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Published on: July 19, 2019
Medullary microvessel degeneration in multiple system atrophy.
V M Miller1, R N Kalaria, R Hall
1Neurovascular Research Unit, Sir James Spence Institute, Royal Victoria Hospital, Newcastle upon Tyne, NE1 4LP, UK. veronica.miller@mail.dcu.ie
Neurobiology of Disease
|May 1, 2007
Summary
Multiple system atrophy (MSA), a rare autonomic disorder, shows medullary microvessel degeneration. This degeneration, indicated by reduced collagen IV and glucose transporter 1, may worsen MSA progression.
Area of Science:
- Neurology
- Pathology
- Autonomic Disorders
Background:
- Multiple system atrophy (MSA) is a rare, fatal autonomic disorder with Parkinsonism and orthostatic hypotension (OH).
- Current understanding of MSA pathophysiology includes autonomic neuron depletion and glial inclusions.
- The role of medullary autonomic microvessels in MSA remains unclear.
Purpose of the Study:
- To investigate medullary autonomic microvessel degeneration as a potential feature of MSA.
- To quantify specific microvessel components in MSA and compare them to controls.
Main Methods:
- Digital pathology was used to analyze medullary autonomic nuclei.
- Expression of basement membrane collagen (Coll IV), alpha-smooth muscle actin (alpha-actin), and glucose transporter 1 (Glut 1) was quantified.
- Samples from 8 MSA patients, 8 OH patients, and 12 controls were analyzed.
Main Results:
- MSA cases showed significantly decreased Coll IV and Glut 1 expression compared to controls (p=0.000 for both).
- Alpha-actin expression did not differ significantly between MSA and control groups.
- No significant differences in Coll IV, alpha-actin, or Glut 1 were observed between OH cases and controls.
Conclusions:
- Medullary microvessel degeneration, evidenced by reduced Coll IV and Glut 1, is a potential finding in MSA.
- This microvascular pathology may be secondary to the primary neuro-glial damage in MSA.
- Microvessel degeneration could contribute to the accelerated, age-related progression of MSA.
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