Microbiome & Chronic Diseases

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Amyloid-beta {90000281}

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Shared Reference Notes

  • [1.1] [#Alzheimer’s disease] [#Chlamydia pneumoniae
    - Among different types of microbes, #Human immunodeficiency virus-1 (HIV-1), #Herpes simplex virus-1 (HSV-1), Chlamydia pneumonia, #Spirochetes and #Candida albicans are frequently detected in the brain of AD patients. - Amyloid-beta protein has demonstrated to exhibit antimicrobial properties upon encountering these pathogens.
  • [1.2] [#Alzheimer’s disease] [#Bacteroides fragilis
    - Presence of #Amyloid deposits was associated with greater abundance of proinflammatory taxa (#Escherichia/#Shigella), which were in turn correlated with proinflammatory cytokines, and with reduced abundance of #Eubacterium rectale and B. fragilis, 2 taxa with anti-inflammatory activity
  • [1.3] [#Alzheimer’s disease] [#Fusobacterium nucleatum] [#Lipopolysaccharide
    - antibodies to F. nucleatum can be detected in the serum of patients with AD or cognitive impairment. - F. nucleatum activates microglial cells causing morphological changes, accelerated proliferation and enhanced expression of TNF-α and IL-1β in microglial cells. - LPS promoted the proliferation of brain microglia - F. nucleatum-induced periodontitis resulted in the exacerbation of Alzheimer’s symptoms in 5XFAD mice including increased cognitive impairment, beta-amyloid accumulation and Tau protein phosphorylation in the mouse cerebrum. - The stimnuli like LPS, Aβ or IFN-γ would activate microglial M1 phenotype, leading to the expression of pro-inflammatory cytokines and irreversible neuron loss. - The main known virulence factors of F. nucleatum include FadA, Fap2, and LPS
  • [1.4] [#Alzheimer’s disease] [#Porphyromonas gingivalis] [#Gingipains
    - AβPP is an infection responsive protein cleaved via the amyloidogenic pathway on exposure to conditioned medium and in the presence of pro-inflammatory mediators.
  • [1.5] [#Alzheimer’s disease
    - many people accumulate amyloid plaques in the brain as they age, but only some of these people go on to develop dementia. - dementia symptoms may result not from the formation of insoluble plaques but from a lack of soluble amyloid beta protein.
  • [1.6] [#Alzheimer’s disease
    - #Fusobacterium nucleatum can increased TNF-α and IL-1β expression in microglial cells, and also in vivo it can increase cognitive impairment, beta-amyloid accumulation and Tau protein phosphorylation in the cerebrum of an AD animal model.
  • [1.7
    - #Chlamydia pneumoniae can infect the olfactory and trigeminal nerves, olfactory bulb and brain within 72 h in mice. - #Chlamydia pneumoniae infection also resulted in dysregulation of key pathways involved in #Alzheimer’s disease pathogenesis at 7 and 28 days after inoculation. - Amyloid beta accumulations were also detected adjacent to the #Chlamydia pneumoniae inclusions in the olfactory system. - Injury to the nasal epithelium resulted in increased peripheral nerve and olfactory bulb infection, but did not alter general CNS infection.
  • [1.8] [#Alzheimer’s disease] [#Saccharomyces boulardii] [#Lipopolysaccharide] [#Probiotic
    - S. boulardii significantly reduced the elevated levels of serum interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, as well as hippocampal levels of NLRP3 and caspase-1 in the LPS model. - S. boulardii alleviated amyloid-β deposition in the rat hippocampus. - S. boulardii could inhibit memory impairment, neuroinflammation, and amyloid-β accumulation induced by LPS, possibly by modifying the gut microbiota.
  • [1.9] [#Alzheimer’s disease] [#Brain-derived tau, #Short Chain Fatty Acid] [#ApoE4 allele
    - Amyloid-Beta is a necessary factor in AD pathogenesis, its accumulation in and of itself is insufficient for neurodegeneration and cognitive decline. - pathological tau accumulation is closely linked with neurodegeneration and cognitive decline in AD and primary tauopathies. - apolipoprotein E (ApoE) isoforms, which strongly influence AD risk and regulate tau-mediated neurodegeneration, differentially affect the gut microbiota. - microbially produced short-chain fatty acids (SCFAs) are mediators of the neuroinflammation-neurodegeneration axis. - Supplementation of SCFAs to GF TE4 mice resulted in more reactive glial morphologies and gene expression as well as increased p-tau pathology.
  • [#Alzheimer’s disease] - high-fat diets and #Obesity are associated with increased risk for developing AD and #Dementia. - the incidence of AD is higher in countries that typically consume high-fat diets as opposed to low-fat diets. - Increased Aβ plaques in the brain after consumption of a high fat diet has been observed in mouse models of amyloidosis. - a #High-fat diet can result in an increase in neuroinflammation and decreased performance on AD-related behavior tests.
  • [#Alzheimer’s disease] - All humans produce Aβ40 and Aβ42 throughout life and levels of these proteins are relatively high in both the CSF and serum throughout life. - Aβ plaques can be present in cognitively normal individuals. This suggests that perhaps Aβ is present for a reason and serves a beneficial physiologic purpose in the human body. - Several bacteria and viruses > enhance amyloidogenic processing and subsequent Aβ production. - Aβ plaques in humans contain viral and bacterial DNA. - Aβ have similar structure to other antimicrobial peptides. - Aβ protects against infection in mouse, cell culture, and C elegans models. - Perhaps Aβ is initially increasingly produced as a response to real or perceived brain infection, but too much Aβ production eventually becomes detrimental by inducing neuronal toxicity, excessive neuroinflammation, and pathological tau seeding.
  • [#Alzheimer’s disease] - levels of Aβ are increased when mice and human are awake and decrease when they are asleep. - These diurnal oscillations in Aβ levels in brain ISF are dissipated and the #Sleep–wake cycle is disrupted after Aβ plaque formation in the APP/PS1 mouse model of amyloidosis. - amelioration of Aβ plaque pathology with Aβ immunotherapy restored a normal #Sleep wake cycle and diurnal oscillations in Aβ levels in the mice. - Lower neuronal activity during #Sleep likely leads to less Aβ production.
  • - higher #Mediterranean diet adherence led to higher grey matter volume, better memory, lower Aβ, and lower phosphorylated tau
  • [1.11] [#Alzheimer’s disease] [#Brain-derived tau
    - adding #Cinnamon or cinnamaldehyde to a cell medium can reduce tau aggregation, Amyloid β and increase cell viability. - #Cinnamon might be useful for preventing and reducing cognitive function impairment.

References Notes

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Common References