Idiopathic Parkinson's disease: possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen

By H. Braak, Udo Rüb, W. Gai, K. Del Tredici. Journal of neural transmission, 2003

1,600 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/fdf67f056aa53225f486c2152c4df5d11fd54acb

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Citations in the corpus

The Impact of Diet and Lifestyle on Gut Microbiota and Human Health (2014, background): “coli and greater endotoxin (LPS) exposure, and these changes correlate with the enteric neuronal damage [143], leading to suggestions that a pathogen may be responsible for PD [144] and a breakdown in mucosal barrier function may play a central role.”
Vagotomy and subsequent risk of Parkinson's disease (2015, background): “nasal and/or gastric route by axonal transport through the vagal nerve.(6,7) A central tenet of the dual hit hypoth-”
Parkinson's disease: a dual‐hit hypothesis (2007, background): “Additional studies not only have corroborated the initial involvement of anterior olfactory structures, but also have pointed to an early involvement of the enteric nerve cell plexuses as well as of the dorsal motor nucleus of the vagus and the intermediate reticular zone in the lower brainstem [21]”
Increased Intestinal Permeability Correlates with Sigmoid Mucosa alpha-Synuclein Staining and Endotoxin Exposure Markers in Early Parkinson's Disease (2011, background): “However, these findings by others, as well as by Braak and colleagues, led to the proposal [14,15] that the ENS may be a route by which a toxin or pathogen initiates the progression of PD over a period of many years.”
A designer AAV variant permits efficient retrograde access to projection neurons (2016, background): “From this perspective, subcortically projecting neurons in the mesocortical regions where pathological protein aggregates first appear, in both Alzheimer’s (Braak and Braak, 1996) and Parkinson’s (Braak et al., 2003) disorders, constitute an attractive intervention target.”
Stress granules as crucibles of ALS pathogenesis (2013, background): “This “bucket-brigade”-like form of propagation helps to explain how disease pathology seems to emerge from epicenters in the brain and spread along anatomically interconnected brain regions during disease progression (Braak et al., 2003; Ravits and La Spada, 2009).”
Unified Staging System for Lewy Body Disorders: Correlation with Nigrostriatal Degeneration, Cognitive Impairment and Motor Dysfunction (2009, background): “Other authors have offered reasons for this special vulnerability, citing thinly myelinated and lengthy axons [15], an unusually high degree of neuronal plasticity [28, 48] or the spatial proximity to the external environment, with its associated exposure to toxins and infectious agents [14, 43, 58]”
Gastric alpha-synuclein immunoreactive inclusions in Meissner's and Auerbach's plexuses in cases staged for Parkinson's disease-related brain pathology. (2006, background): “Known fiber tracts interconnect all brainstem nuclei and cortical areas that consecutively become involved in sPD [7].”
Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson's Disease (2016, neutral): “, 2013), and GI abnormalities such as constipation often precede motor defects by many years (Braak et al., 2003; Verbaan et al., 2007).”
Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults (2008, background): “…CNS and PNS regions in these high-air-pollution–exposed young cohorts follows the characteristic topographical distribution of early PD lesions, as described by Braak and colleagues (Braak et al. 2003, 2006; Del Tredeci et al. 2002), that is, OB, lower brain stem, and ganglionic autonomic cells.”
Multi-organ distribution of phosphorylated α-synuclein histopathology in subjects with Lewy body disorders (2010, neutral): “The former develop a-synuclein histopathology but the latter do not [20].”