Emotion and Alzheimer’s Pathophysiology

The hallmarks of Alzheimer’s disease pathology are the cortical atrophy and decrease of neurons present in the parietal and temporal areas of the brain (Porth, 2005 p. 1238). According to Oddo (2003), the principal neuropathological characteristics of the disease involve the overexpressed (a) amyloid-beta plaques and (b) neurofibrillary tangles comprising of human tau genes. Amyloid-beta plaques are the first to develop followed by the neurofibrillary tangles (Oddo, 2003).

Neuritic or senile plaques are extracellular aggregates of neuronal degeneration produced by the accumulation of amyloid-beta fragments. According to Lezak, Howieson and Loring (2004), the main precursor of the amyloid-beta production is the wrong genetic positioning of another protein – amyloid precursor protein (APP) (p. 209). The protein substance beta-amyloid is theoretically the primary component responsible for nerve damage within the brain.

The build-up of this protein acts like plaques in the brain that eventually disrupts normal passage of electric signals from every nerve endings of the brain (Balch, 2006 p. 194). According to Porth (2005), the amyloid-neuritic plaques are primarily composed of clustered degenerating nerve terminals surrounding a core fragment amyloid beta –peptide, which is responsible for the degradation of cellular components of the neurons (e. g. cytoskeleton, etc. ) (p. 1238).

After the APP produces more amyloid peptide, the fragments gather in the terminal endings of the degenerating nerve fibers to form sludge-like substance destroying the capacity of the neurons to transmit electrical impulses to other linked neurons (Lezak, Howieson and Loring, 2004 p. 209). Once the transmission is blocked, the brain cannot anymore appropriate motor and sensory signals across the body leaving the bodily functions compromised. As the rate of atrophy in brain cells increases, ventricular enlargement occurs as a response to the diminishing mass of brain tissues (Porth, 2005 p.

1238). During the height of plaque formations, the neurofibrilliary tangles develop through the auto-twisting of axon ends after the microtubule carrier transports substances from the body cell to the axon tail (Lezak, Howieson and Loring, 2004 p. 209). In order to maintain the structure of the twisted axon fibers, the genetically altered protein called tau allow the twisting of the axons. According to Imahori, Hoshi and Ishiguro (1998), tau is a microtubule-associated protein capable of attaching itself and stabilizing microtubules.

Once tau is not removed from the cytoplasm, it becomes hyperphosphorylated and stays inside the neuron causing cellular stress and eventually death. The formations of neuritic plaques and neurofibrillary tangles cause brain lesions by replacing the nerve fibers with cellular aggregates. According to Sadock and Kaplan (2007), lesions within the parietal hemispheres of the brain, especially the right hemisphere, can cause profound functional deficits in the emotional capacities of an individual (p. 88-89).

Supported by Welsh (2006), the build-up of plaques can develop lesions that can eventually disrupt the nerve transmissions within the focal brain areas (e. g. cerebrum, hippocampus, etc. ) and, most significantly, the amygdala (p. 213). Once the lesions reached the limbic components of the brain, Alzheimer’s disease can eventually disrupt emotional function of the individual. The limbic system theoretically acts as the primary house of emotional association areas of the brain, which direct the hypothalamus to express both motor and endocrine components of the emotional state (Sadock and Kaplan, 2007 p.

89). Damage in this area can trigger deficiencies in recalling, retrieving and processing of appropriate emotions. Emotions expressed by patients with Alzheimer’s disease are not dependable due to the nature of the disease. According to Balch (2006), emotions and memories expressed by the patient cannot be stored, recalled or retrieved (p. 194). Amygdala and other limbic components perform significant role in memory enhancement for retrieval and processing of emotional information present in the individual’s brain storage (Welsh, 2006 p. 214).

Amygdala is considered as the largest basal forebrain component of the brain functioning as a receptive agent of cortical projections including emotions, sensory functions, memory and hippocampal allocortices (McGaugh, Weinberger and Lynch et al. , 1990 p. 251). As stated by Welsh (2006), “in health adults, the amount of activity in the amygdala (quantified through measurement of blood oxygenation level-dependent signal in functional MRI) during the processing of emotional information corresponds with the likelihood that emotional items will later be remembered” (p.

214). Autopsies of Alzheimer patients reveal significant atrophy in amygdala and pathological alterations, which imply signification relation to the impairment of emotion processing of Alzheimer’s patient (Emilien, Durlach and Antoniadis, 2004 p. 183). According to Lewis, Haviland-Jones and Barrett (2008), patients with damaged amygdala manifest impairments in memory and the ability to recall emotions to respond on a given scenario (p. 610). In the study of Mori, Ikeda and Nobutsugu et al. (1999), they have utilized 51 samples with probable Alzheimer’s disease.

The subjects were tested if they can remember the earthquake (stronger emotional memory) compared to the MRI event (lighter emotional memory), which was done after the four-set interview. Results show that 86. 3% (n=44; exhaustive) recalled the earthquake, while 31. 4% (n=16; exhaustive) remembered the MRI event. Based from the study, stronger emotional event is likely to be remembered than lighter emotional event. After one year, the subjects were also again tested and findings show 70% (n=14 out of 20) were able to recall the earthquake, 30% (n=6 out of 20) had already forgotten the earthquake.

After which, the samples were tested using again the four-set interview to test amygdaloid emotional memory function. In the end, the study found significant relations between amygdaloid atrophy and the capacity of the samples to recall emotional events. As supported by Lewis, Haviland-Jones and Barrett (2008), amygdala mediates emotion and memory processing of the body involving the retrieval, compilation and appropriate behavioral response (p. 610).

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