MRI evidence indicates changes in brain may occur prior to amyloidal deposition. It develops gradually especially affects ADAD mutant carriers.

Alzheimer disease is fatal and according to researchers, it has no cure. Its predisposition affects the mutant carriers and thus can develop early especially among the children carrying genetic mutation for the disease. According to research by Quiroz in the department of psychiatry in Massachusetts general hospital, suggest that ADAD mutant carriers can develop as early as possible among the children with a high certainty unlike the non-carriers who have no brain abnormalities.

Abnormalities in mutant carriers

The amyloid plaques and neurofibrillary tangles are some of the structural and functional assurances of the AD. Their presence in a child or any individual leads to an early definition and diagnosis if the disease. However, there is need to be cautions on the brain changes and, as there is no clear evidence of the functional brain changes that can be associated with the genetic risk of the disease. Actually, there is no single diagnostic test for the Alzheimer’s disease thus the process takes different tests. For example, there was a research conducted in Massachusetts hospital, different variables and sample were used for study and control to enhance definite results. Children and adults with mutation carriers and no carriers are used to determine the predisposition and likelihood of disease development. The research is based on the mutation carriers and the impact and predisposition of the disease in early ages and future development among the adults. Therefore, there are suggestions that alterations in presenilin 1 especially for the mutation carriers occurs among carriers starting at a very early age.

Essential elements of Alzheimer

The in addition, researchers assert that blocking of the beta secretes activity may result to prevention of production of the undesirable beta amyloid. A research was conducted among the children and adults as they try to understand the real issues underlying on the mysteries of the disease. Mutation carriers have a high certainty of development of the disease. In the research, the non-carriers were used a controls and the results shows that the plasma Abeta concentrations had variable ratios.

Reduction of the level of certain neurotransmitters is a characteristic of the Alzheimer’s disease and usually results to healthy functioning of the brain. The disease disrupts proper brain functioning and thus causes intellectual functioning severe enough to lead to brain abnormalities. The disease mainly occurs among older people but there are researchers affirm that the predisposition develops among the carriers. For example, example, there was a beta overproduction, posterior parietal deactivation, high brain volumes and resting state functional connectivity among the carriers. Results show absence of the features among the controls that is the non-carriers, hence are at a minimal chance of having the disease. It develops gradually and thus children with the genetic risk bear the abnormalities. However, non-carriers are virtually certain that they are free from the disease at any given time in their life. The non-carriers have no element of intellectual learning and brain abnormalities. Carriers are highly affected by gradual development of the diseases as they have less memory encoding, poor functioning due to the gradual damages.