Alzheimer’s Disease Research Final Project

Hello everyone!

For my final project I researched Alzheimer’s disease, which is the most common form of dementia and has always been a topic of interest to me. Despite this commonality, there is still no cure for this disease. I was interested to find out more about how the disease manifests itself, to discover the common symptoms of the disease and become familiar with the abnormalities that cause this severe memory loss. I hope you enjoy what I’ve put together!

1. Introduction to Alzheimer’s Disease


Alzheimer’s Disease is a neurodegenerative disease and the most common form of dementia. There is no cure for this disease, despite its discovery in 1906, but extensive research has led to many advanced in Alzheimer’s treatment and care (Alzheimer’s Association, 2014). Alzheimer’s disease progresses with time and eventually strips patients of cognitive functions. This disorder is so prominent that it “accounts for 60% to 70 % of cases of progressive cognitive impairment in elderly patients and the total prevalence of AD in the US is estimated at 2.3 million patients”(Cummings, 2002). These statistics reveal the need to continue researching this disease and work towards developing a cure.

The most difficult aspect in dealing with AD is that dementia is rarely recognized in their early stages. According to the American Academy of Neurology, mini-mental state examination is useful in detecting dementia in its early forms and should be used at check ups in populations with an increased risk of developing this disease (Folstein, 1975). Several associations have also been working to raise awareness regarding the disease in order to inform patients and their families of suspicious symptoms. “Abnormalities in learning new information, difficulty handling complex tasks, impaired reasoning ability, and changes in language or behavioral alterations” are all signs that a patient may be suffering from Alzheimer’s (Cummings, 2002). AD’s most common symptom is an “amnesic type of memory defect”. Patients suffering from this disease eventually lose the ability to recognize their own family members, or lose the ability to perform daily tasks (Cummings, 2002). AD continues to be the most researched neurodegenerative disease and the most puzzling to researchers, which are yet to determine a cure.

Through this web series, we will be finding out more about the clinical characteristics of this disease. We will discover more about the abnormalities in the brain that lead to the development of Alzheimer’s disease by looking at its molecular genetics and pathogenesis. Finally, we will also be learning about known treatments for AD and why these treatments have proved effective.

2. Clinical Characteristics of Alzheimer’s Disease



There are still no definitive laboratory tests designed in order to diagnose Alzheimer’s disease, however certain characteristics are definitely linked to the disease, which aid in determining whether a patient is suffering from AD (Harciarek and Krzysztof, 2005). The typical characteristics of AD are the loss of memory, difficulty in attaining new information or recalling vocabulary, progressive language disorder “beginning with anomia and progressing to aphasia, and disturbances of visuospatial skills” (Cummings, 2002). Alzheimer’s patients have difficulty remembering both current events and past memories due to their inability to encode and store memory. The loss of verbal information is definitely one of the defining aspects of the disease, which progressively worsens and eventually leads to the patient’s inability to communicate (Harciarek and Krzysztof, 2005).

The most commonly used tool for determining problems with verbal deficits is the Auditory-Verbal Learning Test, which is used to detect early occurrences of memory defects and speech impairments. Delayed recall of word lists or persistent evidence of short-term memory loss are all indications that the person may be exhibiting early signs of AD (Harciarek and Krzysztof, 2005). However, there is evidence to suggest that patients with AD will have perfect recollection of old memories, which often cause family members to believe that the patient could not be suffering from a memory problem.

Patients with Alzheimer’s disease are also known to suffer from personality disorder and sudden shifts in emotions. There are a variety of behavioral symptoms that can be seen even in the early stages. These include neuroticism, which essentially means that the patient suffers from intense stress, and sudden mood swings (Gilbert and Herbst, 2014).

Neuropsychiatric symptoms are also very common in Alzheimer’s disease. Patients tend to exhibit diminished interest for past hobbies or people, and reduced concern for previously important aspects of their lives (Cummings, 2002). AD patients also become increasingly agitated in situations with high stress and often display depressive symptoms. In fact, about 50% of AD patients also experience depressive symptoms, and as many as 25% also experience delusions (Cummings, 2002).

Finally, motor system abnormalities are common symptoms of the disease. These symptoms are absent in the early years of AD, so they cannot be used in order to diagnose the disorder. However, in the final years of the disorder, patients suffer from focal abnormalities, gait changes or even seizures. Motor system abnormalities are so severe that most patients die 7 to 10 years after the symptoms begin to manifest (Cummings, 2002).

All of these symptoms are caused by abnormalities in the brain. We will continue by investigating the molecular genetics of Alzheimer’s disease in order to determine the reasons for this disease.

3. Molecular Genetics and Pathogenesis of Alzheimer’s Disease


A pathological diagnosis of Alzheimer’s disease requires the presence of neuritic plaques and neurofibrillary tangles that are abnormal in a healthy individual. Neuritic plaques (or senile plaques) are extracellular deposits of beta amyloid in the gray matter of the brain, which are often associated with degenerative neural structures (Cummings, 2002). Neurofibrillary tangles contain helical filaments of abnormal tau protein that extend into the dendrites. It is the primary marker in Alzheimer’s disease (Cummings, 2002).



Mutations in the brain are also causes of Alzheimer’s disease, and they are valuable in studying the disorder. Mutations in the amyloid precursor protein (APP gene) and the presenilin 2 gene are responsible for the development of the disease. The amyloid protein is deposited in the neuritic plaques. The accumulation of amyloid initiates events contributing to cell death, tangle formation and inflammation (Cummings, 2002). These contribute to the degeneration of the neuronal axon and the loss of synapses, which in turn contribute to neurotransmitter deficits. These are all the main causes of Alzheimer’s disease, and researchers look for these irregularities in order to diagnose the disease.

Researchers such as Gregory and Hodges discovered that the progressive amnestic disorder in Alzheimer’s disease happens because of the breakdown of attentional, perceptual, and visuospatial abilities. “This is due to the breakdown in the structure of semantic memory. These statements are supported by several experiments testing the absence of general knowledge and deficiencies in sensory input and output (Gilbert and Herbst, 2014).

4. Known Treatments for Alzheimer’s Disease



Although there is no cure for Alzheimer’s disease, there have been many treatments that have proven to be effective either in preventing AD or changing the course of the disease when caught in its early stages. These treatments are administered only with the consent of the patient and their family, and mut reflect their values and needs. There are many therapeutic strategies available, as well as disease-modifying treatments.

One of these treatments is known as cholinesterase inhibitors, “which are the only approved medications approved by the US Food and Drug Administration as treatment for AD” (Cummings, 2002). This treatment is considered standard therapy for patients. There are four inhibitors available: tacrine, donepezil, rivastigmine and galantamine. These inhibitors have been proven to produce improvements in cognition, reduction in behavioral disturbances, and stabilization of daily activities (Cummings, 2002). However, although this treatment is widely used and appreciated, some patients do not respond to it. This is because Alzheimer’s disease is known to differ greatly in every individual.

Another treatment is the reduction of amyloid production, which as we learned in the previous section is one of the main reasons for the development of Alzheimer’s disease. Excess production of amyloid leads to the degeneration of the neuronal axon, so reducing amyloid production or removing it “addresses the basic pathophysiology of AD” (Cummings, 2002).

There are other treatments such as hormonal and psychotropic. Hormonal treatments help with the prevention of Alzheimer’s disease, while psychotropic treatments help with the management of behavioral disturbances. Treatments using selective serotonin are used to manage the depressive symptoms of AD (Cummings, 2002). Again, not all patients respond to these treatments, but they have been effective.

The effectiveness of these treatments is determined through placebo-controlled trials in order to determine whether the medication has positive effects in the patients. The most important aspect of curing Alzheimer’s disease is getting tested sporadically in order to be able to detect the disorder at an early age. Dramatic progress has been made in developing treatments for this disease, however none of the therapies are even close to 100% effective. In addition, the advances have had no impact on the prevalence of AD thus far, which continues to be a major global issue (Cummings, 2002). Researchers worldwide are continuously researching Alzheimer’s disease and trying to determine a clinical or therapeutic cure for it.


“Alzheimer’s & Brain Research Milestones | Research Center | Alzheimer’s Association.” Alzheimer’s Association. N.p., n.d. Web. 28 July 2014.

Cummings, J. L.. “Alzheimer Disease.” JAMA: The Journal of the American Medical Association 287.18 (2002): 2335-2338. Print.

Cummings, Jeffrey L.. “Alzheimer Disease.” The Journal of the American Medical Association. N.p., 8 May 2002. Web. 28 July 2014. <>.

Dash, Paul, and Nicole Pittman. Alzheimer’s disease. New York, N.Y.: Demos, 2005. Print.

Folstein MF, Folstein SE, McHugh PR. Mini-mental state.  J Psychiatr Res.1975;12:189-198.

Gilbert, T., and M. Herbst. “Alzheimer’s disease: charting the crossroads between neurology and psychology.” Journal of Neurology, Neurosurgery & Psychiatry 85.2 (2014): 133-134. Print.

Harciarek, Michal, and Krzysztof Jodzio. “Neuropsychological Differences Between Frontotemporal Dementia and Alzheimer’s Disease: A Review.” Neuropsychology Review 15.3 (2005): 131-145. Print.



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