Golgi apparatus in Alzheimer’s disease

Baloyannis, Stavros J.

doi:10.15406/jnsk.2015.02.00056

Cited by 5 publications

(2 citation statements)

References 31 publications

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“…A substantial number of cellular and biochemical mechanisms contribute in shaping the multifactorial pathogenetic background of the disease. In the neuropathological profile of Alzheimer's disease, selective neuronal loss [1], synaptic alterations [2], tau pathology [3], extracellular deposits of polymers of Aβ peptide [4], inflammatory responses [5] and morphological alterations of the cell organelles [6] are the most common phenomena in light and electron microscopy.…”

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confidence: 99%

Mitochondria: Strategic Point in the Field of Alzheimer’s Disease

Baloyannis¹

2016

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confidence: 99%

Mitochondria: Strategic Point in the Field of Alzheimer’s Disease

Baloyannis¹

2016

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“…Electron microscopy enlarges the horizons of morphological alterations in AD visualizing clearly the substantial synaptic loss in association with marked alterations of the organelle involving mostly mitochondria [6], Golgi apparatus (GA) [7,8], and endoplasmic reticulum (ER) [9] clearly observed even in areas of the brain, where dendritic plaques and neurofibrillary tangles are infrequent.…”

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confidence: 99%

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2015

JNSK

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The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease

Rubin

Glazer

2017

Immunobiology

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While a number of endogenous risk factors including age and genetics are established for Alzheimer's disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD.

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Golgi apparatus in Alzheimer’s disease

Cited by 5 publications

References 31 publications

Mitochondria: Strategic Point in the Field of Alzheimer’s Disease

Mitochondria: Strategic Point in the Field of Alzheimer’s Disease

Untitled

The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease

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