Alzheimer’s disease is one of the most common forms of dementia. The disease has no cure as it progresses, before eventually leading to death. Alois Alzheimer, a German neurologist and psychologist, first described the disease in 1906. Frequently, Alzheimer’s disease is diagnosed among people aged over 65 years, though the onset of the disease can occur much earlier. About 26 million people suffered from this disease in 2006 worldwide. Researchers expect the disease to affect about 85 million people internationally by the year 2050. Despite the fact that the disease is developing differently for every individual, there are various common signs and symptoms. According to Alzheimer’s Association (2012), early symptoms are frequently and mistakenly thought to be related to age or stress manifestations. In this regard, this paper discusses Alzheimer’s disease by providing the following: overview of the disease, established causes of the disease, risk factors, prevention of the disease. In addition, the study will also provide the statistics concerning the number of individuals affected by the disease.

Overview of Alzheimer’s Disease

During the onset of the disease, the most common symptoms are problems associated with remembering recent events. When an individual is suspected to be suffering from Alzheimer’s disease, the diagnosis is normally confirmed with tests that analyze thinking abilities and behavior, usually by brain scan. As the disease progresses, the symptoms include irritability, confusions, mood swings, aggression, long-term memory loss, and trouble with language. As the patients’ cognitive abilities decline, they frequently withdraw from their families and society. Body functions are eventually lost, which ultimately results in death. Because Alzheimer`s disease is not similar for every individual, it is very difficult to predict how it will affect an individual. According to Bruce, Davis & Casey (2008), the disease develops for a variable and an unknown amount of time before being fully visible. In addition, the disease can advance undetected for many years. The average life expectancy following the detection of the disease is about seven years.

The cause and advancement of the disease are not well understood. According to studies, the disease is related to tangles and plaques in the brain. Present treatments only attempt to avert the symptoms. Presently, there are no available treatments reversing or stopping the advancement of Alzheimer’s disease. More than one thousand clinical trials, as of 2012, have been performed to assess various compounds in ALS. These clinical trials suggest that mental simulation, balanced diet, and exercise can prevent or delay the cognitive symptoms of AD in healthy older patients. However, these suggestions do not delay brain pathology symptoms. In addition, there is also no supporting evidence that these suggestions are effective.

Because Alzheimer`s disease is degenerative and cannot be cured, a patient depends on other persons for help. Frequently, a close relative or a spouse takes the role of a caregiver. The disease is recognized for burdening caregivers. The pressures resulting from the disease can vary widely. These pressures comprise of psychological, social, economic, and physical elements of the life of caregiver. Alzheimer’s disease in among the most costly illnesses in developed nations.

Causes of Alzheimer`s disease

As mentioned above, the causes of Alzheimer`s disease are still not known. In about 1 to 5 percent of the cases, genetic differences have been perceived to cause the condition. Various competing theories and hypothesis presently attempt to explain various causes of Alzheimer`s disease. These hypotheses include cholinergic hypothesis, amyloid hypothesis, and Tau hypothesis among others (Fanshawe, Prevost, Roberts, Green, Armstron, & Marteau, 2008).

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Cholinergic is the oldest hypothesis that tries to explain the causes of Alzheimer`s disease. Most of the presently available drug therapies and medicine are based on cholinergic hypothesis. According to this hypothesis, Alzheimer’s disease is caused by reduced formation of neurotransmitter acetylcholine. However, this hypothesis has not garnered the widespread support. This is largely because the medications aimed at treating the deficiency of acetylcholine have not been extremely efficient. Other cholinergic impacts have also been suggested. One such impact is the initiation of large-scale aggregation of amyloid that results in generalized neuro-inflammation.

According to amyloid hypothesis, the deposits of beta-amyloid (βA) are the underlying cause of Alzheimer’s disease. The location of gene for the Amyloid precursor protein (APP) on chromosome 21 provides support to this postulate. In addition, the fact the individuals suffering from Down Syndrome, who have an additional gene copy, worldwide experience Alzheimer`s disease by the age of 40 also provides support for this hypothesis. According to Henderson, Benke, Green, Cupples & Farrer (2005), a certain isoform of apoliprotein, APOE4, is a crucial genetic risk factor for Alzheimer’s disease. While APOE4 improves the breakdown of beta amyloid, according to Puglielli, Tanzi, & Kovacs (2003), some APOE isoforms are not extremely efficient at this task. This results in the build-up of excess amyloid in the brain. Transgenic mice that express a mutant form of human amyloid precursor protein showed additional evidence of this hypothesis. These mice develop Alzheimer-like brain pathology with spatial learning deficiencies. In early human trials, a trial vaccine was found to clear the amyloid plaques, though it did not have any substantial impact on dementia. As such, researchers have been forced to deduce non-plaque beta-Amyloid oligomers that are the aggregates of various monomers as its main pathogenic form. According to Roberts, Cupples, Relkin, Whitehouse & Green (2005), these poisonous oligomers, which are also known as amyloid-derived diffusible ligands (ADDLs), change the arrangement of the synapse binding to the surface receptor. As a result, the ADDLs disrupt the neural communication. The prion protein is one of the receptors for beta-Amyloid and it has been associated with both the mad cow disease and Alzheimer`s disease. This possibly links the fundamental mechanism of these neurodegenerative illnesses with that of AD.

The amyloid hypothesis was updated in 2009. The updates suggested that a close relative of beta-amyloid protein, and not beta-amyloid itself, might be the main cause of Alzheimer`s disease. According to this hypothesis, mechanisms associated with amyloid that shortens neuronal connections in human brain during the early life stage might be activated by a process related to ageing in older age. This activation might result in neuronal weakening of the disease. A portion of the amyloid precursor protein, referred to as N-APP, adjoins the beta-amyloid and is chopped from APP by one of the similar enzymes. According to Tilley, Morgan & Kalsheker (1998), N-APP activates the self-destruct pathway, adjoining itself to neuronal receptors that are referred to as death receptor 6 (DR6). Wright, Kunz-Ebrecht & Iliffe (2005) highlight that DR6 is exceedingly expressed in the regions of human brain that are mostly affected by Alzheimer’s disease. Consequently, there is a possibility that DR6 or N-APP pathway might be hijacked in the ageing brain to cause damage. In this hypothesis, the beta-amyloid achieves a complementary role through depressing the synaptic function.

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According to tau hypothesis, the abnormalities of tau protein instigate the surge of Alzheimer’s disease. In this hypothesis, according to Yaffe, Lui & Grady (2000), hyperphosphorylated tau starts to bind to other threads of tau. They finally form neurofibrillary tangles within the nerve cell bodies. The microtubules break up during the formation of neurofibrillary tangles, and therefore collapsing the transport system of neurons. According to Yen (2003), this might result in various malfunctions in biochemical communications among neurons. These malfunctions later cause death of the cells.

Other hypotheses have also been postulated. For instance, Herpes simplex virus type 1 has been suggested to cause Alzheimer’s disease, especially in individuals carrying the vulnerable forms of APOE gene. Some hypotheses also claim that Alzheimer`s disease might be caused by the breakdown of myelin that is related to ageing of brain. The released iron during the breakdown of myelin causes further damage. This is because it interferes with the homeostatic myelin repair process that contributes significantly to the development of proteinaceous deposits like tau and beta-amyloid. According to Yip et al. (2005), dys homeostasis and oxidative stress of biometal metabolism might be crucial in causing Alzheimer’s disease.

Risk Factors for Alzheimer’s Disease

Studies have identified various risk factors related to dementia. It is not possible to eliminate each of the risk factors. According to Yaffe, Lui & Grady (2000), this is because human beings cannot avoid age, which is one of the most significant risk factors. Though it is possible to develop Alzheimer`s disease during early life, the possibility of doing so largely depends on age. One in 50 persons between the age of 65 and 70 has a form of dementia, compared to one in 5 persons over the age of 80. In this regard, this section discusses various risk factors that cause people to develop Alzheimer’s disease.

Cholesterol as a Risk Factor

The first risk factor is the consumption of cholesterol. As mentioned above, APOE is one of the primary apoliproteins in the plasma. APOE is also the principal carrier of cholesterol in the human brain. In human beings, there are three significant alleles of APOE gene. They include ε2, ε3, and ε4. According to Puglielli, Tanzi & Kovacs (2003), the isoforms of proteins produced by three alleles vary in the amino acids at positions 158 and 112: ε2 (Cys 112, Cys 158), ε4 (Arg 112, Arg 158), and ε3 (Cys 112, Arg 158). ε3 is the most common allele of the three. ε4 is present in at least one copy in about 25 percent of the population.

Various independent investigations have regularly affirmed that APOE ε4 allele is the most common risk factor for Alzheimer`s disease. According to Yen’s (2003) research, the risk for Alzheimer’s disease conferred by this allele increases in a dose-reliant way. People who are homozygous for ε4 alleles, approximately 2 percent of the population, are eight times more likely to suffer from Alzheimer`s disease than those who are homozygote for ε3 allele. Nevertheless, APOE ε4 is neither essential nor enough to cause Alzheimer’s disease. According to Wright, Kunz-Ebrecht & Iliffe (2005), this allele only increases the likelihood of developing Alzheimer’s disease.

The relationship between APOE and Alzheimer’s disease remains hugely undefined at the mechanistic level. Studies using the transgenic mouse model show that APOE significantly contributes to deposition of Aβ. In addition, the deposition of amyloid has been found to be strictly reliant on expression levels of APOE in a dose-reliant way. PDAPP mice that are hemizygous for APOE have been found to have about 60 percent decline in amyloid deposition, while no fibrillar or non-fibrillar Aβ has been found in the region of the brain of homozygous mice. According to ROOO, the absence of APOE affected the extracellular accumulation. However, it did not affect the formation of Aβ. The reintroduction of APOE human genes in the PDAPP mice restores the deposition of fibrillar Aβ. The deposition of Aβ linked to severe neuritic dystrophy is more evident with the APOE ε4 isoform.

Recent investigations have also indicated that the internalization of Aβ is not essentially followed by its degradation. Instead of degradation, Aβ tends to aggregate in the endocrytic compartment and can be secreted in a more toxic form in fibrillar Aβ. As a result, APOE might eventually contribute to the aggregation of Aβ by mediating its internalization process. Additionally, APOE ε4 has been shown to bind Aβ more effectively and encourage the formation of Aβ fibril than the APOE ε3 isoform. According to Alzheimer’s Association (2012), a possible scenario is that APOE could encourage Aβ aggregation in the endosomal compartment following the enzymatic digestion of lipid and receptor-mediated internalization. This renders APOE to be lipid-free and be able to interact with Aβ. This is supported by the facilitation of the formation of Aβ fibril as observed in Alzheimer disease mice that express the APOE ε4 isoform.

Besides directly enabling the aggregation and internalization of Aβ, APOE ε4 might also interfere with the cholesterol homeostasis of the brain by altering the formation of lipoprotein. In the plasma, APOE ε4 tends to associate with VLDL particles that contain more cholesterol. On the other hand, APOE ε3 associates with HDL. Homozygous individuals for APOE ε4 allele have high levels of cholesterol in their plasma, and high levels of 24S-hydroxycholeterol in their cerebrospinal fluid (CSF). According to Yaffe, Lui & Grady (2000), 24S-hydroxycholesterol is a catabolic derivative of cholesterol. This catabolic derivative represents the primary metabolic route for the clearance of cholesterol from human brain. The lipoproteins produced in human brain are extremely different, in terms of density, position, and other properties, from the particles present in the plasma. It is also perceivable that various forms of APOE alter the brain cholesterol homeostasis by preferentially associating with certain lipoprotein particles. Perhaps, this is because APOE shows differential preference for VLDL particles present in the plasma. The primary nature of APOE in brain lipoproteins would emphasize small differences in the affinity of lipoproteins for isoforms of APOE. As a result, the role of APOE in maintaining the homeostasis of cholesterol might significantly contribute to the elevated risk for Alzheimer`s disease linked to APOE ε4 (Alzheimer’s Association, 2012).

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Genetic Risk Factor for Alzheimer’s Disease

In various families, Alzheimer’s disease is inherited as an autosomal dominant illness. However, in many cases, inheritance of the disorder seems to be multi-factorial. A monozygotic investigation shows an inconsistent concordance of between 18 and 14 percent. This shows that the disease cannot be entirely explained by a single autosomal dominant gene. A comparative risk of about 3.5% has been shown for individuals with not less than one first-degree comparative suffering from dementia.

Three genes have been identified and linked to the occurrence of Alzheimer’s disease. The mutations of these genes cause early-onset Familial Alzheimer’s Disease (FAD). This disease is inherited in an autosomal dominant way. The genes are presenilin 1 (PS-1), amyloid precursor protein (APP) and PS-2 genes. Yen (2003) points out that the APP gene maps to chromosome 21q21.1. Mutations in the APP gene are said to be responsible for about 5 percent of cases of familial Alzheimer`s disease. According to Fanshawe, Prevost, Roberts, Green, Armstron & Marteau (2008), mutations in this gene result in early development of Alzheimer`s disease with onset age being between 43 and 62 years. Mutations in this gene might lead to altered metabolism of APP. This results in an increased production of the 42-amino-acid form or Aβ protein. This is the main form present in senile plaques and perceived to be more amyloidogenic than the shorter forms of Aβ.

PS-1, which is a second familial AD locus, was detected by the analysis of genetic linkage at chromosome 14q24. The mutations in this gene are perceived to cause about 80 percent of the inherited Alzheimer’s disease cases. The onset age of Alzheimer`s disease due to the mutations in this gene is as early as 29 years. Up to date, not less than 35 missense mutations have been detected in PS-1 gene in the affected families. The notion that most mutations in this gene are missense ones points out that Alzheimer pathology is an outcome of its abnormal functioning caused by mutation. Presently, the role of PS protein remains unknown though it is recognized to be a transmembrane protein. As such, PS protein might perform the role of a cell surface receptor, or act as ion channel or membrane structural protein. According to Tilley, Morgan & Kalsheker (1998), PS-1 gene product is essential during development. This is because PS-1 gene knockout mice show deformations of skeletal, impaired neurogenesis and neuronal cell death.

Cardiovascular Diseases as a Risk Factor

Risk factors linked to stroke and heart diseases, such as high blood pressure and high cholesterol, might increase the risk of an individual to develop Alzheimer’s disease. According to Bruce, Davis & Casey (2008), high blood pressure might damage blood vessels in human brain. As a result, it disrupts the regions that are essential in decision-making, verbal skills and memory. This significantly contributes to the advancement of the disease. According to Alzheimer’s Association (2012), high levels of cholesterol might prevent the ability of blood to remove protein from the brain. Some studies have also cited that concussion and traumatic brain injury increase the risks of developing Alzheimer’s disease.

Prevention of Alzheimer’s disease

Alzheimer is a complex disease that has no recognized cure or prevention. Some studies have instilled hope among many people that one day it will be possible to slow the advancement of the disease, delay the symptoms or prevent it from occurring. Despite the existence of preliminary evidence of some interventions like cardiovascular risk reduction and physical activity, nothing has been found to inhibit the dementia. This section discusses various ways of preventing or delaying the symptoms of Alzheimer`s disease.

Dietary habits can help in preventing Alzheimer’s disease. Various studies have suggested that food consumed by an individual raises or reduces the risk of developing the disease. Consuming such products as fruits, grains, vegetables and food that is low in fat and sugar can significantly reduce the risks of developing Alzheimer`s disease. This is because these products reduce the occurrences of chronic illnesses. However, there are some exciting reports that might one day show that Alzheimer`s disease can be prevented through proper dietary habits. Many of these reports have also been shown to be part of entire healthy lifestyles that are likely to safeguard against developing other illnesses as well. For instance, researchers found out that clinical participants, who conformed to the traditional Mediterranean diet, have relatively slower decrease in the mini-mental state examination (MMSE) cognitive decline. According to Alzheimer’s Association (2012), Mediterranean diet might be protective against various illnesses, such as macular degeneration that is related to age. In addition, Vitamin D3 has been found to have neuroprotective impacts, which might preserve the cognitive function of an individual. This vitamin is generated naturally from sunlight exposure to a person`s skin.
Some researchers have also shown that products such as strawberries, blueberries and cranberries can result in enhanced cognitive functions in aging animals and humans (Alzheimer’s Association, 2012). Curcumin, a spice present in turmeric, is used to improve the flavor of meat and curries in Indian cuisine. Researchers have been examining the impacts of curcumin on human brain. According to recent studies, curcumin might reduce the levels of beta-amyloid plaques linked to Alzheimer’s disease. Using vegetable oil instead of animal oil might also prevent Alzheimer’s disease. Virgin oils are not only healthy but might also prevent AD. Oleocanthal, which is a natural compound present in virgin oils, transforms the structure of ADDLs, which are toxic proteins. ADDLs increase the risks of developing AD.

Exercising can also reduce the risks of developing Alzheimer’s disease. Medical practitioners encourage people to have exercise plans in order to improve their health. Investigations on individuals with mild cognitive impairment (MCI) show that exercises enhance cognitive agility. Another independent study also indicated that the risk of developing Alzheimer’s disease is 35 to 40 percent lower in individuals who exercise regularly than in those who do not exercise. As much as it is not proven that exercises can inhibit AD or delay its progression, investigations on animals and preliminary human studies have attracted scientists` attention. As a way of preventing or delaying Alzheimer’s disease, exercises might be helpful in decreasing frailness, maintaining the strength of the muscles, and elevating mood.

Building brain reserves and social engagement might prevent or delay the symptoms of Alzheimer`s disease. According to Alzheimer’s Association (2012), building cognitive reserve is a long process, which starts at childhood as one expands his or her reading skills. Classical neurological theory points out that the human brain form a huge number of neurons or nerve cells. However, many of these cells also die. Those neurons that do not die survive by connecting with other neurons during the stage of rapid growth of the nervous system. This stage occurs during childhood or adolescence. Learning a musical instrument, progressive reading of challenging books, playing chess, engaging in mental activity and creating art assist in the formation of these neural connections, which can last a lifetime. This appears to be protective against cognitive decline.


Alzheimer`s disease occurs in four distinct stages (Bruce, Davis, & Casey, 2008). Each stage has its own symptoms. The stages are pre-dementia, early, moderate and advanced. During the pre-dementia stage, symptoms are mistakenly attributed to stress of ageing. Neuropsychological analysis might show cognitive problems for about 8 years before an individual fulfils the clinical requirement for diagnosis. The patient also has problems with executive functions of planning, attentiveness, abstract thinking, flexibility or impairments in semantic memory. During this stage, apathy can also be seen and remains the most persistent symptom throughout the course of the illness.

During the early progression of Alzheimer`s disease, a patient experiences problems with executive functions, language, execution of movements or apraxia, and perception or agnosia. According to Bruce, Davis & Casey (2008), Alzheimer`s disease does not equally affect the entire memory capacities. Episodic or older memories, learned facts or semantic memory, and implicit memory are affected to a lesser extent than new memories.

During moderate progression of the disease, speech difficulties are evident because of the incapability to remember vocabulary. This usually results in incorrect word substitutions. Writing and reading skills are also eventually lost during this stage. Memory difficulties intensify and an individual might fail to recognize his or her close relatives.

During the advanced stage, an individual is reliant on caregivers. Language is reduced to single words, which results in complete loss of speech. Other common symptoms during this stage include extreme apathy, aggressiveness, and exhaustion. Mobility and muscle mass deteriorate to an extent that they are bedridden.

Types of Treatment

There are five medications used to treat the cognitive problems of Alzheimer`s disease. Four of these treatments are acetylcholinesterase inhibitors that are rivastigmine, donepezil, galantamine and tacrine (Bruce, Davis, & Casey, 2008). The last treatment is memantine, which is used as an NMDA receptor antagonist. However, none of these drugs has an indication for halting or delaying the advancement of the disorder.

Prevalence of Alzheimer

Approximately 5.4 million Americans of all ages suffered from Alzheimer`s disease in 2012. This figure comprises of 5.2 million people age 65 years and older. It is evident that 200 thousand individuals aged less than 65 years had early-onset Alzheimer`s disease (Alzheimer’s Association, 2012).

The number of women suffering from Alzheimer`s disease and other dementias is more than that of men. Approximately two thirds of the Alzheimer population consist of women (Alzheimer’s Association, 2012). This reflects about 3.4 million women suffering from Alzheimer`s disease. Men comprise of about 1.8 million of the entire Alzheimer population (Alzheimer’s Association, 2012).

Alzheimer`s disease is emerging as a more common cause of death in the US and other nations. Deaths due to other illnesses have continued declining, whereas deaths due to Alzheimer`s disease seem to be rising (Alzheimer’s Association, 2012). Deaths caused by Alzheimer`s disease increased by 66 percent from 2000 to 2008. Deaths caused by other diseases decreased by about 13 percent. The figure below compares deaths caused by Alzheimer`s disease and other diseases (Alzheimer’s Association, 2012).


Alzheimer’s disease is one of the most common dementia forms. The disease has no cure as it progresses eventually leading to death. The cause and advancement of the disease are not well understood. According to studies, the disease is related to tangles and plaques in the brain. Present treatments only assist in averting the symptoms. Alzheimer`s disease occurs in four distinct stages. Each stage has its own symptoms. The stages are pre-dementia, early, moderate and advanced. One in every 50 persons between the ages of 65 and 70 years has a form of dementia, compared to one in 5 persons over the age of 80.

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