The Distribution of Lewy Bodies in the Central and Autonomic Nervous Systems in Idiopathic Paralysis Agitans

Jäger, W.; Bethlem, J.

doi:10.1136/jnnp.23.4.283

Cited by 261 publications

(36 citation statements)

References 9 publications

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“…We may speculate that the involvement of the peripheral nervous system in Parkinson's disease, suggested by the presence of Lewy bodies in sympathetic ganglia (Jager and Bethlem, 1960), is not present in postencephalitic Parkinsonism, and that postencephalitic patients are consequently less prone to suffer changes in blood pressure regulation.…”

Section: Resultsmentioning

confidence: 95%

Response of patients with postencephalitic Parkinsonism to levodopa

Duvoisin

Lobo-Antunes

Yahr

1972

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Resultsmentioning

confidence: 95%

Response of patients with postencephalitic Parkinsonism to levodopa

Duvoisin

Lobo-Antunes

Yahr

1972

Journal of Neurology, Neurosurgery & Psychiatry

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“…The description of Lewy bodies within the sympathetic and parasympathetic ganglia, adrenal medulla and selected GI tract regions within autopsied subjects with PD and DLB [78–82] has shown that peripheral nervous system LTS is certainly present but there has been insufficient data regarding the findings in prodromal phases of disease. Autopsy studies of relatively small numbers of subjects with ILBD have demonstrated a high prevalence of LTS within the spinal cord, sympathetic ganglia, adrenal medulla and upper GI tract [18,78,79,84–87] but no study to date has found LTS in the spinal cord or in peripheral nervous system sites in the absence of brain involvement, with the possible exception of Fumimura et al [82] who reported one case out of 783 with adrenal medulla as the only site with LTS. One other case report exists of Lewy body pathology restricted to the heart and stellate ganglion [88].…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Submandibular Gland Synucleinopathy in Parkinson’s Disease, Dementia with Lewy Bodies and other Lewy Body Disorders

Beach

Adler

Serrano

et al. 2016

JPD

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BACKGROUND Clinical misdiagnosis, particularly at early disease stages, is a roadblock to finding new therapies for Lewy body disorders. Biopsy of a peripheral site might provide improved diagnostic accuracy. Previously, we reported, from both autopsy and needle biopsy, a high prevalence of submandibular gland synucleinopathy in Parkinson’s disease (PD). Here, we report on an extension of these studies to subjects with dementia with Lewy bodies (DLB) and other Lewy body disorders in 228 autopsied subjects from the Arizona Study of Aging and Neurodegenerative Disorders. OBJECTIVE To provide an estimate of the prevalence of histological synucleinopathy in the submandibular glands of subjects with PD and other Lewy body disorders. METHODS Submandibular gland sections from autopsied subjects were stained with an immunohistochemical method for α-synuclein phosphorylated at serine 129. Included were 146 cases with CNS Lewy-type synucleinopathy (LTS), composed of 46 PD, 28 DLB, 14 incidental Lewy body disease (ILBD), 33 Alzheimer’s disease with Lewy bodies (ADLB) and 2 with progressive supranuclear palsy and Lewy bodies (PSPLB). Control subjects included 79 normal elderly, 15 AD, 12 PSP, 2 corticobasal degeneration (CBD) and 2 multiple system atrophy (MSA). RESULTS Submandibular gland LTS was found in 42/47 (89%) of the PD subjects, 20/28 (71%) DLB, 4/33 (12%) ADLB and 1/9 (11%) ILBD subjects but none of the 110 control subjects. CONCLUSIONS These results provide support for further clinical trials of in vivo submandibular gland diagnostic biopsy for PD and DLB. An accurate peripheral biopsy diagnosis would assist subject selection for clinical trials and could also be used to verify other biomarkers.

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“…However, the presence of Lewy bodies did not become the standard for post-mortem diagnosis of PD until after Lewy’s death. Currently, the presence, number and specific anatomical localization of Lewy bodies as well as Lewy neurites, proteinaceous inclusions within neuronal projections, are used for the post-mortem diagnosis of PD (den and Bethlem 1960; Braak and Braak 2000; Braak et al 2002, 2003, 2004, 2006). …”

Section: 3 Pathological Features Of Pdmentioning

confidence: 99%

Parkinson’s Disease

Mhyre¹,

Boyd²,

Hamill³

et al. 2012

Subcellular Biochemistry

336

203

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Parkinson’s disease (PD) is the most common age-related motoric neurodegenerative disease initially described in the 1800’s by James Parkinson as the ‘Shaking Palsy’. Loss of the neurotransmitter dopamine was recognized as underlying the pathophysiology of the motor dysfunction; subsequently discovery of dopamine replacement therapies brought substantial symptomatic benefit to PD patients. However, these therapies do not fully treat the clinical syndrome nor do they alter the natural history of this disorder motivating clinicians and researchers to further investigate the clinical phenotype, pathophysiology/pathobiology and etiology of this devastating disease. Although the exact cause of sporadic PD remains enigmatic studies of familial and rare toxicant forms of this disorder have laid the foundation for genome wide explorations and environmental studies. The combination of methodical clinical evaluation, systematic pathological studies and detailed genetic analyses have revealed that PD is a multifaceted disorder with a wide-range of clinical symptoms and pathology that include regions outside the dopamine system. One common thread in PD is the presence of intracytoplasmic inclusions that contain the protein, α-synuclein. The presence of toxic aggregated forms of α-synuclein (e.g., amyloid structures) are purported to be a harbinger of subsequent pathology. In fact, PD is both a cerebral amyloid disease and the most common synucleinopathy, that is, diseases that display accumulations of α-synuclein. Here we present our current understanding of PD etiology, pathology, clinical symptoms and therapeutic approaches with an emphasis on misfolded α-synuclein.

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The Distribution of Lewy Bodies in the Central and Autonomic Nervous Systems in Idiopathic Paralysis Agitans

Cited by 261 publications

References 9 publications

Response of patients with postencephalitic Parkinsonism to levodopa

Response of patients with postencephalitic Parkinsonism to levodopa

Prevalence of Submandibular Gland Synucleinopathy in Parkinson’s Disease, Dementia with Lewy Bodies and other Lewy Body Disorders

Parkinson’s Disease

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