Introduction to Alzheimer’s Disease
Discuss about the Dementia Specifically Alzheimer’s Disease.
In the past few years, the Australia government and a lot of organization have had problems in grasping and understanding the national challenge created by dementia. Dementia is a broad term used to describe a group of symptoms such as loss of memory, poor problem solving, difficulties with thinking and poor speech or use of language that is mainly due to damaging of the brain. It is the failure in the cognitive area in a human being strong enough to interfere with their daily activities (McKhann et al., 2011). There are several types of dementia which include frontotemporal dementia, hunting’s disease, mixed dementia, normal pressure hydrocephalus, vascular dementia and Alzheimer’s disease. Alzheimer’s disease is the most common type of dementia with two-thirds of people diagnosed with dementia found suffering from it (Blennow, 2015). Generally, it mostly affects old people from age 65 and above. Though most characteristics of dementia and AD are common memory loss only or one of the symptoms cannot be used to conclude that a person has Alzheimer’s disease unless confirmed by a medical procedure that will also be discussed below. Some of the symptoms of Alzheimer’s disease are a hallucination, mood changes, forgetfulness, and difficulty in completion of sentences or tasks and poor judgment amongst others (Albert et al., 2013). This disease is following meaning as time progresses its symptoms also increase because of this at early stage t might not be visible. Approximately 44 million people worldwide have Alzheimer’s disease, and recently a study has shown that the rate of old people dying because of heart failure has deceased with 1 out of 3 killing because of the AD or other dementia types. I am therefore going to discuss Alzheimer’s disease a form of dementia especially in looking at its symptoms in details concerning its neurological processes and clinical signs by use of the current relevant research.
Cognitive impairment is the critical determinant of Alzheimer’s disease as a form of dementia, though other causes of cognitive impairment might also be stroke and delirium. One should be able to differentiate between cognitive changes that are resulting from or indicating Alzheimer’s disease and those that are because of excitement which is because of treatments (Wang et al. 2013), infections or fatal medical concerns left untreated.
Alzheimer’s disease as mentioned earlier spreads slowly and gradually, and at the early stages, the patient with Alzheimer’s disease might not show any alteration that can be different from that of an old person. With difficulties in using factors such as brain sensory, motor ability, and visual areas to differentiate aging characteristics and AD.
Types of Dementia
This went on until the development of a group called National Institute of Neurological and communicative disorder and stroke and the Alzheimer’s disease and Related Disorder Association provided a way of recognizing dementia (Goedert, 2017). This diagnosis was based on two areas by use of post-mortem. The vital pathological lesions in Alzheimer’s disease were a senile plaque, and neurofibrils tangles and these contain tau protein.
Alzheimer’s disease, therefore, is caused by the accumulation of two different protein namely tau and beta-amyloid (Mavrogiorgou et al., 2011). The man emphasis is on tau protein which after pathological accumulation in gliofibrialiary or neurofibrillary tangles causes tauopathy a disease characterized by deterioration of brain neutrons and neural pathway.
Tau proteins are a high soluble protein that has the function of stabilizing microtubes which are found in cytoskeleton in the cytoplasm (Wang, 2016). They are mainly located in the middle part of the nervous system, and they are formed during differential splicing by the gene. This protein that does not have a specific structure may dissociate from microtubules to create masses of protein in insoluble state building a neurodegenerative disease which could be an AD.
A neural pathway is a group of neutrons connected; neutrons are part of the nervous system that enables communication between different parts of the brain. With time there is an increase of this tau protein spreading in mind (Transneuronal spread) causing Alzheimer’s disease.
Alois Alzheimer first discovered neurofibrillary tangles in his patient who was suffering from the AD, this tangles (NFTs) are a combination of tau protein that is mostly referred to as the primary indicator of Alzheimer’s disease (Hanson et al., 2017). They are unusual fibrous materials in the perikaryal cytoplasm of the neutron that can be almost impossible to see by the use of traditional morphological staining technique since they require the presence of specialized equipment or experienced histotechnologists. The pattern of spread and distribution of neurofibrillary tangles are predictable and predetermined with a lot of its involvement seen in the entorhinal cortex and the regions of the hippocampus, the neocortex, and the amygdala.
In addition to neourofibliary tangles, another pathological lesion that is seen in patients with Alzheimer’s disease is a senile plaque. Also known as neurotic plaques, this is deposits of amyloid beta found in the grey matter of the brain. The increase of microglial and astrocytes can be related to senile plaque deposit, and they can also be byproducts of aging (Suh, 2002). Part of this protein contains Aβ peptide sequence, this senile plaque is formed when Aβ peptide is split from the amyloid protein. The beta-β or gamma-y are further divided to process APP, and APP is also cut to leave the carboxyl part of the Aβ fragment, with the increase of accumulation of APP the carboxyl is further cleavage o form amyloid beta on the transmembrane. It can be noted that this formation is healthy, but the accrual of Aβ that result in deposits is an unusual scenario. The senile plaque which can be identified by light microscopy accumulates over time especially beta-amyloid 42 to be an identity of Alzheimer’s disease (Findeis, 2007).
Causes of Alzheimer’s Disease
Iron plays a crucial role in the neurological function, and it has received a very little attention regarding how it is regulated in the body, a study compared iron protein transferrin, ferritin, and iron itself, between under 65, over 65 and patients with Alzheimer’s disease. In a normal circumstance, there should always be a lot of transferrin in white matter than grey matter then ferritin greater than transferrin. In AD transferrin in the brain kept on reducing while the behavior of iron and ferritin remained unpredictable, with the reduction of transferrin-a lot of salt was used resulting to less salt than required in the brain leading to effects in the motor ability of the individual(Frisoni et al., 2010).
The first step in treatment of any disorder or disease start s by identifying its existence, the same case applies to Alzheimer’s disease and several ways can be involved in determining those suffering from AD examples could be issuing of questionnaires that assess some areas on AD, the other one could be use of tools in finding the possibility of AD example screening tools and the last one could be by observing some cynical symptoms of patients that are likely to be suffering from this disease. It should be noted that the way people respond to Alzheimer’s disease may be defended especially in the early stages depending on the environment and how people react to them.AD dementia refers to an ow syndrome that arises from Alzheimer’s disease pathophysiological process, and some of the clinical symptoms of patients who have Alzheimer’s disease are:
Reduction or decline from the average work rate or the ability to undertake duties at the working areas that cannot be explained by derrilium disorder especially at old age
Cognitive impairment which can be detected by looking at the knowledge that is stored or that can be remembered by the individual (Rege et al., 2014)
Disability in the acquisition of new information that is accompanied by asking of a lot of questions repeatedly requesting for the same information. Loosing of personal equipment’s or belongings like their toothbrush, clothes and even books if they had any, forgetting about activities and events that they had example even wedding ceremony or burials, it can also include setting lost every time in the paths they follow while undertaking their usual day routine
Reduced reasoning ability and difficulty in dealing with complex situations which entail making of poor decisions on matters, poor management of finances and safety measures, cannot plan activities that are detailed and complex.
Role of Tau Protein in Alzheimer’s Disease
Poor visualization which includes the inability to remember and recognize familiar faces, poor putting on of their clothes and failure to use or run simple equipment’s (Vago, 2008).
Impaired use of language which entails poor reading skills, poor speaking speed and pronunciation of words and incomplete sentences due to problems of remembering the words.
Lastly, there is a change in behavior and personality which include frequent changes in mood that can be indicated by social withdrawals, lack of motivation, a lot of empathy and sympathy, lack of interest in their favorite previous activity and other unpredictable behaviors.
Conclusion
To a considerable extent, the neurological structures and effects of Alzheimer’s dementia in the brain is directly related and affects the clinical symptoms that are observed in people with this illness.
In looking at the problems with memory loss that result in disability in acquiring new information and in the forgetfulness of patients with the AD. We can see that this is the effect of AD pathology that interferes with the ability to form new memories since the pathology affect the short and long-term memory in the early stages of the disease (Hohsfield, 2015)
The problems with communication can be explained by the effect of the proteins on the neutrons that hinder communication within the neural system of a human being hence one cannot communicate.
The loss of motor function in the body of the disease could be because of their old age hence weak muscles, but in the AD it is due to the defect of iron (Mattson et al., 2009) as there is a reduction of transferrin as discussed above.
References
Albert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., … & Snyder, P. J. (2013). The diagnosis of mild cognitive impairment due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. FOCUS, 11(1), 96-106.
Blennow, K., & Zetterberg, H. (2015). The past and the future of Alzheimer’s disease CSF biomarkers—a journey toward validated biochemical tests covering the whole spectrum of molecular events. Frontiers in neuroscience, 9, 345.
Connor, J. R., Snyder, B. S., Beard, J. L., Fine, R. E., & Mufson, E. J. (1992). Regional distribution of iron and iron?regulatory proteins in the brain in aging and Alzheimer’s disease. Journal of neuroscience research, 31(2), 327-335.
Finders, M. A. (2007). The role of amyloid β peptide 42 in Alzheimer’s disease. Pharmacology & therapeutics, 116(2), 266-286.
Frisoni, G. B., Fox, N. C., Jack Jr, C. R., Scheltens, P., & Thompson, P. M. (2010). The clinical use of structural MRI in Alzheimer disease. Nature Reviews Neurology, 6(2), 67.
Goedert, M., & Spillantini, M. G. (2017). Propagation of Tau aggregates. Molecular brain, 10(1), 18.
Hansson, O., Grothe, M. J., Strandberg, T. O., Ohlsson, T., Hägerström, D., Jögi, J., … & Schöll, M. (2017). Tau pathology distribution in Alzheimer’s disease corresponds differentially to cognition-relevant functional brain networks. Frontiers in neuroscience, 11, 167.
Hohsfield, L. A., & Humpel, C. (2015). Migration of blood cells to β-amyloid plaques in Alzheimer’s disease. Experimental gerontology, 65, 8-15.
Mattsson, N., Zetterberg, H., Hansson, O., Andreasen, N., Parnetti, L., Jonsson, M., … & Rich, K. (2009). CSF biomarkers and incipient Alzheimer disease in patients with mild cognitive impairment. Jama, 302(4), 385-393.
Mavrogiorgou, P., Gertz, H. J., Ferszt, R., Wolf, R., Bär, K. J., & Juckel, G. (2011). Are routine methods good enough to stain senile plaques and neurofibrillary tangles in different brain regions of demented patients? Psychiatria Danubina, 23(4.), 334-339.
McKhann, G. M., Knopman, D. S., Chertkow, H., Hyman, B. T., Jack, C. R., Kawas, C. H., … & Mohs, R. C. (2011). The diagnosis of dementia due to Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimer’s & dementia: the journal of the Alzheimer’s Association, 7(3), 263-269.
Rege, S. D., Geetha, T., Griffin, G. D., Broderick, T. L., & Babu, J. R. (2014). Neuroprotective effects of resveratrol in Alzheimer disease pathology. Frontiers in aging neuroscience, 6, 218.
Suh, Y. H., & Checler, F. (2002). Amyloid precursor protein, presenilins, and α-synuclein: molecular pathogenesis and pharmacological applications in Alzheimer’s disease. Pharmacological reviews, 54(3), 469-525.
Vago, D. R., & Kesner, R. P. (2008). Disruption of the direct perforant path input to the CA1 subregion of the dorsal hippocampus interferes with spatial working memory and novelty detection. Behavioural brain research, 189(2), 273-283.
Wang, J. Z., Xia, Y. Y., Grundke-Iqbal, I., & Iqbal, K. (2013). Abnormal hyperphosphorylation of tau: sites, regulation, and molecular mechanism of neurofibrillary degeneration. Journal of Alzheimer’s Disease, 33(s1), S123-S139.
Wang, Y., & Mandelkow, E. (2016). Tau in physiology and pathology. Nature Reviews Neuroscience, 17(1), 22.
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