Two New Lesions in Alzheimer's Disease

Averback, P.

doi:10.1016/s0140-6736(83)91256-4

Cited by 103 publications

(32 citation statements)

References 6 publications

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“…Accordingly, periodontal invasive spirochetes were detected along the trigeminal nerve and in trigeminal ganglia [96]. They might also propagate along the fila olfactoria and tractus olfactorius, which would be in harmony with the olfactory hypothesis [122-124] and with previous observations showing that the olfactory tract and bulb are affected in the earliest stages of the degenerative process in AD [125]. …”

Section: Mechanisms Involved In Spirochete-host Interaction and Theirmentioning

confidence: 68%

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

Miklóssy

2011

J Neuroinflammation

309

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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Section: Mechanisms Involved In Spirochete-host Interaction and Theirmentioning

confidence: 68%

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

Miklóssy

2011

J Neuroinflammation

309

284

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“…84, 85 In addition, the anterior olfactory nucleus and olfactory bulb are the two primary brain regions commonly affected in AD. 86, 87 Indeed, change in olfactory identification has been strongly associated with pathological changes in the medial temporal lobe structures. 88 These studies strongly imply a primary role for olfactory dysfunction as an indicator of pathological cognitive decline and dementia.…”

Section: Discussionmentioning

confidence: 99%

Olfactory discrimination predicts cognitive decline among community-dwelling older adults

et al. 2012

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The presence of olfactory dysfunction in individuals at higher risk of Alzheimer's disease has significant diagnostic and screening implications for preventive and ameliorative drug trials. Olfactory threshold, discrimination and identification can be reliably recorded in the early stages of neurodegenerative diseases. The current study has examined the ability of various olfactory functions in predicting cognitive decline in a community-dwelling sample. A group of 308 participants, aged 46–86 years old, were recruited for this study. After 3 years of follow-up, participants were divided into cognitively declined and non-declined groups based on their performance on a neuropsychological battery. Assessment of olfactory functions using the Sniffin' Sticks battery indicated that, contrary to previous findings, olfactory discrimination, but not olfactory identification, significantly predicted subsequent cognitive decline (odds ratio=0.869; P<0.05; 95% confidence interval=0.764−0.988). The current study findings confirm previously reported associations between olfactory and cognitive functions, and indicate that impairment in olfactory discrimination can predict future cognitive decline. These findings further our current understanding of the association between cognition and olfaction, and support olfactory assessment in screening those at higher risk of dementia.

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“…Olfactory thresholds also correlate with degree of dementia (Murphy et al, 1990). Increased olfactory impairment in those with Alzheimer’s disease (AD) and those at risk for AD may be due to physiological changes during early stages of the disease, specifically in areas involved in olfactory processing such as the olfactory bulb, anterior olfactory nucleus, parahippocampal gyrus, hippocampus, amygdala, and orbitalfrontal, insular and temporal neocortex (Averback, 1983; Braak and Braak, 1997, Christen-Zaech, et al, 2003; Esiri and Wilcock, 1984; Getchell et al, 2003; Ohm and Braak, 1987; Price 1993, 1997; Price et al, 1991; Reyes et al, 1985; Struble and Clark, 1992). …”

Section: Introductionmentioning

confidence: 99%

Abnormal event-related potentials in young and middle-aged adults with the ApoE ε4 allele

Corby¹,

Morgan²,

Murphy³

2012

International Journal of Psychophysiology

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The largest genetic susceptibility factor for Alzheimer’s disease is the Apolipoprotein E (ApoE) ε4 allele. Cognitive decline and olfactory impairment are greater in those positive for the ε4 allele. This study sought to determine if the olfactory event-related potential (OERP), compared to the visual ERP, would be sensitive to these subtle declines. Participants included 40 individuals from two age groups, half of each group were ε4 allele positive and half were ε4 negative. Visual ERPs did not demonstrate significant differences between ApoE groups. OERPs demonstrated robust age by ApoE interactions. P3 latencies were significantly longer in ε4 young and middle age participants. These findings suggest that very early olfactory and cognitive changes related to ApoE status are detectible via the OERP.

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Two New Lesions in Alzheimer's Disease

Cited by 103 publications

References 6 publications

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

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

Olfactory discrimination predicts cognitive decline among community-dwelling older adults

Abnormal event-related potentials in young and middle-aged adults with the ApoE ε4 allele

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