Propionibacterium acnes in the cortex of patients with Alzheimer's disease

Hh, Kornhuber

doi:10.1007/bf02274902

Cited by 31 publications

(17 citation statements)

References 15 publications

(16 reference statements)

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“…However, the consistently high levels seen here in AD samples compared to normal brains and the apparent minimal contribution of post mortem interval along with the lack of significant contact with skin makes contamination an unlikely explanation for the P. acnes content of these data. Furthermore, the physiological characteristics of P. acnes (Buchanan et al, 1982; Bhatia et al, 2004; McDowell et al, 2013; Tanghetti, 2013), including its known ability to grow slowly in the cortex (Kornhuber, 1996), would make P. acnes a good candidate for a bacterial source of neuroinflammation in AD brains and the bacterial reads seen here would warrant further investigation.…”

Section: Discussionmentioning

confidence: 90%

“…acnes to non-specifically stimulate the innate immune system is well documented (Tanghetti, 2013): it secretes chemotactic and proinflammatory cytokine-inducing factors and can activate complement pathways and produces hyaluronidases, proteases and neuraminidases, thought to cause epithelial permeabilization and inflammatory infiltration (Bhatia et al, 2004). It is interesting to note that P. acnes was cultured from three out of four biopsies from AD-affected brains (Kornhuber, 1996). P. acnes is a well-documented contaminant of NGS techniques as shown by no template controls and of clinical samples that have unavoidable contact with skin (Lusk, 2014; Salter et al, 2014; Mollerup et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

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16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain

Emery

Shoemark²,

Batstone

et al. 2017

Front. Aging Neurosci.

256

211

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The neurological deterioration associated with Alzheimer’s disease (AD), involving accumulation of amyloid-beta peptides and neurofibrillary tangles, is associated with evident neuroinflammation. This is now seen to be a significant contributor to pathology. Recently the tenet of the privileged status of the brain, regarding microbial compromise, has been questioned, particularly in terms of neurodegenerative diseases. It is now being considered that microbiological incursion into the central nervous system could be either an initiator or significant contributor to these. This is a novel study using 16S ribosomal gene-specific Next generation sequencing (NGS) of extracted brain tissue. A comparison was made of the bacterial species content of both frozen and formaldehyde fixed sections of a small cohort of Alzheimer-affected cases with those of cognitively unimpaired (normal). Our findings suggest an increase in bacterial populations in Alzheimer brain tissue compared with normal.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain

Emery

Shoemark²,

Batstone

et al. 2017

Front. Aging Neurosci.

256

211

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“…These experimental data [107,89] indicate that as observed in syphilis [29,61,62] and Lyme neuroborreliosis [85,89], the evasion of spirochetes can result in their survival and proliferation and the production of lesions similar to senile plaques, tangles and granulovacuolar-degenerations (Figure 3). Additional experimental data include transmission of Aβ amyloidosis to experimental animals [200-203], the observations showing the immune regulatory function of APP [171-173], the antimicrobial properties of Aβ [174] and the improvement in symptoms of AD patients following antibiotic treatment [204-208]. Further research and clinical trials would be primordial.…”

Section: Analysis Of Causal Relationship Between Spirochetes and Ad Fmentioning

confidence: 99%

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria

Miklóssy

2011

J Neuroinflammation

316

284

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It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 × 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases. Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro by exposure of mammalian cells to spirochetes. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

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“…The surviving cells are able to expel strongly inflammatory components including LPSs [16]. The imputed role of pathogens in AD has been extensively reported for about over 200 different helical bacterial spirochete species [17], which may co-infect with other Gram-negative phylotypes [18][19][20][21][22][23][24][25][26][27][28][29].…”

Section: Introductionmentioning

confidence: 99%

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

Andreadou

Pantazaki

Daniilidou

et al. 2017

JAD

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Abstract. Alzheimer's disease (AD) has been attributed to chronic bacterial infections. The recognition of human microbiota as a substantial contributor to health and disease is relatively recent and growing. During evolution, mammals live in a symbiotic state with myriads of microorganisms that survive at a diversity of tissue micro-surroundings. Microbes produce a plethora of secretory products [amyloids, lipopolysaccharides, virulence factors rhamnolipids (RLs), toxins, and a great number of neuroactive compounds]. The contribution of infectious microbial components to the pathophysiology of the human central nervous system including AD is considered potentially substantial, but the involvement of the RLs has never been reported. Here, RLs were isolated from serum and identified through various conventional methods including the colorimetric orcinol method, thin-layer chromatography, attenuated total reflection Fourier transform infrared (ATR-FTIR), and dot blot using antibodies against RLs. Dot blot demonstrated elevated RL levels in sera of AD patients compared to controls (p = 0.014). Moreover, ELISA showed similarly elevated RL levels in cerebrospinal fluid of both AD (0.188 versus 0.080) (p = 0.04) and mild cognitive impairment (0.188 versus 0.129) (p = 0.088) patients compared to healthy, and are wellcorrelated with the AD stages severity assessed using the Mini-Mental State Examination. These results provide conclusive evidence for the newly-reported implication of RLs in AD, adding it to the list of bacterial components, opening new avenues for AD investigation. Moreover, they strengthen and vindicate the divergence of research toward the exploration of bacterial involvement in AD generation and progression.

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Propionibacterium acnes in the cortex of patients with Alzheimer's disease

Cited by 31 publications

References 15 publications

16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain

16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

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