Where Does Parkinson Disease Pathology Begin in the Brain?

By K. Del Tredici, Udo Rüb, R. D. de Vos, J. Bohl, H. Braak. Journal of Neuropathology and Experimental Neurology, 2002

805 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/855965ed2b89ef8ee41a73dcb130b30ea25ee1e3

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Dennis W. Dickson
2. K. Del Tredici
3. Udo Rüb
4. P. Jenner
5. H. Braak
6. A. Schober
7. D. Dexter

In Neurology

1. Dennis W. Dickson
2. K. Del Tredici
3. H. Braak
4. D. Dexter
5. Udo Rüb
6. E. Ghebremedhin
7. P. Jenner
8. C. Hawkes

In Sensory Systems

1. Dennis W. Dickson

Citations in the corpus

• Parkinson disease: from pathology to molecular disease mechanisms. (2013, background): “For example, constipation as a common NMS is associated with neuronal loss and the presence of Lewy bodies in the dorsal motor nucleus of the vagus, which provides parasympathetic innervation to the stomach and intestine [10,20,159], and changes such as these can be initiated by injection of proteas”
• Staging of the intracerebral inclusion body pathology associated with idiopathic Parkinson's disease (preclinical and clinical stages) (2002, background): “The various types of vulnerable nerve cells show clearcut differences in their respective susceptibilities to the degenerative process underlying IPD [5, 8].”
• Parkinson's disease and parkinsonism: neuropathology. (2012, methodology): “The cerebellar dentate nucleus usually has atrophy and discoloration of the white matter in the dentate hilus, with similar atrophy and discoloration in the cerebellar outflow pathway.”
• Idiopathic hyposmia as a preclinical sign of Parkinson's disease (2004, background): “Recent neuropathological observations show extensive extranigral neuropathological changes in idiopathic PD, including the olfactory bulb and related portions of the anterior olfactory nucleus.(17,36,37) In the novel and challenging pathological staging system for PD put forward by Braak and colleag”
• National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach (2011, neutral): “Although not part of this classification scheme, it is important to realize that LBD also occurs frequently in the olfactory bulb in older adults and should be sampled when possible [20].”
• Association of olfactory dysfunction with risk for future Parkinson's disease (2008, background): “Inclusion criteria were: (1) parkinsonism (eg, bradykinesia or resting tremor combined with rigidity or postural reflex impairment); (2) a progressive disorder; (3) any two of a marked response to L-dopa, asymmetry of signs, asymmetry at onset, or initial onset tremor; and (4) absence of any causati”
• Unified Staging System for Lewy Body Disorders: Correlation with Nigrostriatal Degeneration, Cognitive Impairment and Motor Dysfunction (2009, background): “Investigations that have mapped the topographical distribution and density of Lewy bodies and their associated abnormal neurites have indicated that these are spread much more widely throughout the neuraxis than formerly appreciated [22, 30, 31, 39, 46, 49, 50, 57, 69, 80, 81].”
• Multi-organ distribution of phosphorylated α-synuclein histopathology in subjects with Lewy body disorders (2010, background): “The topographical distribution and density of Lewy bodies and their associated abnormal neurites are much greater than formerly appreciated [8,28,31,33,37,44,46,61,64,70,71,77,82].”
• Stages in the development of Parkinson’s disease-related pathology (2004, background): “…first lesions develop at two predilection sites simultaneously, namely, at the dorsal motor nucleus of the vagal nerve plus adjoining interme- diate reticular zone and the olfactory bulb together with related portions of the anterior olfactory nucleus (Del Tredici et al. 2002; Braak et al. 2003a).”
• National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease (2012, neutral): “We recommend that genetic risk and biomarkers (chemical and neuroimaging) be used in research settings to complement neuropathologic data for the postmortem diagnosis Box 2: LBD (includes Parkinson disease and DLB) Method Recommended brain regions for tiered evaluation are in Table 1.”