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I was probably 6 or seven years old when I realized that both my neighbors and family members were hinting that my grandmother was senile. I noticed that she had started forgetting many things including the names of my younger brother. At times, she would forget how to put the scarf on and at other times she would wait for our long dead grandfather at the door. In other instances, she was unable to comprehend what people were telling her and she could start on some activity only to forget. Later, she was diagnosed with Alzheimer's disease (Oliver, H., Nader, K. and Nadel, L., 2013).

Alzheimer's disease is a progressive neurogenerative disorder which increases so first in prevalence as the population ages (Lee, 2004). This results from the effects of flat retrograde amnesia whereby there is a uniform loss of memory from the past periods. This shows that my grandmother is undergoing impaired episodic memory (Kihara, T and Shimohama, S., 2004). In addition, she appears to be suffering from a poor semantic memory. This is because semantic memory represents the factual and conceptual knowledge which is not related to any given memory like how to tie a scarf.  It is worth noting that, episodic memory deterioration is the ultimate clinical feature associated with Alzheimer's disease (Cowan, 2008).

Just like in my grandmother’s case, a person suffering from any of the above disorders will have higher chances of forgetting. For instance, vascular dementia is closely linked to the damage of the blood vessels which supply blood to the brain (Poulin, 2011).

These vessels carry oxygen rich blood to nourish the brain with enough oxygen to discharge its duties (Poulin, S.P. et al., 2011). The main difference in memory between a memory disorder and normal aging is the amount beta-amyloid deposits, the tangles of hippocampal neurofibrillary or the neuritic plaques within the cortex. Therefore, Alzheimer’s disease (AD) is that neurodegenerative pathology whereby amyloid-beta (Abeta) peptide accumulates within parts of the brain resulting to plague deposition and progressive decline of the various cognitive functions. Research has shown that injection of beta amyloid into a rats brain can damage neurons and lead to symptoms which resemble the ones associated with alzheimers disease. This has been proven by use of a new transgenic rat line which researchers coded McGill-R-Thy1-APP, developed in order to express the human being’s amyloid-beta precursor protein (AbetaPP) having both the Indiana and Swedish mutations under the control of murine Thy1.2 promoter (Leon, 2010).  This mono-transgenic line shows an extended stage of intraneuronal Abeta accumulation, which is already apparent within the 1st week after birth. It is widespread all over the various cortical areas as well as the hippocampus (CA1, CA2, CA3, and dentate gyrus). The homozygous Tg animals with time produce extracellular Abeta deposits. By the time these rats reach 6 months of age, a thick, thioflavine S-positive, amyloid plaques apparent in association with glial activation as well as the surrounding dystrophic neuritis (Leon, 2010).

Further, scientists developing new drugs to ensure symptomatic relief cognitive disturbances of AD can gain from much more detailed understanding of the various neurochemistry and neural correlates of the episodic memory in the AD clients (Machado, 2009).  This disease results once amyloid plaques have formed in the brain. These clamps of improperly formed proteins end up condensing outside the neurons and between the connections from one cell to the other. These proteins are made in such a way that they can be cut at specific places so that they can carry out their functions as intended. In case of Alzheimer’s, these proteins cleave within the wrong locations and lead to the formation of abnormal proteins. These proteins build up in between the cells. Therefore, the plaques reduce the capability of neurons to transmit signals from one to the other and this result in cognition failure as well as memory impairment. The synaptic connections may be destroyed and cells may also die hence adding to one’s possibility of forgetting and worsening the cognitive symptoms.

On the concept of consolidation, there exist two versions (Cowan, 2008). First, there is a total increase in the memory strength over a period of time. Secondly, consolidation is composed of decreases in trace fragility (Lee et al., 2004). As such, the overall irretrievability reduces over time although the memory trace is more resistant to decay as well as retrograde amnesia. Despite the problems my grandmother was undergoing through, she had not completely lost her memory.

She could recall the undone activities at intervals, meaning that she only forgot for a while, and then came back to her senses (Cowan, 2008). Therefore, increased research endeavors are continuing to ensure that medical intervention to Alzheimer’s disease is found. 

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