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Correlation Alzheimer Diseas Neuropathologic

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Correlation Alzheimer Diseas Neuropathologic

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Correlation Alzheimer Diseas Neuropathologic

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Alzheimer Disease which is also known as AD occurs mostly in the old age people. It is a disease in which a person loses his power of thinking and the brain cells does not work as they do in the normal young age. In case of Dementia, there could be loss of memory in the older aged people. The diagnosis of the disease and the pathology of the disease are discussed. Also the relationship of the Alzheimer disease with the clinical symptoms is mentioned in this essay. It is determined that there are few types of neuropathological cognitive impairments like plaque and neurofibrillary tangles management. AD is characterized by two such principles lesion, plaque and tangles. The major protein components are elucidated from the studies since it was identifies 100 years ago. This led to metabolic cascades which involves plaques and tangles. This essay discovers the major pathological lesions which are linked with molecular biology and the relationship with clinical disease AD.
Alzheimer disease is one of the most common reasons for the happening of dementia and chronic neurodegenerative disorder within people who are aged. Dementia is a type of syndrome which progresses in the illness that affects memory, behavior, everyday performance and thinking of any person (Geri & Jim, 2016). It usually affects people who are aged but also only 2% of the people develop this disease before the age of 65 years. With respect to the worlds Alzheimer report in the year 2014, there were 44 million people who are living with dementia all across the world. People with this number are going to be double by the year 2030 and triple by the year 2050. It was researched that approximately 5.2 million Americans had this disease in the year 2014. It is also said the Women are more affected as compared to men (Sorensen, 2009). There are a few factors which lead to AD. These are genetics, head trauma, diabetes mellitus, hyperlipidemia, environmental factors and vascular factors. There are as such no treatments for AD which reduces or stops death and malfunctioning of the neurons in brain. However, there are many drugs and therapies which aims to slow or stop neuron malfunctioning. At present, there are five drugs which are approved by United States and the administration of drugs for the improvement of the symptoms of AD. This will be done with the increase on the number of the neurotransmitters in the brain. It is studied that Medicare and Medicaid covered about $150 billion of the total health care for the long duration of the individuals who are suffering from AD and other dementias (Miklossy, 2011).
The studies which are clinical and neuropathlogical have huge knowledge of the path psychology and progression of this disease.  AD is related to the accumulation of abnormal proteins such as amyloid?β [aβ which progresses gradually in the brain and leads to the progressive synaptic, axonal and neuronal damage. Such changes happen years prior to the symptoms appearance. The changes occur with the stereo-typical pattern of early medical temporal lobe involvement, which is followed by the progressive damage of the neocortical.
Knowledge of people with the clinical manifestations and biology of Alzheimer disease has been increasing greatly. The relation between the clinical symptoms and the AD is very critical. The original criteria features which requires revision includes:
Facts of the historical pathology of the disease might be founded all across the broad spectrum of the clinical symptoms. This includes the individuals who are normal cognitively or from their brains, people with MCI and people with dementia too. This term patho-psychological is used to encompass the ante mortem changes which are biological and they precede the postmortemneu-ropathological diagnosis of the AD and also as the neuropathological substrate. Dementia in AD refers to the syndrome which is clinical and that arises as the result of the AD pathophysiological progress (Kayed, Jackson, Estes, & Barrett, 2011).
There is lack of the acknowledgement of the feature distinguishing with the other conditions in dementia. They occur in the aged population and it is not completely recognized years ago. For example: Bodies which are lewy and dementia, vascular dementia, variations in the behavior which is called frontotemporal dementia and progressive aphasia. All these are characterized extensively.
Results are not included which are based on the magnetic imaging, positron emission tomography imaging and cerebrospinal fluid assays in the making of the decision. The efforts which are put initially for the incorporation of the diagnosis of the AD dementia and MCI, they need to be linked with more detailed approach to the diagnostic process (Briggs, Kennelly, & Neil, 2016).
There is the implication that the impairment of the memory is always the initial cognitive discrepancy in all the patients who are suffering from AD. There have been experiences which have shown that there are a few nonmagnetic presentations of the pathopsychological process of the AD. The common ones of all have the syndrome of posterior cortical atrophy and logopenic primary progressive aphasia.
There is a lack of the information about the genetics of the AD as well. Mutations in three genes – presenilin 1 and 2 and amyloid precursor can cause the early onset, autosomal dominantly inherited AD.
The age cutoffs which are proposed for the diagnosis of the AD was 40 years when it was worked upon decades ago but rarely it differs its pathopsysiology from the aged people say of age 60 and above.
Alzheimer disease and especially dementia which occurs in the people who are above 90 years of the age are also the part of the spectrum similar to the young people. However, the clinical pathological correlations are attenuated. High level heterogeneity of the AD which is possibly due to dementia included the group of patients who will be diagnosed as Minor or mild cognitive impairment also known as MCI.
It depends on the historical examination is done of the brain specimen that definite diagnosis of the AD can be done. This type of diagnosis is based on the identification of the series of the morphological abnormalities which are distributed in stereotyped patterns. It is significant that one should realize that any of the alterations in which the neuropathological diagnosis of this disease is made might also seen to some degree in the brains of the old aged people who within their whole life have displayed cognitive functions. Mostly of the times it needs recognition of the involvement in the areas of the brain by these types of lessons for the neuropathologist to be able to state that AD was the reason of the patient’s impairment which is cognitive (Lim, 2013).
Sometimes, all this might consist of the distinctions which need experience and expertise and other times, just an honest neuropathologist might be needed for the requirement to state that this diagnosis could or could not be left with the degree of the probability and not the certainty. This could be true when one examines the brains of the patients who are dying with the old age range. The individuals who are dying at the old age, there is this overlap of neuropathological changes in between those which are found with profound dementia and those who are intact with the cognitive function and that function is extensive.  Such type of distinctions is difficult. Yes, the correlations in between the extent and the distribution of such type of lesions are presently under detailed scientific study with the usage of the brain specimen taken out from the individuals in the large cohorts of advanced old patients who underwent deep and rigorous longitudinal neuropsysiological research (Lane & Hardy, 2017).
AD is the type of disease which was founded by Aliod Alzheimer gives the description that has the presence of the fibrous inclusions within the perikaryal cytoplasm of the pyramidal neurons. Such type of inclusions is known as Alzheimer neurofibrillary tangles and today too it is considered a cardinal economics lesion which is linked with the disease and a need for making the pathological diagnosis. Neurofibrillary tangles are tough to see with the old traditional morphological stain which is used by pathologists, hematoxylin and eosin. The nature of such tangles has been studies in details since the past few decades and people have learned about the structural components about these tangles (Foster, 2007).
If the structure is seen, these tangles are composed of the abnormal fibers which measures up to 10 nm in the diameter and occurs in pairs and are wound in the helical fashion which the periodicity of 80 nm. Such observations tell that such type if structures are called paired helical filaments. The first constituent of these tangles is the microtubule associated protein tau. This tau in neurofibrillary tangle is abnormally phosphorylated with the phosphate groups which are attached to the very specific sites on the molecule. There are also the numbers of proteins constituents which are linked with these tangles. They are ubiquitin, cholinesterase and beta-amyloid 4 but tau is considered to be as the critical factor for many of the structures (Snyder, 2015).
There are patterns which are present in the distribution of the neurofibrillary tangles in the case of AD and the major part is instead stereotyped and predictable. A very profound involvement can be seen in the 2nd layer neurons of the entorhinal cortex, the CA1 and subicular regions of t he hippocampus, deeper layers like 3rd, 5th and 6th and the amygdale of the neocortex.  Researchers have displayed that the extent and the distribution of these tangles in such disease relates with the degree of dementia and for how long the illness have been in the patient. This information displays that such abnormalities have direct effect on the brain’s functioning capacity. Nevertheless, it is clear that factors which contribute in the production of the clinical features of the disease are other and not these. However the tangles are considered as a cardinal histopathological feature of AD, it still should be kept in the mind that this lesion might also meet in association with many other states of the diseases. This process consists of the disorders like postencephalitic, posttraumatic dementia or dementia pugalistica, Parkinsonism, type C Niemann-Pick disease, and amyotrophic lateral sclerosis/parkinsonism dementia complex of Guam. This is still not clear as to why disease with such a huge range of etiological mechanisms must show this particular neuropathological abnormality (Nelson & Alafuzoff, 2013).
Other cardinal pathological lesion that is seen in the patients who are dealing with AD is the senile plaque. These plaques are complicated structures which can be defined by the presence of the central core build up of 4-kD protein with the Beta-pleated sheet configuration called as βA4. The beta pleated sheet of this protein grants the capability to keep together the planar dye Congo red and produce birefringence when lit by polarized light. And at last it grants the physical definition of the amyloid (Castellani, Zhu, Lee, Smith, & Perry, 2009).
The brains of the old people and cases of the patients who have AD might also have a few forms of βA4 containing plaques. Sometimes, the taxonomy employed for the lesions in the literature could be confusing. The plaque has the central core of βA4 protein which is arranged in the radial style and it is surrounded by corona of neuritis which are formed abnormally (Knopman, Chertkow, & Hyman, 2011). This abnormal neuritis mark strongly with silver impregnation stains which are used to know the neurofibrillary tangles. Such structures consist of the deep bodies, packets of couples helical filaments and membranous profiles. In the border of the neurotic plaque, the researchers encounter one to a few microglia cells and less frequently reactive atrocities. Whether such microglia cells are involved actively in a neuro inflammatory path genetic cascade or they react to the presence of the constituents within lesions remain a matter of deep argument.
In the few years, most of the neuropathological literatures relates the details of AD and it clinicopathological correlation tend to engage detailed researches and exams of the end stage of the disease (Korolev, 2014). There still stays confusion about the documents which lacks cognitive impairment and yet who brains displays neuropathological findings of Alzheimer disease at autopsy (Perl, 2010). This seems to be a significant issue as it challenges the principles of the processes which underlie AD changes and are the single cause of the cognitive impairment. For addressing this issue, longitudinal studies of the patients who are enrolled being normal by brains and still followed for several decades can be used to study the clinical and corresponding molecular pathologic changes in AD. Accurate analysis always requires preliminary modelling of what exactly is expected at the population level based on what is already known about such type of disease (Santos, .Snyde, Alber, Zhang, & Wu, 2017).
The summary points which are presented in the neuropathology of aging related brain disease should be taken into account of diverse medical, biochemical, technical and anatomic considerations. Pathologies related to concomitant are usually very cliché in the brains that are aging. Such diseases and most other factors are collectively formidable issues to aligning pathology and cognition with strictly linear scales. However, co pathologies (CVD), hippocampus sclerosis, synucleinopathies etc. contribute to the cognitive impairment. The universal observation of tough independent relation in between plaques and tangles with the disease which is dementia means that AD neuropathological changes will most likely be important. The detailed literature on CPC correlations related to AD and dementia, a body of research is based on the work that is done around the whole world with multiple patients and that indicates a type of sequence which might begin with the specific genetics and environmental factors that might spread AβP’s. Neuritis plaques link the extracellular Aβ deposition and intracellular neurofibrillary (Protein of TAU) pathology. Data which is cross sectional indicates that pretangles and NFT’s develops first in the stem of the brain and medical temporal; lobe structures. Within the patients with the measurable disease and commodities which are lacking, the extent of cognitive impairment parallels the depth of neocortical NFT pathology (Imbimbo, Lombard, & Pomara, 2005). In the conclusion, it can be said that there are predictable relation between Alzheimer disease pathologic hallmarks and cognitive impairments.
Briggs, R., Kennelly, S. P., & Neil, D. O. (2016). Drug treatments in Alzheimer’s disease. Clinical Medicine , 16 (3), 247-253.
Castellani, R. J., Zhu, X., Lee, H. G., Smith, psychology., & Perry, G. (2009). Molecular Pathogenesis of Alzheimer’s Disease: Reductionist. International Journal of Molecular Sciences .
Foster, N. L. (2007). A new framework for the diagnosis of Alzheimer’s disease. The Lancet Neurology , 6 (8), 667-669.
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Imbimbo, B. P., Lombard, J., & Pomara, N. (2005). Pathophysiology of Alzheimer’s Disease. Neuroimaging Clinics of North America , 15.
Kayed, R., Jackson, G., Estes, D. M., & Barrett, A. D. (2011). Alzheimers Disease: Review of Emerging Treatment Role for Intravenous Immunoglobulins. Journal of Cetral Nervous System Disease .
Knopman, D. S., Chertkow, H., & Hyman, B. T. (2011). The diagnosis of dementia due to Alzheimer’s disease:. Alzheimer’s & Dementia , 1-7.
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Lim, A. (2013). AlzheimerDisease: A historical Perspective. Historical Perspectives in Neuroscience , 1 (1).
Miklossy, J. (2011). Alzheimer’s disease – a neurospirochetosis Analysis of the evidence following Koch’s and Hill’s criteria. Miklossy Journal of Neuroinflammation .
Nelson, P. T., & Alafuzoff, I. (2013). Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature. J Neuropathol Exp Neurol. , 71 (5), 362-381.
Perl, D. P. (2010). Neuropathology of Alzheimer’s Disease. Mt Sinai J Med. , 77 (1), 32-42.
Santos, C. Y., .Snyde, P. J., Alber, J., Zhang, M., & Wu, W. C. (2017). Pathophysiologic relationship between Alzheimer’s disease, cerebrovascular disease, and cardiovascular risk: A review and synthesis. Alzheimer and Dementia , 7, 69-87.
Snyder, P. J. (2015). Introducing Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, an open access journal of the Alzheimer’s Association. Alzheimer and Demetia , 1, 1-4.
Sorensen, A. A. (2009). Alzheimer’s Disease Research: Scientific Productivity and Impact of the Top 100 Investigators in the Field. Journal of Alzheimer’s Disease , 16, 451-465.

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