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Alzheimer’s disease is a deadly progressive form of atrophy that affects millions of people around the globe. Alzheimer’s disease also referred to as AD accounts for 70% of dementia cases diagnosed. Two significant reasons linked to the development of AD are genetic influences and lifestyle/environmental factors, while two of its primary effects are death of nerve cells and tissue loss within the brain as well as interference in the patient’s daily life. One of the main causes for Alzheimer’s is the genetic component related to family bloodlines. Genes manipulate the function of every cell in our bodies, including basic characteristics and potential disease development.
There is a predominance of maternal transmission in later onset and paternal transmission in early onset . The bulk of this paper will deal with the SOD1 gene mutations as the proposed cause for some types of FALS. Many other hypothesis have been developed and will be briefly addressed at this point. Autoimmune disease and mutations in the glutamate receptor are other proposed causes. Autoimmune disease has been studied as a possible agent for the cause of FALS .
1995 May 15;9(10):1149-63. Review. PubMed PMID: 7758941. Wolf FI, Fasanella S, Tedesco B, Torsello A, Sgambato A, Faraglia B, Palozza P, Boninsegna A, Cittadini A. Regulation of magnesium content during proliferation of mammary epithelial cells (HC-11). Front Biosci.
People who have the Late-onset Alzheimer’s originates from a complicated series of brain changes that occur over a long period of time. Current drug treatments are given to slow down the cognitive damage temporally. Scientist are currently researching that the disease may be triggered by different factors however age is the most known factor . This nerve racking disease called Alzheimer’s also known as AD was discovered in 1906 by Dr Alois Alzheimer a German physician, this was not considered a critical Disease until the 1970s.It all began with a documented case of a woman by the name Of Auguste D in her in fifties who showed signs of a cognitive disorder as it relates to her memory and socializing with her family. She later died and this great physician decided to do an autopsy on her brain, he then noticed a shrinkage in and around the nerve cells of her brain which led significantly to the discovery of this disease.
‘Huntington’s disease (HD) is an autosomal dominant progressive neurodegenerative disorder characterized by personality changes, motor impairment and subcortical dementia. It is associated with a selective neuronal cell death occurring primarily in the cortex and striatum.’ (Scherzinger et al, 1997). HD causes emotional problems, uncontrolled movements and the loss of thinking ability. It can lead to disability and death from the illness. There are two forms of this disease: adult-onset and early-onset (juvenile).
Alzheimer’s Disease INTRODUCTION Alzheimer’s disease is a progressive degenerative disorder of insidious onset, characterized by memory loss, confusion, and a variety of cognitive disabilities. It is the major cause of dementia in the elderly and is characterized by the presence of neuropathologic lesions including: neurofibrillary tangles in the neuronal perikarya and in pyramidal neurons of the hippocampus, entorhinal cortex and neocortex, nucleus basalis of Meynert, and periaqueductal gray. Neuritic (senile) plaques often with a central or core deposition of amyloid within the plaque and in some cases with amyloid infiltration of blood vessel walls (amyloid angiopathy) and the adjacent perivascular neuropil; loss of neurons, most often in the hippocampus, neocortex, locus coeruleus, and nucleus basalis; and disturbance of acetylcholine transmitter activity marked by lowered levels of acetylcholine and choline acetyltransferase (4). ETIOLOGY Alzheimer’s disease may strike as early as age 40, but is most common after the age of 60. As the average life expectancy continues to increase so too does the incidence of AD.
Annals of Neurology, 25(6):607-13. Kordower, J. H. et.al. 1991. Putative chromaffin cell survival and enhanced host-derived TH-fiber innervation following a functional adrenal medulla autograft for Parkinson’s disease. Annals of Neurology, 29(4):405-12.
Most investigations using transgenic animal models of Alzheimer’s disease (AD) have reported a decrease in hippocampal neurogenesis (Demars et al., 2010, Hamilton et al., 2010, Naumann et al., 2010). Currently, is considered that the impairment in neurogenesis can be an important factor during the onset and progression of AD. Most authors consider hippocampal neurogenesis necessary to maintain hippocampal cognitive abilities, therefore, the damage in the proliferative system has to be functionally detrimental (See references in Mu and Gage, 2011). Most animal models with the familial type mutations that cause AD show that when toxic amyloid beta peptides (Aβ42) are present, hippocampal neurogenesis decreases. In addition, we know that knocking out of presenilin-1 in the hippocampus impairs proliferation.