Idiopathic Parkinson's disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen
Abstract
The progressive, neurodegenerative process underlying idiopathic Parkinson's disease is associated with the formation of proteinaceous inclusion bodies that involve a few susceptible neuronal types of the human nervous system. In the lower brain stem, the process begins in the dorsal motor nucleus of the vagus nerve and advances from there essentially upwards through susceptible regions of the medulla oblongata, pontine tegmentum, midbrain, and basal forebrain until it reaches the cerebral cortex. With time, multiple components of the autonomic, limbic, and motor systems become severely impaired. All of the vulnerable subcortical grays and cortical areas are closely interconnected. Incidental cases of idiopathic Parkinson's disease may show involvement of both the enteric nervous system and the dorsal motor nucleus of the vagus nerve. This observation, combined with the working hypothesis that the stereotypic topographic expansion pattern of the lesions may resemble that of a falling row of dominos, prompts the question whether the disorder might originate outside of the central nervous system, caused by a yet unidentified pathogen that is capable of passing the mucosal barrier of the gastrointestinal tract and, via postganglionic enteric neurons, entering the central nervous system along unmyelinated praeganglionic fibers generated from the visceromotor projection cells of the vagus nerve. By way of retrograde axonal and transneuronal transport, such a causative pathogen could reach selectively vulnerable subcortical nuclei and, unimpeded, gain access to the cerebral cortex. The here hypothesized mechanism offers one possible explanation for the sequential and apparently uninterrupted manner in which vulnerable brain regions, subcortical grays and cortical areas become involved in idiopathic Parkinson's disease.
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Inflammation and oxidative stress are caused by swallowing nasal secretions, which leads to the accumulation of α-synuclein in the CNS.
“Inflammation and oxidative stress are caused by swallowing nasal secretions, which leads to the accumulation of a-synuclein in the CNS.134”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [134]
The vagal nerve might provide a path for the spread of alpha-synuclein pathology from the enteric nervous system to the brain through the brainstem, midbrain, basal forebrain, and cortical areas.
“The vagal nerve might provide a path for the spread of alpha-synuclein pathology from the ENS to the brain through the brainstem, midbrain, basal forebrain and finally the cortical areas (Braak et al., 2003;Hawkes et al., 2007)”
From The Gut-Brain Axis in Parkinson’s Disease: Possibilities for Food-Based Therapies (2017) · cites this paper as Braak et al., 2003
A toxin or pathogen and associated immune/inflammatory responses might start the detrimental process in the enteric nervous system and/or olfactory bulbs and spread via the vagal nerve and olfactory tract to the substantia nigra and further areas of the central nervous system.
“where a toxin or a pathogen and associated immune/inflammatory responses might start the detrimental process and spread according to a specific pattern, via the vagal nerve and olfactory tract respectively, to the SN and further areas of the CNS”
From The Gut-Brain Axis in Parkinson’s Disease: Possibilities for Food-Based Therapies (2017) · cites this paper as Braak et al., 2003
Alpha-synuclein deposition in neurons might begin in the enteric nervous system and/or in the olfactory bulbs.
“new evidence suggests that alpha-synuclein deposition in neurons might begin in the ENS and/or in the OB”
From The Gut-Brain Axis in Parkinson’s Disease: Possibilities for Food-Based Therapies (2017) · cites this paper as Braak et al., 2003
Braak and colleagues hypothesized that alpha-synuclein pathology might start in the olfactory bulbs and/or enteric nervous system by an unknown pathogen and/or environmental toxin and then progress to the substantia nigra and further areas of the central nervous system.
“Braak and colleagues hypothesized that alpha-synuclein pathology might start in either the OB and/or in the ENS possibly by an unknown pathogen and/or environmental toxin and then progresses towards the SN and further areas in the CNS.”
From The Gut-Brain Axis in Parkinson’s Disease: Possibilities for Food-Based Therapies (2017) · cites this paper as Braak et al., 2003
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“It has been suggested that α-syn pathology may begin within the ENS and propagate up to midbrain regions through the vagal nerve afferents [35, 54, 55].”
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“The neuropathological hallmarks of PD include the loss of dopaminergic neurons in substantia nigra (SN) and the formation of neuronal protein inclusions known as Lewy bodies (LB) (Braak et al., 2003).”
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Aspects of innate immunity and Parkinson's disease
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Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain
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“Non-motor symptoms, such as autonomic failure, fatigue, depression, and anxiety are also prevalent and this is likely due to an additional involvement of non-dopaminergic systems [2].”
BackgroundALS Untangled No. 21: Fecal transplants
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- Authors
- Braak, H., R�b, U., Gai, W. P., & Del Tredici, K.
- Affiliations
- Goethe University Frankfurt (DE)
- Flinders University (AU)
- ORCID
- Braak, H.
- Venue
- Journal of Neural Transmission
- Published
- 2003-05-01
- Volume
- 110
- Issue
- 5
- Pages
- 517-536
- ISSN
- 0300-9564 (ISSN-L)
- 1435-1463
- OpenAlex
- W2044908785
- Cited by
- 1,683
- References
- 102
- Citations by year
- 2026: 72 · 2025: 118 · 2024: 120 · 2023: 132 · 2022: 161 · 2021: 170 · 2020: 129 · 2019: 107 · 2018: 84 · 2017: 84 · 2016: 67 · 2015: 66 · 2014: 56 · 2013: 55 · 2012: 44
- FWCI
- 8.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neural Transmission (publishedVersion)
- PubMed (publishedVersion)
- Flinders Academic Commons (Flinders University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- idiopathic Parkinson's disease, neuroinvasion, neurodegeneration, dorsal motor nucleus of the vagus, enteric nervous system, transneuronal transport, retrograde axonal transport, subcortical gray matter
- MeSH terms
- Brain, Brain Stem, Humans, Neural Pathways, Neurons, Parkinson Disease, Severity of Illness Index, Vagus Nerve, Disease Progression
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