Alzheimer's Disease

Alzheimer’s Disease and Stroke

main article: Alzheimer’s Disease and Stroke
author: Roslyn Cheung

Alzheimer's Disease and Stroke
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Image source: Ians. (2012). Tiny stroke could bring on
Alzheimer’s [Photograph]. Retrieved March 28, 2013, from

Dementia, stroke, or both is diagnosed in 1 out of every 3 people[1]. Given this statistic and the fact that Alzheimer's disease (AD) and stroke regularly co-occur[2], it is evident that AD needs to be studied in conjunction with stroke. Past research has found that the risk of dementia is increased after the occurrence of stroke[2]. A number of different mechanisms, such as axonal changes, have been studied to identify their role in the development of AD after the experience of a stroke[3]. Although the association between AD and stroke has been studied in the past, limited research is available regarding the topic of AD as a risk factor for stroke[2]. Nevertheless, some studies, such as cohort studies and studies on animal models, are available to gain knowledge of the occurrence and effects of stroke in AD patients. In addition, AD and stroke have many common risk factors, such as hypertension; therefore, treating these risk factors will be efficient in the prevention of both AD and stroke[1]. Furthermore, endogenous neuroprotectants have been studied for their use in the prevention of stroke and neurodegenerative disorders, such as AD[4].

1. Hachinski, V. Stroke and Alzheimer disease: fellow travelers or partners in crime? Arch Neurol 68, 797-798 (2011).
2. Tolppanen, A. et al. Incidence of stroke in people with Alzheimer disease: a national register-based approach. Neurology 80, 353-358 (2013).
3. Zhang, Q. et al. Transient focal cerebral ischemia/reperfusion induces early and chronic axonal changes in rats: its importance for the risk of Alzheimer’s disease. PLoS ONE 7, e33722 (2012).
4. Yu, Z., Liu, N., Liu, J., Yang, K. & Wang, X. Neuroglobin, a novel target for endogenous neuroprotection against stroke and neurodegenerative disorders. Int J Mol Sci 13, 6995-7014 (2012).

Alzheimer's Disease Models

main article: Alzheimer's Disease Models
author: Luisa Garzon

Figure 1. (a) Fertilized eggs are taken from a donor mouse. (b) DNA that contains genes linked to AD is injected into the nucleus of the fertilized eggs. (c) The eggs are inserted into a surrogate mothers, where they will mature to form pups. (d) Of the pups that are born, only about 10–20% contain the transgene. Adapted from Ashe 2009
Alzheimer's disease (AD) is the most common cause of dementia; it currently affects 1 in 8 older individuals in North America [1]. Ever since it was described around the 1900s by Alois_Alzheimer and Emil_Kraepelin, significant efforts have been made in order to cure this disease or to at least be able to treat it. Such efforts include the development of animal and cellular models, which have been attained by using diverse genetic modifications in order to mimic the spectrum of symptoms and with the purpose of gaining some insights on the disease. It is because of the use of these models that scientists have been able define critical disease-related mechanisms, and evaluate new treatments.

Transgenic mouse models of AD have been created to express the major pathological hallmarks of the disease, more specifically the amyloid_plaques [2], the neurofibrillary_tangles [3] and the substantial neurodegeneration [4] observed in patients. However, our understanding of Alzheimer’s disease pathogenesis is currently limited by difficulties in obtaining live neurons from patients and the inability to model the sporadic form of the disease. It may be possible to overcome these challenges by reprogramming cells from AD patients.

1. Alzheimer’s Association. (2012). Alzheimer’s disease facts and figures. Chicago, IL: US. National Office. Accessed: March 25th, 2013 at 8:00 p.m.
2. Fraser P.E., Lévesque L., & McLachlan D.R. (1993). Biochemistry of Alzheimer's disease amyloid plaques. Clinical Biochemistry 26(5), 339 – 349.
3. Grundke-Iqbal I., Iqbal K., Tung Y.C., Quinlan M., Wisniewski H.M., & Binder L.I. (1986). Abnormal phosphorylation of the microtubule-associated protein tau (tau) in alzheimer cytoskeletal pathology. PNAS 83(13), 4913 – 4917
4. Crouch P.J., Harding S.M.E., White A.R., Camakaris J., Bush A.I., & Masters C.L. (2008). Mechanisms of Aβ mediated neurodegeneration in Alzheimer's disease International Journal of Biochemistry and Cell Biology 40(2), 181 – 198.

Effects of Lifestyle on the Prevalence of Alzheimer's Disease

main article: Effects of Lifestyle on the Prevalence of Alzheimer's Disease
author: Charlotte Redfern

Alzheimer's Disease
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Retrieved from:

Alzheimer's disease (AD) is a form of dementia that currently affects millions of people in North America alone[1]. Its increasing prevalence, lack of cure, and course of progress makes AD an important area of research. In AD, massive loss of neurons affects several regions of the brain, including the hippocampus and prefrontal cortex. This neurodegeneration is due to the buildup of tau protein tangles and β-amyloid plaques that disrupts neuron communication, resulting in symptoms that involve memory loss and cognitive decline. Alzheimer’s is a chronic disease that develops over a long period of time. The majority of cases are not simply due to genetics but are sporadic and can be influenced by several risk factors including some environmental factors and lifestyle choices. An individual’s diet choices, their use of cannabis, their cognitive reserve, and their life events have all been found to play a role in either prolonging or advancing the onset of Alzheimer’s disease. With no known cure these risk factors have become important in early intervention for delaying the pathogenesis of Alzheimer’s[2].

1. Alzheimer’s association (2013). Retreived from:
2. Humpel C. (2011). Chronic mild cerebrovascular dysfunction as a cause for Alzheimer's disease?. Experimental gerontology 46(4): 225–232.

Genetics of Alzheimer's Disease

main article: Genetics of Alzheimer's Disease
author: Farah Al-Dajani

Genetics involve looking at the DNA
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Taken from

As with many neurodegenerative diseases, Alzheimer’s Disease (AD) can be associated with genetics. It is therefore important to study the role that genetics play in this disease with respect to its onset and progress, in order to better understand it and develop treatments. For instance, a specific allele (ApoE ε4) is known to increase one’s risk of getting AD in a dosage dependent manner. Namely, a person who has two copies of this allele has a much higher risk than one who has one copy of it; and a person who has no copy of these allele would have a lower risk than the aforementioned two [1]. Awareness of the presence of those alleles in one’s genome may influence the person to try to minimize their risk of acquiring AD or prolong their age of onset via other mechanisms, such as diet and lifestyle. Furthermore, other genes have also been found to contribute to AD onset albeit in a different way. Those genes follow Mendelian Genetics, and mutations in them account for a minority of the cases [1]. Yet, it is still important to study them, as they are linked to an earlier onset and more aggressive progression of the disease [1]. Studies looking at genes involved have furthered our knowledge in relation to Alzheimer’s Disease, ultimately aiding in the development of treatment strategies.

1. Reitz C, Brayne C, Mayeux R. Epidemiology of Alzheimer disease. Nature Reviews Neurology 3, 137-152, (2011)

Immunology of Alzheimer's Disease

main article: Immunology of Alzheimer's Disease
author: Karan-46

Microglial Cells
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Figure 1. Microglial cells interact with neurons within the CNS

Alzheimer’s disease (AD) is a common form of dementia mostly found within patients over the age of sixty-five. During Alzheimer’s, there is an accumulation of amyloid-beta plaques and intracellular neurofibrillary tangles within various brain regions. This results in cytotoxicity induced by the amyloid plaques. On the other hand, due to the aggregation of plaques and tangles, there is an activation of microglia cells, specifically by the misfolding of the truncated tau proteins[Bibliography item 2 not found.]. Microglia cells release specific chemicals to escape through the blood brain barrier and are essential for getting rid of any toxic or pathogenic invaders which are found within the brain. However, it is still controversial if the activation of microglia cells is causing negative effects within the brain. Within neuroimmunological research, evidence has been accumulated to support both, the advantages and disadvantages of microglia activation[Bibliography item 9 not found.]. Specifically, one of the major receptors responsible for the recruitment of microglia is CCR-2 (CC-chemokine receptor 2)[Bibliography item 18 not found.]. CCR-2 recruits microglia within the brain to prevent inflammation and can be looked at as a particular target for the treatment of Alzheimer’s disease.[Bibliography item 18 not found.]

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miRNA in Alzheimer's Disease

main article: miRNA in Alzheimer's Disease
author: Omar Oubari
Alzheimer’s Disease (AD) is a neurodegenerative disease that is projected to affect more than 1.3 million people in Canada in the near future [1]. It is characterized by increased inflammation, oxidative stress and a loss of neurons in several brain regions including the hippocampus and the prefrontal cortex gradually leading to memory loss and cognitive impairment. Some of the main changes in the proteome leading to Alzheimer’s Disease include hyperphosphorylation of the microtubule-associated tau proteins and overexpression of β-amyloid plaques due to a dysregulation in the splicing of its precursor protein, the amyloid precursor protein (APP) [2]. AD detection is currently limited to imaging techniques such as fMRI or PET scans [3] during the late stages of the disease so preventive measures are then difficult to implement and no treatments are available. miRNAs, small non-coding RNAs that regulate gene expression have recently been implicated in Alzheimer’s Disease in that their dysregulation leads to the proteomic changes that result in AD. They play a role in the disease onset and their abundance in body fluids such as the blood and the cerebrospinal fluid (CSF) make them potential biomarkers for early detection of the disease using everyday laboratory techniques such as northern blot and RT-PCR [4]. miRNAs act through the RNA interference pathway which can be used to silence gene expression. This technique can be used as a potential treatment for AD by targeting the aberrantly expressed proteins to alleviate some symptoms of the disease during its early phases [5].

1. Alzheimer’s Society Toronto (2010). Statistics. Retrieved from:
2. Tan, L. et al., Non-coding RNAs in Alzheimer’s disease. Molecular Neurobiology 47:382-393 (2013)
3. Risacher, S., Saykin, A., Neuroimaging and Other Biomarkers for Alzheimer’s Disease: The Changing Landscape of Early Detection. Annu. Rev. Clin. Psychol 9:18.1-18.28 (2012)
4. Ciesla, M. et al., MicroRNAs as biomarkers of disease onset. Anal Bioanal Chem 401:2051-2061 (2011)
5. Lee, ST. et al., miR-206 Regulates Brain-Derived Neurotrophic Factors in Alzheimer’s Disease Model. Ann Neurol 72:269-277 (2012)

Sex and Gender in Alzeheimer's Disease

main article: Sex and Gender in Alzeheimer's Disease
author: June Jee Yoon Bang

Male vs. Female
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Alzheimer's Disease (AD) is a form of dementia that currently affects 5.4 million people in North America alone.[1] Its high prevalence rate and course of progression, which result in the individuals being dependent on care from others, make this disease relevant to study. In AD, massive loss of neurons affects several regions of the brain, including the hippocampus and prefrontal cortex, which are involved in memory processes and cognition, thereby causing memory loss and cognitive decline. The role of sex and gender in the disease is interesting because AD is more prevalent and severe in women than in men. There are many factors that can contribute to the differential occurence between the sexes, ranging from lifestyle and genetics to biological metabolism and neuroanatomy. Furthermore, due to the post-mortem diagnosis of the disease, progression or onset of the disease among the different sexes are very challenging to interpret.

Though this observation is not fully understood, it is believed that the gene APOE e4, widely known as a AD risk factor, may increase the inheritance and risk for AD in a sex dependent manner.[2] The innate differences of brain anatomy and biological metabolism in men and women may also be key potential effectors to this differential AD onset when aging.[Bibliography item example3 not found.], [Bibliography item example4 not found.]

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Shock Therapy Treatment in Alzheimer's Disease

main article: Shock Therapy Treatment in Alzheimer's Disease
author: (account deleted)

Shock Therapy
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Image Retrieved From:

Alzheimer's Disease (AD) is a neurodegenerative disorder that is characterized by loss of neurons in several brain regions, including the hippocampusand prefrontal cortex [1] . This deterioration of memory pathways and regions results in the disease’s defining symptom of memory loss. Recent leading research has shown that shock therapy treatment in Alzheimer and non-Alzheimer’s patients has been demonstrated to improve memory, brain cognition and stimulate regrowth of brain regions affected by the disease [1][2]. This treatment method has also been successful in improving both Parkinson's disease, and Major Depressive disorders . Although shock therapy has a negative connotation from its history of misuse to treat psychiatric patients, the methods used today are modernized and safe. Electrodes are inserted into the brain inducing deep brain stimulation with low electrical currents, targeting specific brain regions [1]. While shock therapy treatment is still in the trial phase for Alzheimer’s disease, it is proving to have significant potential as a treatment. With further research, shock therapy can be a possible cure for Alzheimer’s disease.

1. Laxton et al. A Phase I Trial of Deep Brain Stimulation of Memory Circuits in Alzheimer’s Disease. American Neurological Association 00;1-13.(2010)
2. Suthana et al. Memory Enhancment and Deep-Brain Stimulation of the Entorhinal Area” The New England Journal of Medicine 366;502-510. (2012)

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