Yıl 2018, Cilt: 10 Sayı : 3 Sayfalar 793 - 793 2018-08-18
Dysbiosis of gut microbiota and Alzheimer’s Disease
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Öz Alzheimer's Disease (AD) is a degenerative, chronic, progressive disease of CNS. Pathological changes that develop in the course of the disease lead to memory loss, alteration of thought, and deterioration of other brain functions. The disease progresses slowly, resulting in cell death and brain damage (Jiang 2017; Knopman 2016). Increased permeability of the intestinal and blood brain barrier due to microbial dysbosis plays a role in the pathogenesis of AD and other neurodegenerative disorders associated with aging. In addition, intestinal microbiota bacterial populations secrete amyloids and lipopolysaccharides in large quantities, which may contribute to the modulation of signaling pathways and the production of proinflammatory cytokines associated with the pathogenesis of AD (Jiang 2017). Amyloid precursor protein (APP) , which constitutes Aβ plaques and is normally secreted by intestinal bacteria, is expressed by the enteric nervous system. However, the accumulation corrupts the CNS functions. Escherichia Coli and Salmonella Enterica are some of the many bacterial strains that express and secrete APP and play a role in the pathogenesis of AD (Tse 2017). Production and clearance of Aβ in CNS is a dynamic change and some bacteria and fungi are amyloid secretions, which disrupt the dynamic balance of Aβ protein in CNS and increase the amyloid levels. This causes Aβ protein accumulation in the brain and a high risk of AD (Hill 2015).It is very important for cognitive function in serotonin, 95% of serotonin is synthesized in intestines and intestinal microorganisms play an important role in the synthesis of serotonin. There is evidence that serotonin may reduce the formation of Aβ plaques and thus reduce AD risk (Hill 2015; Jiang 2017).

Anahtar Kelimeler

Microbiota, Dysbiosis, Alzheimer disease
Hill JM, Lukiw WJ. 2015. Microbial-generated amyloids and Alzheimer's disease (AD). Front Aging Neurosci. 7:9.
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Yayımlanma Tarihi 18 Ağustos 2018
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Yayımlanma Tarihi : 18 Ağustos 2018

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