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Pure autonomic failure without synucleinopathy.

Risa Isonaka1, Courtney Holmes1, Glen A Cook2

  • 1Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 9000 Rockville Pike MSC-1620, Building 10 Room 5N220, Bethesda, MD, 20892-1620, USA.

Clinical Autonomic Research : Official Journal of the Clinical Autonomic Research Society
|February 12, 2017
PubMed
Summary
This summary is machine-generated.

Pure autonomic failure involves sympathetic nerve damage but may not involve Lewy bodies or alpha-synuclein protein in the brain or nerves. This finding challenges the classification of pure autonomic failure as a Lewy body disease.

Keywords:
CatecholamineNorepinephrinePure autonomic failureSympatheticSynuclein

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Area of Science:

  • Neurology
  • Pathology
  • Autonomic Nervous System Disorders

Background:

  • Pure autonomic failure (PAF) is a chronic autonomic disorder.
  • It presents with neurogenic orthostatic hypotension and sympathetic denervation.
  • PAF has been hypothesized to be a Lewy body disease involving alpha-synuclein deposition.

Observation:

  • A patient with diagnosed PAF experienced sudden cardiac arrest and was autopsied.
  • Neuropathological examination of brain and sympathetic ganglion tissues was performed.
  • Immunohistochemistry and neurochemical studies were utilized.

Findings:

  • No Lewy bodies, Lewy neurites, or alpha-synuclein were found in the brain.
  • Significant reduction in tyrosine hydroxylase was observed in sympathetic ganglion tissue.
  • Alpha-synuclein was undetectable in sympathetic ganglion tissue, even in residual nerve fibers.

Implications:

  • Sympathetic noradrenergic denervation in PAF can occur independently of Lewy bodies or alpha-synuclein.
  • This challenges the direct classification of all PAF cases as Lewy body diseases.
  • Further research is needed to understand the diversePathophysiology of autonomic failure.