The Neuron-inflammatory Effects of Intracellular A[beta]

Released on by Lindsay Welikovitch
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  • The Neuron-inflammatory Effects of Intracellular A[beta] Book Detail

  • Author : Lindsay Welikovitch
  • Release Date : 2021
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  • File Size : 11,11 MB
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The Neuron-inflammatory Effects of Intracellular A[beta] by Lindsay Welikovitch PDF Summary

Book Description: "AbstractDespite being the most common cause of dementia worldwide, there are still no available drugs to prevent or cure Alzheimer’s disease (AD). In addition to the deposition of amyloid-[beta] (A[beta]) plaques and tau neurofibrillary tangles (NFT) as hallmark brain lesions, the AD neuropathology comprises a significant immunological component. That inflammation is likely a contributory factor in the AD pathogenesis is evidenced by the fact that chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) in cognitively healthy adults protects against disease development. It is widely presumed that dense amyloid plaques and accumulating cellular debris represent the primary inflammatory stimuli within the AD brain. However, inflammation is frequently observed in AD transgenic animal models devoid of plaques and cell death. Since the basis of this early inflammatory reaction remains unexplored, investigations characterizing these preclinical AD immune processes may reveal promising therapeutic targets for early disease intervention. Chapter 1 of this Thesis serves as a review of the fundamental characteristics of the AD neuropathology and an evaluation of the current status of the field at large. While low molecular weight soluble oligomers are the most potent amyloid species within the brain, several technical limitations have historically prevented direct inspection of the soluble amyloid pool within the human brain; thus, it is unclear exactly how it evolves before overt plaque deposits become apparent. Using exquisitely preserved post-mortem human brain material, in Chapter 2, we demonstrate that soluble amyloid peptides and oligomers accumulate within the intraneuronal compartment in brain areas that are most vulnerable to early pathology and degeneration. Our findings implicate the buildup of intraneuronal A[beta] as a potential pathogenic factor in AD, instigating cellular damage from the ‘inside-out’. Chapter 3 describes the neuroinflammatory effects of this same iA[beta] pool within a transgenic rat model of the AD-like amyloid pathology, as well as human brain. Given that inflammation is a major determinant in driving disease progression, we asked how iA[beta] might provoke a plaque-independent neuroinflammatory environment. By analyzing neuron-specific inflammatory gene and protein expression, we discovered that neurons burdened with increasing levels of soluble A[beta] engage in well-known inflammatory signaling cascades and are associated with responsive microglial cells. Together, our findings reveal the neuron as an understated suspect in triggering harmful neuroinflammation during early stages of disease. Finally, in Chapter 4, we will review the known biological mechanisms that mediate iA[beta]-toxicity and consider how they might trigger a neuronal inflammatory reaction. By discussing the processes underlying complex neuroglial interactions during health and disease, we will examine how they may similarly contribute to the development and progression of neural deficits during early AD. And lastly, we will reconcile certain aspects of the disputed amyloid cascade hypothesis with a novel ‘plaque-independent’ amyloid hypothesis, while proposing novel therapeutic avenues for combatting disease onset"--

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