Parkinson's disease with involvement of the parasympathetic ganglia

Takeda, Shingo; Yamazaki, Kazunori; Miyakawa, Takashi; Arai, Hiroyuki

doi:10.1007/bf00369454

Cited by 60 publications

(42 citation statements)

References 8 publications

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“…It has been suggested, for example, that olfactory dysfunction, depression and autonomic nervous system dysfunction may be predictive for subsequent PD [3,22,29]. Olfactory bulb and peripheral autonomic nervous system synucleinopathy, are very common if not universal findings in PD [10][11][12]14,37,39,46,48,49]. Olfactory dysfunction and olfactory bulb synucleinopathy have been reported to be present in ILBD cases and hence smell tests and/or olfactory bulb biopsy may be useful for early diagnosis in PD and/or DLB.…”

Section: Resultsmentioning

confidence: 99%

“…The differences between studies may be due to differing immunohistochemical methods, differing subject ages and differing sampling sites. Although Parkinson's disease (PD) is generally considered a disease of the central nervous system (CNS), it has long been known that Lewy bodies may also be found in the peripheral autonomic nervous system in PD subjects [15,18,36,37,46,49]. Recent studies using immunohistochemical staining for α-synuclein have found that the peripheral autonomic nervous system is a common site of affectation in ILBD.…”

Section: Introductionmentioning

confidence: 99%

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Reduced striatal tyrosine hydroxylase in incidental Lewy body disease

Beach¹,

Adler

Sue³

et al. 2007

Acta Neuropathol

121

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Incidental Lewy body disease (ILBD) is the term used when Lewy bodies are found in the nervous system of subjects without clinically documented parkinsonism or dementia. The prevalence of ILBD in the elderly population has been estimated at between 3.8 and 30%, depending on subject age and anatomical site of sampling. It has been speculated that ILBD represents the preclinical stage of Parkinson's disease (PD) and/or dementia with Lewy bodies (DLB). Studies of ILBD could potentially identify early diagnostic signs of these disorders. At present, however, it is impossible to know whether ILBD is a precursor to PD or DLB or is just a benign finding of normal aging. We hypothesized that, if ILBD represents an early stage of PD or DLB, it should be associated with depletion of striatal dopaminergic markers. Eleven subjects with ILBD and 27 control subjects were studied. The ILBD subjects ranged in age from 74 to 96 years (mean 86.5) while the control subjects' age ranged from 75 to 102 years (mean 86.7). Controls and subjects did not differ in terms of age,

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reduced striatal tyrosine hydroxylase in incidental Lewy body disease

Beach¹,

Adler

Sue³

et al. 2007

Acta Neuropathol

121

View full text Add to dashboard Cite

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“…Cite this article as Cold Spring Harb Perspect Biol 2016;8:a023630 purple) (Bloch et al 2006;Braak et al 2006;Braak and Del Tredici 2009;Del Tredici et al 2010; see also den Hartog Jager and Bethlem 1960; Wakabayashi et al 1988Wakabayashi et al , 1989Wakabayashi et al , 1990Wakabayashi et al , 1993Takeda et al 1993;Wakabayashi and Takahashi 1997a,b;Cersó simo et al 2011;Beach et al 2013;Adler et al 2014). The brain is closely connected with postganglionic ENS neurons via axons of the preganglionic parasympathetic motor neurons of the dmX.…”

Section: Tau and A-synuclein Dissemination In Ad And Pdmentioning

confidence: 99%

“…(Legend continues on following page.) 1960;Wakabayashi et al 1988Wakabayashi et al , 1989Wakabayashi et al , 1990Wakabayashi et al , 1993Takeda et al 1993; Wakabayashi and Takahashi 1997a,b; Cersó simo et al 2011;Beach et al 2013; Adler et al 2014). The brain is closely connected with postganglionic ENS neurons via axons of the preganglionic parasympathetic motor neurons of the dmX.…”

mentioning

confidence: 99%

Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases

Braak

Tredici

2016

Cold Spring Harb Perspect Biol

108

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Experimental data indicate that transneuronal propagation of abnormal protein aggregates in neurodegenerative proteinopathies, such as sporadic Alzheimer's disease (AD) and Parkinson's disease (PD), is capable of a self-propagating process that leads to a progression of neurodegeneration and accumulation of prion-like particles. The mechanisms by which misfolded tau and a-synuclein possibly spread from one involved nerve cell to the next in the neuronal chain to induce abnormal aggregation are still unknown. Based on findings from studies of human autopsy cases, we review potential pathways and mechanisms related to axonal and transneuronal dissemination of tau (sporadic AD) and a-synuclein (sporadic PD) aggregates between anatomically interconnected regions. S poradic Alzheimer's disease (AD) and Parkinson's disease (PD) are human neurodegenerative disorders that do not occur in other vertebrate species. Pathological hallmark lesions in AD and PD involve only a few types of nerve cells, mainly projection neurons. These lesions develop at predetermined predilection sites and progress according to predictable patterns (Braak and Del Tredici 2009, 2015). In AD, disease-related lesions remain confined to the central nervous system (CNS), whereas in PD they develop not only in the CNS but also in the enteric (ENS) and peripheral (PNS) nervous systems. Both diseases are caused by misfolding of specific proteins that are associated with aberrant aggregation. AD is primarily characterized by pathological forms of the intraneuronal protein tau (Goedert et al. 2006;Iqbal et al. 2009) and, thereafter gradually, by extracellular deposits of the b-amyloid protein (Ab) (Alafuzoff et al. 2009;Haass et al. 2012;Masters and Selkoe 2012). In mature nerve cells, the highest concentrations of the protein tau usually are found in the axon. Key lesions in sporadic PD consist of aggregated forms of a-synuclein, a protein located chiefly in axons and their presynaptic terminals (Eisenberg and Jucker 2012;Jucker and Walker 2013;Kaufman and Diamond 2013;Goedert et al. 2014). Notably, all brain regions and all types of nerve cells consecutively involved in AD or PD are anatomically interconnected over considerable distances, thereby indicating that physical contact among such interconnected nerve cells plays a key role in the pathogenesis of both illnesses (Pearson et al. 1985;Saper et al. 1987;Pearson and Powell 1989;Pearson 1996;Duyckaerts et al. 1997;Braak and Del Tredici 2011b). Ab is deposited extracellularly and thus is not known to transfer from one nerve cell to the next in the neuronal chain (Fiala 2007;Kaufman and Diamond 2013).Here, we focus on potential pathways and mechanisms related to the postulated transmission and transneuronal dissemination of tau and a-synuclein between involved neurons and as yet uninvolved neurons in anatomically connected regions (Brundin et al. 2008Clavaguera et al. 2009Clavaguera et al. , 2013aDesplats et al. 2009;Luk et al. 2009;Angot et al. 2010 Angot et al. , 2012Frost and Diamond 2010;Goedert...

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“…[5][6][7][8][9] In some PD and dementia with Lewy bodies patients, Lewy pathology is present in the peripheral vagal nerve and ganglia. 10,11 These axons originate in the DMV. There are reports of strong Lewy pathology in the DMV preganglionic parasympathetic neurons of nearly all PD patients studied (see below).…”

Section: Introductionmentioning

confidence: 99%