There are three genes that are found to cause Alzheimer’s disease. These include (Melesie and Dinsa, 2013):
– APP, a membrane, located on chromosome 21
– Presenilin 1 located on chromosome 14
– Presenilin 2 located on chromosome 1
They lead to excessive production of the cells and result in deterioration of the causal genes.
The functionality of brain can be studied based on microscopic and macroscopic features. The macroscopic features are meant to study the medial temporal lobes and the activities of motor, visual and sensory regions. The pattern is usually detected with MRI scan but it is stereotypic by nature. The microscopic features include neurofibrillary tangles and the study of composition of various components within the brain (Pozo et al., 2011). These help to study the morphology and topography of the brain with better accuracy.
Cholinesterase is an enzyme that attempts to break down the acetylcholine which is neurotransmitters. People with Alzheimer’s disease display lower levels of this neurotransmitter. Cholinesterase inhibitors are meant to enhance the brain function. Still, the progress does not happen rapidly. It can be seen in measurable levels. Donepezil is suggested as the treatment methodology for Alzheimer’s disease in USA (Duthey, 2013). Glutamatergic agents are supposed to be the unnoticed groups of neurotoxic organisms that release large volumes of amino acids. Most of the patients suffering from Alzheimer’s disease face loss of pyramidal neurons that are glutamatergic. When these receptors are stimulated excessively, the neuronal loss can affect the pathophysiology to a greater level.
The neuropathologic criteria for this disease are as follows:
1. Topographic staging
2. Cut off of the quantitative values of the tangles and plaques
3. Age adjustment
The actual metrics available to study the tangles are semi quantitative. Therefore, new techniques are identified to determine even the mild lesions and study the contribution of brain damage to uncertainty (Jellinger, 2014).
Melesie and Dinsa (2013) have also identified few risk factors that contribute to this disease. These include cerebral infarcts, multiple microinfarcts and status lacunaris. Alzheimer’s disease has a dimension in the vascular structure as well. The major factors include atherosclerosis, reduced glucose metabolism, reduced perfusion and cerebral embolism.
Neuropathology can be analysed in early stages of Alzheimer’s disease, too. Patients facing mild cognitive impairment are already exposed to cognitive issues and this can affect baseline level. Such impairments are more likely to cause dementia. The autopsy studies for patients with MCI are scarce but they have also noted a mid level between demented patients and cognitive subjects. As already mentioned, Alzheimer’s disease is not restricted to people in their old ages. People in normal age also fall prey to Alzheimer’s disease (Pozo et al, 2011). Sometimes, it could be the mild cognitive impairment (MCI) within a person resulting in dementia or this disease. However, there is a significant overlap between the disease and lewy bodies. These seem to have similar impacts on the brains of patients and the progressive neural system undergoes a fatal failure. The entire process is irreversible by nature in the neural system.

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