Researchers know Alzheimer disease involves gradual brain cell failure, the purpose as to why the cells fail isn’t well-defined. As other chronic conditions, specialists believe that Alzheimer’s advances as a complicated result of numerous factors other than any one superseding cause. The paramount risk factors for Alzheimer’s are genetics, traumatic brain injury, and age. The unearthing of further risk influences will increase our understanding as to why Alzheimer’s develops in some individuals and not others.
Alzheimer disease has a convincing but complicated genetic origin and has already exhibited allelic and locality of heterogeneity and polygenic inheritance. It is possible that added complications, including gene-gene relations, is also involved in the etiology of Alzheimer disease. Though rare mutations in various genes can perturb early-onset of Alzheimer disease, only usual adaptation in apolipoprotein E (APOE) has a considerable effect on the added common late-onset form of Alzheimer disease. Modern genome-wide association studies in late on-set Alzheimer disease have recognized up to “21 additional novel genetic loci for Alzheimer disease, including genes from multiple pathways, such as beta-amyloid processing and clearance, calcium signaling, and extracellular matrix” (Hohman, 2016 p. 142). But APOE, the identified genetic loci have very meek results, and in total the branded genetic influences in late on-set Alzheimer disease still only explain “about 33% of the broad-sense heritability, which has been estimated to be 60%–80%” (Hohman, 2016 p. 142). One likely cause of further heritability is gene-gene interactions. Identified genetics might adopt influence of disease and risk through interactions with one another, as well with other not yet discovered genetic factors. Furthermore, novel genetics with no evident independent main effect on late on-set Alzheimer disease risk could intermingle with each other to considerably increase risk (Hohman, 2016 p. 142).
Traumatic Brain Injury
Accruing evidence associates traumatic brain injury (TBI) as a provoking result in the development of Alzheimer disease although, description of whether and how TBI might trigger a long-term course of neurodegeneration remains debated. A treacherous growth in TBI has been perceived to match the high-tech advances of the twentieth century, with a sizeable ratio of brain injuries arising from motor vehicle accidents (Lye & Shores, 2000, p.115). Developments in the administration of the acute phases of neurotrauma have reduced the quantity of losses associated with TBI, however the lasting sequelae of brain trauma in persons enduring TBI remain a substantial medical challenge. In sight of the growth in the frequency of both TBI and Alzheimer disease in modern times, the likelihood that brain trauma might lead to earlier progression of Alzheimer disease later in life has an important social and medical implication for health services planning and precautionary efforts.
Aging is the most important risk factor for Alzheimer’s disease. Hereditary forms of the illness are rarely expressed clinically before the fifth decade of life. Hence, a better understanding of how old age contributes to Alzheimer disease pathogenesis will likely provide critical clues on potential treatments. Interestingly, thermoregulatory deficits appear at the same time in life when the incidence of Alzheimer disease greatly increases (Tournissac et al., 2017 p. 25). “The common incidence of subclinical cognitive decline and neuropathology has led to the hypothesis that age-related cognitive decline may be fully mediated by co-occurrence of various neuropathologies. That is, advancing age is associated with disease-related neuropathologies that are the primary causes of cognitive decline. Age is the largest risk factor for Alzheimer’s disease. However, AD can develop at any point during the adult life span as early as the fourth decade” (Hohman, et al., 2017 p.120).
Having a degenerative disease such as Alzheimer’s disease is a disease that’s difficult to observe someone going through. The research that articulates the major causes of Alzheimer disease projects an alarming thought as to whom can be affected by the disease. Walking in a Christian life and attempting to treat those with Alzheimer’s disease, one would have to approach it in a loving and compassionate way. There’s only one scripture in the bible that directly addresses such an illness and that’s in Ecclesiastes 12:1-8 where it states “remember your Creator in the days of your youth, before the days of trouble come and the years approach when you will say, “I find no pleasure in them” before the sun and the light and the moon and the stars grow dark, and the clouds return after the rain’ when the keepers of the house tremble, and the strong men stoop, when the grinders cease because they are few and those looking through the windows grow dim…”. A key to managing with a generative disease such as Alzheimer’s is to always remember that God is good regardless of the circumstances, God’s will does not change. The same God that is mentioned in the Bible is the same God who is with us today. His words and promises still hold true and just. Scripture tells us, “and we know that for those who love God all things work together for good, for those who are called according to His purpose” (Romans 8:28). For some people, degenerative disease is one of those things that is in works for “all things”. God does not tell us that all things that we go through are good, but He does work for the good in all things as God is a redeemer.


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