Lindsay, 2002). Early onset Alzheimer’s disease is associated with the gene apolipoprotein E (APOE4) (Harvard Health Publishing, 2019). Having one copy of this gene increases an individual’s risk of developing Alzheimer’s by three-fold (Harvard Health Publishing, 2019). In rare cases, two copies of this gene are inherited which increases the risk of developing it by 10-15 times (Harvard Health Publishing, 2019). People with Down Syndrome carry an extra copy of chromosome 21, which contains the gene for amyloid precursor protein. An overload of this protein can result in an accumulation of Beta-amyloid plaques, resulting in an increased risk of Alzheimer’s. Approximately 40-70% of people with Down Syndrome develop Alzheimer’s disease (Salehi, et al., 2016). Current research suggests that ethnicity is also linked to Alzheimer’s. At a population level elderly Latinos are 1.5 times more likely than elderly Caucasians to develop Alzheimer’s disease, and African Americans are nearly twice as likely as Caucasian populations (Resendez, et al., 2019). This is likely influenced by high rates of cardiovascular disease in these populations, which is known to be a modifiable risk factor for Alzheimer’s (Alzheimer’s Association, 2019a & Recendez et al., 2019). RISK FACTORS The causes of Alzheimer’s are not fully understood, but it is thought to be a result of a combination of genetic and environmental factors (Mayo Clinic, 2018). There are several recognized modifiable risk factors which are thought to affect the risk of development of Alzheimer’s disease (Mayo Clinic, 2018). The recognized environmental risk factors are exposure to toxic chemicals, heavy metals, and pesticides, extended exposure to high levels of air pollution, and traumatic brain injury (Lindsay, 2002). Some biological modifiable risk factors are cardiovascular disease, smoking, obesity, hypertension, depression, and type two diabetes which have all been found to be associated with increased risk of Alzheimer’s disease (Alzheimer Society Canada, 2018b). Cardiovascular disease is suspected to increase the risk of acquiring Alzheimer’s because of the damage to blood vessels it causes. When damage to blood vessels in the brain occurs there is a higher probability of beta-amyloid plaques forming in the brain (Alzheimer’s Association, 2019a & De Bruin et al., 2014). Risk factors found to be have protective qualities and be associated with a decreased risk of Alzheimer’s are an increased level of education, leisure activities, being physically active, and consuming a Mediterranean diet which consists primarily of whole grains, fish, legumes, fruit and vegetables, and does not include red meat (Alzheimer Society Canada, 2018b). All these modifiable risk factors alter the level of risk people in the at-risk populations, and the general population have of developing Alzheimer’s disease.
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