The Alzheimer’s disease is a form of chronic neurodegenerative disease which slowly worsens over time. It is determined to be 60-70% responsible for causing dementia among individuals. In this assignment, a brief overview of Alzheimer’s disease is discussed.
The neuropathology of the Alzheimer’s disease informs that it is mainly identified by the loss of synapses and neurons present in the cerebral cortex region of the brain. This loss of the brain tissues results in forming gross atrophy of the infected region that includes degeneration in the parietal and temporal lobe and parts of cingulated gyrus and frontal cortex. The pathology of Alzheimer’s disease further informs that it is caused by mainly two processes that are intracellular build-up of tau protein and extracellular deposition of beta-amyloid-Aβ. The proteins are insoluble in nature and the key component of sensile plaques is Aβ and tau is for neurofibrilar tangles formed in the brain in Alzheimer’s disease.
Alzheimer’s disease is a disease of the brain which leads to large number cell death and atrophy of the brain tissues leading the individual to face hindrance in managing their everyday life. Thus, it is important to know about Alzheimer’s disease as it is going to assist in taking timely medical intervention to reduce damage to brain tissues helping the individual to lead a normal life. Moreover, effective knowledge for Alzheimer’s disease is important is to avoid the risk factors related to the disease and for eroding any stigma to ensure timely medical intervention.
Prokop, S., Miller, K.R., Drost, N., Handrick, S., Mathur, V., Luo, J., Wegner, A., Wyss-Coray, T. and Heppner, F.L., 2015. Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer's disease-like mice. Journal of Experimental Medicine, 212(11), pp.1811-1818.
Prokop, S., Miller, K.R., Drost, N., Handrick, S., Mathur, V., Luo, J., Wegner, A., Wyss-Coray, T. and Heppner, F.L., 2015. Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice. Journal of Experimental Medicine, 212(11), pp.1811-1818.
Prokop, S., Miller, K.R., Drost, N., Handrick, S., Mathur, V., Luo, J., Wegner, A., Wyss-Coray, T. and Heppner, F.L., 2015. Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice. Journal of Experimental Medicine, 212(11), pp.1811-1818.
Alzheimer’s disease is a disease of the brain which leads to large number cell death and atrophy of the brain tissues leading the individual to face hindrance in managing their everyday life. Thus, it is important to know about Alzheimer’s disease as it is going to assist in taking timely medical intervention to reduce damage to brain tissues helping the individual to lead a normal life. Moreover, effective knowledge for Alzheimer’s disease is important is to avoid the risk factors related to the disease and for eroding any stigma to ensure timely medical intervention.
In Alzheimer's disease, at the structural level, the limbic system of which the hippocampus is a part is attacked that causes the individual to experience impairment of memory and frequent mood chances. The cerebral cortex region is damaged which is responsible for controlling emotional outbursts in individuals. The damage of the brain stem occurs in late stages of the Alzheimer’s disease which leads to impairment of organ functions. At the cellular-level, in Alzheimer's disease, the neuron of the brain which is responsible for communicating signals and learning memory is damaged and later leads to death. This results the brain in Alzheimer’s disease to shrink gradually and become less functional leading to show symptoms of dementia.
Prokop, S., Miller, K.R., Drost, N., Handrick, S., Mathur, V., Luo, J., Wegner, A., Wyss-Coray, T. and Heppner, F.L., 2015. Impact of peripheral myeloid cells on amyloid-β pathology in Alzheimer’s disease–like mice. Journal of Experimental Medicine, 212(11), pp.1811-1818.
Raskin, J., Cummings, J., Hardy, J., Schuh, K. and A Dean, R., 2015. Neurobiology of Alzheimer’s disease: integrated molecular, physiological, anatomical, biomarker, and cognitive dimensions. Current Alzheimer research, 12(8), pp.712-722.
Raskin, J., Cummings, J., Hardy, J., Schuh, K. and A Dean, R., 2015. Neurobiology of Alzheimer’s disease: integrated molecular, physiological, anatomical, biomarker, and cognitive dimensions. Current Alzheimer research, 12(8), pp.712-722.
Raskin, J., Cummings, J., Hardy, J., Schuh, K. and A Dean, R., 2015. Neurobiology of Alzheimer’s disease: integrated molecular, physiological, anatomical, biomarker, and cognitive dimensions. Current Alzheimer research, 12(8), pp.712-722.
The loss of memory is the most common symptom in patients suffering from Alzheimer’s disease. The other symptoms include trouble planning as well as problem-solving due to damage and death of the brain cells. The loss of memory leads to create challenge in executing daily task that is one of the symptoms related to the disease. The symptoms such as confusion of time and place, incapable to form meaningful conversation, changes in vision, social withdrawal, mood changes, lapse in judgement and others related to Alzheimer’s disease.
One of the treatment options for Alzheimer’s disease is the clearance of existing aggregates and deposition of amyloid protein in the brain. In order to execute this purpose, two strategies are mainly applied that includes activation of enzymes which are able to reduce amyloid proteins and modulation of beta-amyloid transportation between the brain and peripheral circulation. This strategic treatment is only able to be resolved by the use of medication inhibitors/ modulators of RAGE. Moreover, active immunotherapy is also a potential treatment opportunity for Alzheimer’s disease that is being currently used. Further, Aricept is the only medication approved for Alzheimer’s disease by the FDA to control the disease. The hyperphosphorylated Tau protein aggegrates are seen to result in neurotoxicity of the brain in Alzheimer’s disease. The methylene blue dye derivatives are seen to show some promising activity in inhibiting formation of tau protein aggregates and thus are an effective treatment for Alzheimer’s disease.
Rosenberg, P.B., Nowrangi, M.A. and Lyketsos, C.G., 2015. Neuropsychiatric symptoms in Alzheimer's disease: what might be associated brain circuits?. Molecular aspects of medicine, 43, pp.25-37.
Rosenberg, P.B., Nowrangi, M.A. and Lyketsos, C.G., 2015. Neuropsychiatric symptoms in Alzheimer's disease: what might be associated brain circuits?. Molecular aspects of medicine, 43, pp.25-37.
Folch, J., Petrov, D., Ettcheto, M., Abad, S., Sánchez-López, E., García, M.L., Olloquequi, J., Beas-Zarate, C., Auladell, C. and Camins, A., 2016. Current research therapeutic strategies for Alzheimer’s disease treatment. Neural Plasticity, 2016.pp.1-15.
www.accessdata.fda.gov 2004, Drug Approval Package: Aricept, Available at:
One of the treatment options for Alzheimer’s disease is the clearance of existing aggregates and deposition of amyloid protein in the brain. In order to execute this purpose, two strategies are mainly applied that includes activation of enzymes which are able to reduce amyloid proteins and modulation of beta-amyloid transportation between the brain and peripheral circulation. This strategic treatment is only able to be resolved by the use of medication inhibitors/ modulators of RAGE. Moreover, active immunotherapy is also a potential treatment opportunity for Alzheimer’s disease that is being currently used. Further, Aricept is the only medication approved for Alzheimer’s disease by the FDA to control the disease. The hyperphosphorylated Tau protein aggegrates are seen to result in neurotoxicity of the brain in Alzheimer’s disease. The methylene blue dye derivatives are seen to show some promising activity in inhibiting formation of tau protein aggregates and thus are an effective treatment for Alzheimer’s disease.
The discussion informs that Alzheimer’s disease is involved with brain tissues damage that leads individuals to lose memory. There is no cure for the disease but the treatment is available which is mainly indicated at inhibiting the formation of beta-amyloid and tau protein aggregates in the brain.
Folch, J., Petrov, D., Ettcheto, M., Abad, S., Sánchez-López, E., García, M.L., Olloquequi, J., Beas-Zarate, C., Auladell, C. and Camins, A., 2016. Current research therapeutic strategies for Alzheimer’s disease treatment. Neural Plasticity, 2016.pp.1-15.
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