Alzheimer’s Disease (AD) is a degenerative brain disease that causes a significant amount of damage to neurons and eventually other parts of the brain. As the disease progresses the individual afflicted will lose the ability to perform basic functions such as walking and swallowing. The final stages of Alzheimer’s leave the individual bed-ridden and in need of constant care until death occurs (Alzheimer’s Association, 2016).
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AD has been recognized as the most common cause of dementia, which is the loss of cognitive functions such as reasoning and remembering and the loss of behavioral functions that affects daily life. Alzheimer’s is also the sixth leading cause of death in the United States. Recent findings have indicated that it may rank third as cause of death for the elderly, right behind heart disease and cancer (NIA, 2016).
There are two main types of Alzheimer’s Disease that are mentioned frequently. The first being Early-Onset Alzheimer’s Disease (EOAD). EOAD is seen in those under the age of 65 and only accounts for around 1-5% of all cases of Alzheimer’s. The second type is Late-Onset Alzheimer’s Disease (LOAD) and it is seen in those who are 65 years of age or older and accounts for more than 95% of all cases of Alzheimer’s (Reitz & Mayeux, 2014; Uddin et al., 2018). While there is much research done now over this destructive disease, when it was first discovered it was promptly brushed aside.
In 1901, Alois Alzheimer began observations on 50-year-old Auguste Deter. Deter was admitted into the Frankfurt Psychiatric Hospital when her husband noticed that her behavior had become erratic and unpredictable. During Alzheimer’s observations he noted that as time passed Deter became more disoriented and had a significant loss in memory and an increase in deliriums (Hippius & Neundörfer, 2003). In the spring of 1906 Deter passed away. Alzheimer proceeded to conduct a post mortem, particularly of the brain. He found that the brain was evenly atrophied, and the large vascular tissues showed signs of arteriosclerosis (Alzheimer, Stelzmann, Schnitzlein, & Murtagh, 1907).
Many specimens were prepared using the Bielschowsky’s silver method, which allows for the detection of axons, neurofibrils, and senile plaques. Alzheimer observed that the neurofibrils had changed significantly in size and shape, thickening and becoming bundled together. He also found that even when the cell disintegrated, the fibrils remained which he supposed was a result of a chemical change that had also allowed the fibrils to accept dyes whereas normal fibrils did not. These changes were seen in around a quarter to a third of all the neurons in the cortex, though many neurons had disappeared in the upper layers. There was an abundance of miliary foci found in the upper layers of the cortex that were caused by deposition of what Alzheimer referred to as a “special substance”. Alzheimer also noted that glial cells developed many fibers, along with adipose saccules (Alzheimer, Stelzmann, Schnitzlein, & Murtagh, 1907).
In the fall of 1906 Alzheimer presented his findings upon the urging of his colleague Dr. Emil Kraeplin. Unfortunately, his findings were brushed aside and Mrs. Deter was diagnosed with a case of “pre-senile dementia”. Though this did not deter Alzheimer from continuing with similar research, finding similar cases to publish in the following years. Dr. Kraeplin saw value in Alzheimer’s findings and wanted the case to be noticed. Thus in 1910 Kraeplin published Mrs. Deter’s case in a volume of his psychiatry textbook, which was at the time highly respected. He also named this “pre-senile dementia” after Alois Alzheimer, dubbing it Alzheimer’s disease (Hippius & Neundörfer, 2003; Ellison, 2018).
In the 1960’s two psychiatrists, Tomlinson and Roth, conducted research that found that the senile plaques, what Alzheimer referred to as miliary foci, were very important in the elderly because they are seen at differing rates in nearly all elderly. As 1970 came around Roth began to question the need for the age criteria to separate the pre-senile and senile dementia of the Alzheimer’s type. Robert Katzman supposed that the age criteria that separated this pre-senile and senile dementia of the Alzheimer’s type should be thrown away altogether in 1976. Starting from the 1980’s to present day, Alzheimer’s has been recognized as a cause of dementia instead of a dementia itself and was deemed the most common cause of dementia (Ellison, 2018). Because of this new view of Alzheimer’s researchers began to delve into what caused Alzheimer’s Disease and how it developed.
Currently there are no definitive causes of Alzheimer’s Disease, though there are many causal factors. Even with the presence of these factors the individual does not always develop Alzheimer’s. There are also individuals that do not possess the causal factors and go on to develop AD (Alzheimer’s Association, 2016; O Lane, Dacks, Shineman, & Fillit, 2013). However, these factors still give researchers insight into how this disease occurs for most individual. The choligenergic hypothesis is the thought process that AD symptoms can be caused by a deficit of acetylcholine, which is needed for memory function (Ellison, 2018). This prompted the production of cholinesterase inhibitors to increase levels of acetylcholine in the brain or to prevent it from being destroyed (Voisin et al., 2004; Ellison, 2018). The amyloid cascade hypothesis has to do with the accumulation of beta-amyloid protein in the brain due to the inability to clear the blood brain barrier. This accumulation causes senile plaques, or what we now call amyloid plaques and is thought to inhibit communication between neurons and contributes to the death of cells (Alzheimer’s Association, 2016; Ellison, 2018).
Tau protein tangles, or neurofibrillary tangles, are caused when there are abnormalities of the tau protein. These tangles block the transfer of nutrients inside of neurons and may lead to cell death (Reitz & Mayeux, 2014; Alzheimer’s Association, 2016). A healthy tau protein forms microtubules that allow for transport of nutrients to and from different parts of the neuron. However, an abnormal tau protein causes these microtubules to collapse, inhibiting the transport of nutrients (Ellison, 2018).
The APOE gene is responsible for producing the apolipoprotein E or ApoE protein. This protein combines with fats to form lipoproteins that carry cholesterol and other fats across the blood brain barrier and through the bloodstream. The APOE gene has three major alleles, APOE 2, APOE 3, and APOE 4. The usual pathway of an APOE protein is to become lipidated with fats or cholesterol and bind to beta-amyloid proteins and cross over the blood brain barrier via a low-density lipoprotein receptor-related protein 1 (LRP1). However, the APOE 4 isn’t as functionally efficient as APOE 2 or APOE 3 and is unable to cross the blood brain barrier via LRP1 as fast, thus internalizing a significant amount of beta-amyloid protein, leading to amyloid plaques (Dong, Gim, Yeo, & Kim, 2017). Dubois et al. (2018) conducted a study on the relation of amyloid deposition to complaints of cognitive dissonance. They found that there were more participants who were APOE 4 allele carriers and positive for amyloid deposits than those that were APOE 4 allele carriers and negative for amyloid deposits (Dubois et al., 2018). These are the four main causal factors of AD that have been agreed upon by the majority of researchers today. Many of them lead to the loss of neurons which causes the most well known symptom of Alzheimer’s, memory loss. While memory loss is detrimental to the individual and their families there are also many other severe symptoms that change the individuals way of living.
AD can be developing in individuals several years before symptoms are shown. There is an approximate seven to ten-year lifespan of the disease that individuals experience once symptoms to occur. For the first five years mild symptoms are seen during the early stages of the disease. These can include short-term memory loss, confusion of space and time, speech complications, behavioral changes such as aggression or withdrawal from social life. There can also be a decrease in problem solving abilities and a significant increase in sleep disturbances. As the disease progresses and enters years six through ten the symptoms become much more severe, impairing function in daily life completely. Individuals begin to need aid with activities such as grooming, dressing, and eating. This is also where we see long-term memory loss occurring. Towards the very end of the disease course we start to see all cognitive and function dwindle down even further. An inability to swallow or control the bladder is seen, individuals become non-ambulatory and mute, in need of constant care and supervision until these complications result in death of the individual (Holtzman, Morris, & Goate, 2011; Alzheimer’s Association, 2016).
Many risk factors have been identified that may result in an individual being more susceptible to developing Alzheimer’s Disease. AD is an age-related disease, meaning as your age increase your risk for developing AD increases. Family history plays a large part in risk because of the many genetics that can be passed down during reproduction such as Down syndrome and the APOE 4 allele (Liebing, 2014). Down syndrome has been seen to increase risk of developing a dementia that is caused by Alzheimer’s Disease or a similar dementia. This may be due to the partial or double copy of chromosome 21 which is known to code for a gene that produces Amyloid Precursor Protein (APP). APP is cut into beta-amyloid fragments in those with Alzheimer’s, and in turn accumulate producing amyloid plaques Those with Mild Cognitive Impairment (MCI) experience an increased risk of Alzheimer’s, especially those with MCI that involves memory impediment. (Alzheimer’s Association, 2016; Ellison, 2018).
Another surprising risk factor is education. There are three main schools of thought for this. One being that cognitive reserve may be depleted over time, susceptibility increasing as well. This cognitive reserve could be measured based on educational attainment, therefore those who achieve higher education may have a larger cognitive reserve. Some believe that if an individual does not continue mental activity through adulthood, synaptic density could decrease, making it easier for remaining synapses to be blocked by buildup, resulting in symptoms of Alzheimer’s. This thought goes along with other risk factors such as depression and social isolation. There are also those who claim that individuals who attain a higher education, gain skills to pass a neuropsychological test. These individuals could be developing AD but would be able to skew the results of these tests so that it would seem as though they were functioning normally. Gatz et al. (2001) conducted a study using twins to assess whether education attainment decreased risk of developing Alzheimer’s. The study showed that there was a slight increase in risk of Alzheimer’s in those that did not go on to achieve a higher education (Gatz et al., 2001). There has been a trend seen in Alzheimer’s patients where patients often have a cerebrovascular disease as well as vascular risk factors. These vascular risk factors are thought to emerge due to the build-up of amyloid in the brain, though a study done by Eldholm et al. (2018) suggests that if these risk factors are left untreated, they could progress cognitive decline at a faster rate (Eldholm et al., 2018). Individuals who are diagnosed with AD are rising dramatically and are projected to continue to rise in the near future.
The estimated number of individuals that are currently diagnosed with Alzheimer’s is around 5 million in the United States. This number is expected to double or triple in size by the year 2050 resulting in an estimated 14 to 15 million individuals to be diagnosed with AD (Hebert, Weuve, Scherr, & Evans, 2013). Globally the prevalence of AD estimated to be as high as 24 million. If no changes in preventative care of mortality rate occur, this number will double every twenty years, resulting in the diagnosis of approximately 90 million individuals. These estimates are due to the increase of longevity in the elderly as well as the increase in overall population of the elderly. (Ferri et al., 2005). Currently there are only a handful of medical treatments that are offered to the public.
Acetylcholinesterase inhibitors are the most well-known medicinal treatment for Alzheimer’s Disease. There are currently three on the market: Donepezil, Rivastigmine, and Galantamine. These drugs prevent the breakdown of acetylcholine, which is needed for functionality of memory and learning processes. This increase of acetylcholine allows for proper communication between neurons (Voisin, Reynish, Portet, Feldman, &Vellas, 2004). Memantine is a N-methyl-D-aspartate (NMDA) receptor antagonist (McKeage, 2009). The NMDA receptor is activated when bonded with the excitatory neurotransmitter glutamate. If glutamate excessively activates excitatory receptors such as the NMDA receptor, it can cause the death of CNS neurons (Newcomer, Farber & Olney, 2000). This occurs because of an overproduction of glutamate. Memantine aids in decreasing the amount of activation by bonding with a portion of NMDA receptors (McKeage, 2009). Animal therapy has been shown to bring relief and joy to patients with Alzheimer’s Disease. Patients have been reported to become much more vocal and proactive in their choices when there is interaction with the animal (Swall, Ebbeskog, Lundh Hagelin, & Fagerberg, 2017). Animal therapy has also been used to encourage Alzheimer’s patients to increase their food intake to increase their weight. A study done by Edwards & Beck (2002) resulted in a significant increase in food intake and weight gain in AD patients when a fish tank was set up in the dining area. (Edwards & Beck, 2002). With the expected dramatic increase of individuals with AD there is a need for more effective treatments.
There has been a call to start focusing on preclinical Alzheimer’s in order to synthesize treatments that can intervene before a significant amount of damage can occur. Work has been started on plotting out the occurrence of Alzheimer’s before symptoms are shown and forecasts are being made on how prevention methods could reduce the detriment of Alzheimer’s (Brookmeyer, Abdalla, Kawas, & Corrada, 2018). With preclinical Alzheimer’s studies becoming more prevalent there will also be a need to further assess biomarkers that help us to key in on the progress of Alzheimer’s in individuals who are not presenting symptoms yet. This will help to develop medications that can intervene on the progression of the disease (Iturria-Medina et al., 2016).
Souvenaid is a nutrition supplement originating in the Netherlands. The supplement contains phospholipids, choline, folic acid, selenium, vitamins B6, B12, C, and E, and many other nutrients that are said to improve on the deficiencies that could be limiting the formation of synaptic connections in Alzheimer’s patients (Ritchie et al., 2014). Genistein is another supplement that can be found in soybean products and other legumes in the forms of glucoside genistin when digested. Genistein has been found to possibly reduce the formation of beta-amyloid, which could reduce the formation of amyloid plaques in Alzheimer’s patients (Devi, Shanmuganathan, Manayi, & Nabavi, 2016).
Because LRP1 is responsible for transfer of beta-amyloid across the blood brain barrier, many are trying to figure out a way to achieve a boost of expression or a maintenance of function of the LRP1 receptor. There have also been propositions of using the LRP1 receptor to deliver drugs to the central nervous system more effectively (Storck & Pietrzik, 2017).
Neuroinflammation presented in Alzheimer’s patients is thought to occur because of the accumulation of beta-amyloid, causing innate immune cells to activate and become sustained in activation. This leads to a constant inflammation in the brain. If we were to better intervene on this process, it could reduce the amount of degeneration (Bronzuoli, Iacomino, Steardo, & Scuderi, 2016; Ardura-Fabregat et al., 2017). Degradation caused by AD could be better solved if a large focus on the preclinical stages of the disease occurred.
Alzheimer’s Disease has come a long way since its first discovery in 1906. From being misrepresented as another form of dementia to becoming a dementia causing disease. Symptoms, risk factors, and causal factors have been identified and while we still know very little about what causes Alzheimer’s Disease there have been many advancements made in the past 40 years that have helped to aid individuals suffering. There is still much more to learn and much more research to be done. Specifically, there should be a focus of the preclinical side of AD. This could bring about new treatments options that may slow the progression of the disease by many years or halt it from occurring overall in the exponential amount of individuals expected to develop this disease.
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