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Neurodegenerative Disorders: Alzheimer’s Disease Essay

2265 words - 10 pages

Neurodegenerative Disorders: Alzheimer’s Disease

1. Amyloid Precursor Protein (APP)
Alzheimer’s disease (AD) remains a major cause of senile dementia, which is characterised by an impairment of neuronal and synaptic function in addition to the accumulation of β-amyloid plaque and formation of neurofibrillary tangles within distinct portions of the brain (De Strooper and Annaert, 2000). Progression of this distinct pathology of neurodegeneration does not typically vary from patient to patient, beginning in cerebral cortex before targeting the hippocampus, neocortex as well as the sub-cortical nuclei (Braak and Braak, 1995). The role of amyloid precursor protein (APP) in the ...view middle of the document...

Extracellular cleavage of APP at the carboxyl terminus of Aβ is mediated by γ- secretase, giving rise to the formation of one of two products: either p3, which is a 3kDa product generated in collaboration with α-secretase activity, or Aβ, which is generated in cooperation with BACE1 activity, in addition to the APP intracellular domain (AICD) (Iwatsubo, 2004).
Figure 1: The α-secretase pathway leads to the formation of P3 and is non- amyloidogenic, whereas the β-secretase pathway is amyloidogenic, resulting in the formation of the amyloid plaque-forming Aβ protein. Products of both pathways are critical for the maintenance of neuron development and function and usually only about 10% of APP enters the amyloidogenic pathway depending on age, and other environmental causes (Figure adapted from La Ferla et al., 2007)
Figure 1: The α-secretase pathway leads to the formation of P3 and is non- amyloidogenic, whereas the β-secretase pathway is amyloidogenic, resulting in the formation of the amyloid plaque-forming Aβ protein. Products of both pathways are critical for the maintenance of neuron development and function and usually only about 10% of APP enters the amyloidogenic pathway depending on age, and other environmental causes (Figure adapted from La Ferla et al., 2007)
APP Processing
APP Processing


Other proteins besides Aβ have been implicated in the pathogenesis of AD, most notably Tau and to a lesser extent, Apiloprotein E (ApoE). Tau is a microtubule-associated protein that when hyper-phosphorylated comprises the main component of neurofibrillary tangles, another hallmark of AD. When Tau is hyper-phosphorylated, conformational changes within the protein prevent normal binding to microtubules. Tau instead detaches and forms helical filaments making them more prone to aggregation, and it is this accumulation of Tau protein along with microtubule rearrangements that trigger neurodegeneration (Götz et al., 2004).
ApoE is normally found circulating in the cardiovascular system where it interacts with low density lipoprotein receptors (LDLRs) to regulate plasma lipoprotein as well as cholesterol levels. This protein is manufactured in the liver before being transported to numerous organs of the body. In the brain however, ApoE is generated by astrocytes and is thought to contribute to neuronal growth and plasticity in addition to the formation of synapses and dendrites. Three alleles of the apoE gene exist, giving rise to three distinct isoforms, ApoE2, E3 and E4. Each isoform is associated with a distinct risk of disease, and the presence of the ApoE4 isoform has been linked to an increased propensity to develop AD (Warrington and Rodriguez, 2010).

2. Models of Alzheimer’s Disease

Due to the remarkable genomic similarities between mouse and man, transgenic mice have traditionally been utilised as models of human disease in an attempt to uncover novel therapies. This method of overexpressing or...

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