What Is The Importance Of The NE-Ergic System Degeneration In Ne Levels?

The brain changes in size and weight as a person ages. There is also a narrowing of the gyri, enlargement of the ventricles, and widening of the cerebral sulci. In AD, these changes are accelerated, causing issues such as atrophy of the cerebral cortex and loss of cortical neurons. In addition, the pre-central gyrus of the frontal lobe, superior temporal gyrus, hippocampus, and substantia nigra are all affected. Changes in neurofibrillary tangles (tangled masses of fibrous tissue throughout the neurons) , amyloid-rich senile or neuritic plague (degenerating nerve terminals in the hippocampus which contain proteins that form neurotoxic plague in the brain) and granulovascular degeneration can all occur as well.

Alzheimer’s Disease is a disease of the future. With the growing aged population, this disease, which affects primarily the elderly, will become of increasing relevance to the medical profession. Also, the high frequency of Alzheimer’s, and the high cost in labor, money, and material of caring for its victims shall put considerable burden on the society as a whole. Here, however, these issues are not going to be debated. Instead the pathology of Alzheimer’s will be reviewed to the extent it is known today.

Some area’s affected by neuronal loss are the cerebral cortex, the hippocampus, locus coeruleus, and cerebellum. Even with a single TBI, neuronal loss does occur, and evidence suggests this neuronal loss continues beyond the initial injury phase. White matter degeneration does occur as well, and while this study has little information on this, it is noted that white matter injury as well as axonal pathology has been suggested as a mechanism of rapid Aβ genesis. Also seen in neurodegeneration is neuroinflammation that is beyond repair. This inflammation continues after the initial injury in the white matter region, including the corpus callosum. Finally, changes in the cerebellar pathology are noted, in particular loss of cerebellar neurons. Smith, Johnson, & Stewart (2013) note atrophy and demyelination of the folial white matter present in those affected by

The occipital lobe is in a posterior position and the function of the occipital lobe is vision including perception and colour and movement (Stannard Gromisch, 2012). Atrophy is described as a process of tissue wastage or cell death (Lippincott Williams & Wilkins, 2006). According to (Jones & Gaillard, 2005-2013) the pathology of PCA includes Neuritic plagues and neurofibrillary tangles which are found in the parieto-occipital and temporo-occipital areas, as well as occasionally in the primary visual cortex. It is thought that PCA is a version of AD, with very little difference in the pathology. “Neuritic plagues or senile plagues are extracellular and composed of a central core of beta-amyloid peptides aggregated together with fibrils of beta-amyloid, dystrophic neurites, reactive astrocytes, phagocytic cells, and other proteins and protein fragments derived from degenerating cells or liberated from neurons” (Weerakkody & Gaillard, 2005-2013).

As a medical practitioner, I was always fascinated by the complexities of the human nervous system. A few years later, during my neurology residency training, I developed special interests in the field of neurodegenerative disorders and dementias. These are largely non-curable disorders

Figure 1 is a figure of the cross-section of a human brain. A huge degradation can be seen in the right section of the brain, which has been affected by Alzheimer’s disease.

Alzheimer’s Disease (AD) is the most common type of dementia and the sixth-leading cause of death in the United States. This neurological condition is brought on by the malfunction or death of neurons in the brain, causing changes to one’s memory, behavior, and ability to think and reason logically and clearly. There is no cure for the disease and very little available to treat the symptoms. While AD was discovered over 100 years ago by German psychiatrist Alois Alzheimer, it has only been in the last few decades that research and science have started to understand the inner workings of the neurological degeneration and possible hypothesis as to its cause. However, the physiologic changes that trigger the change in neurons still remains unknown. AD worsens as it progresses and life expectancy following diagnosis is approximately seven years; fewer than three percent of individuals will live more than 15 years after their diagnosis (Mölsä, Martlla, Rinne, 1995).

As previously discussed, the cause of AD is not well understood, which makes the diagnosis of AD more difficult as there is not one biological marker (Atchison & Dirette, 2012). AD is diagnosed by eliminating other conditions that display similar symptoms, such as Parkinson’s disease or cardiovascular disease (Atchison & Dirette, 2012). Once other conditions are ruled out, diagnostic tools such as magnetic resonance volumetry, magnetic resonance spectroscopy, diffusion-tensor imaging, cerebrospinal fluid assays, positron emission tomography, and electroencephalography can be used to detect some of the brain abnormalities that are characteristic of AD (Atchison & Dirette, 2012). These diagnostic tools are not always the most accurate, and there is not a demand for better diagnostic tools due to the lack of effective treatment options following an AD diagnosis (Atchison & Dirette, 2012).

Microglia, in the same way as vascular cells, can bind to Aβ resulting in an amplified production of cytokines, glutamate and nitric oxide (6, 7). Some studies suggest that chemokines can recruit monocytes from the peripheral blood into plaque bearing brain.(8) Related to this neuroinflammation are the alterations of type I and type II Interferon (IFN) levels in AD mice model, PDGFB-APPSwInd (J20), where an enhanced type I IFN signaling at the brain barriers and hippocampus, and decreased type II IFN response, only at the barriers were observed.(9) Of interest the blockage of IFN type I response at the central nervous system is able to partial revert the cognitive decline in aged mice.(10) However the role of this blockage on an AD mice model is still

The epsilon4 allele of apolipoprotein E4 (ApoE4) which is located in chromosome 19 is linked to the onset and progression of AD. The synaptic loss is due to a loss of cholinergic neurones which transmits nerve signals in the brain which are known to be linked to memory formation (figure 2). Amyloid plaques cause this loss.

Nevertheless, both types of AD are recognised pathologically by the build-up of intracellular neurofibrillary tangles, extracellular amyloid plaques, and massive neuronal and synaptic loss (Carmo & Cuello, 2013). Neurofibrillary tangles are aggregates of hyper-phosphorylated tau protein and plaques are mostly insoluble deposits of β-amyloid, resulting from the cutting of the amyloid precursor protein (APP) (Farooqui & Farooqui, 2011). The discovery of mutations in the APP gene which cause familial AD lead to the articulation of the amyloid cascade hypothesis (ACH) (Hardy & Asllop, 1991). A large amount of evidence supports this view; however a number of findings are contrary to its proposal. As a result, Armstrong (2011) proposed a revision of the hypothesis, postulating that the main trigger for the development of the disease is the ageing of the brain and related wear and tear such as head trauma and stress; collectively referred to as the “allostatic load” (Carroll, 2002). Furthermore, a greater emphasis has now been placed on the role of small, soluble amyloid oligomers which seem to be the cause of early cell dysfunction in AD, rather than the large, insoluble amyloid fibrils. (Ferreira, Vieira & De Felice, 2007).

The neuropathological hallmarks of AD are the presence of plaques and neurofibrillary tangles. (18 -20)

Therefore, RNFL measurements have been extensively used in research to assess neurodegeneration (Jones-Odeh, 2015; Satue et al., 2010). Several studies have demonstrated significant thinning of the superior quadrant of the RNFL in patients with AD compared with control subjects, which has been calculated by some researcher to be around 10 to 11 μm (Berisha et al., 2007; Keslet et al., 2011; Ohno-Matsui, 2011).

Emerging evidence demonstrates neuroinflammation as a crucial pathophysiology of AD, specifically impacted by microglia and astroglia. 3 The microglia are distributed evenly across the brain and are activated by protein aggregation and neuronal cell death. 3 Specifically related to AD, the two chief proteins involved are amyloid-B and tau.3 An accumulation of microglia around amyloid-B plaques has been documented in post-mortem human brains and in animal models with AD.3 Research has yet to clearly determine if microglial activation plays a beneficial or detrimental role in the progression of AD..3 Some reports suggest that microglia are attracted to

Another clue may be the effects the aging process has on the brain as it is harming the neurons in the brain causing the disease (NIA, 2012). Regardless of the cause, AD is a life altering disease in every aspect of the victim’s life.