The most common chronic disease of the memory is Alzheimer’s disease, which is characterized by the continuous degeneration of neurons in the brain while being replaced senile plaques and neurofibrillary tangles (Sadock and Kaplan, 2007 p. 88). According to Balch (2006), “Alzheimer’s disease is characterized by the progressive mental deterioration to such a degree that it interferes with one’s ability to function socially and at work” (p. 193). The most frightening effects of the disease are the degradation of cognitive capacity, memory and emotions of the person.
Initial courses of the disease progression are the gradual cellular damage in the hippocampus until it invades the nearby prefrontal and parietal areas of the brain. According to Sadock and Kaplan (2007), Alzheimer’s disease usually disrupts the motor and sensory functions related to the parietal area of the brain, such as language comprehension and visual organization (p. 88). Alzheimer patients also manifest general symptoms in behavioral and psychological domains manifested in their disturbed perceptions of reality, thoughts, mood and behavior (Behavioral and Psychological Symptoms of Dementia – BPSD; Blackburn and Dulmus, p.
333). Risk factors of the disease are usually genetics and aging. According to Porth (2005), the risk for developing Alzheimer’s disease increases as an individual ages, which justifies the number of Alzheimer patients in the increased older demographics of United States (p. 1238). Hereditary risk of acquiring the disease is doubled if anyone from the first-degree level acquired Alzheimer’s disease, while only a small number of cases have attained the disease through genetic mutation (Lezak, Howieson and Loring, 2004 p.
208). On the other hand, the impact of the disease in emotional capacity of an individual becomes more expressed during the terminal phase of the disease. According to the study of Hargrave, Maddock and Stone (2002), Alzheimer patients lack the basic capacities of emotion processing mechanisms, namely (a) facial emotion matching, (b) facial emotion labeling, and (c) emotion differentiation. In Alzheimer patients, memory impairments are often linked with the impairments of their emotion processing centers.
Anatomical structures involved in the memory impairment, such as amygdala, hippocampus, limbic system, right hemisphere, etc, are also involved in the impairment of emotion functions (Hatano, Okada and Tanabe, 2000 p. 108). According to different studies, the two components associated to the impairments of emotion among Alzheimer’s patients are (a) deficits in perception of emotion associated in the damages of the right temporoparietal region and (b) deficits in negative emotions involving the damage of amygdala – one of the essential components of the limbic system (Morris and Becker, 2004 p.
268). The damages in these areas are caused by neuropathological malformations causing lesions in the brain. In the study of Sheng, Mrak and Griffin (1997), they have found that cellular inflammation brought by the activated brain microglia acts as the driving force in the diffusion of amyloid deposits into neuritic plaques. According to the study, the activated microglia overexpresses a neuroactive cytokine interleukin-1 leading to the evolution of amyloid plaques among patients with Alzheimer’s disease.
On the other hand, the genetic neuropathological component of the disease – neurofibrillary tangles – has been observed to increase according to the neuronal loss and severity of the disease progression (Gomez-Isla, Hollister and West et al. , 1997). Neurofibrillary tangles are protein derivatives comprising of hyperphosphorylation and taus microtubule, which acts as insoluble aggregates in the brain (Perry, 2006 p. 219-220). According to the study of Oddo (2003), Amyloid-beta plaques first developed prior to the neurofibrillary tangles.
Increase in the levels of neurofibrillary tangles and plaques cause the replacement of brain neurons, which eventually disrupts the normal pathways of nerve transmission (Blazer, Steffens and Busse, 2004 p. 213). Aside from the decrease and replacement of brain neurons, decline in the cognitive function has also been associated to the lesions present in the synapses preventing the transmission of signals from different nerve cells of the brain (Sadock and Kaplan, 2007 p. 88).