Published July 30, 2012 | Version v1
Journal article Open

In vivo microglia activation in very early dementia with Lewy bodies, comparison with Parkinson's disease.

  • 1. Neurorehabilitation Unit, Department of Clinical Neurosciences, San Raffaele Scientific Institute and Vita-Salute University, Milan, Italy
  • 2. Neurorehabilitation Unit, Department of Clinical Neurosciences, San Raffaele Scientific Institute and Vita-Salute University, Milan, Italy; Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy and Vita-Salute San Raffaele University, Milan, Italy
  • 3. Proteome Biochemistry Unit, San Raffaele Scientific Institute, Milan, Italy
  • 4. Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy
  • 5. Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy; IBFM-CNR, Segrate, Italy and University of Milano-Bicocca, Monza, Italy
  • 6. Nuclear Medicine Unit and Division of Neuroscience, San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University, Milan, Italy and IBFM-CNR, Segrate, Italy

Description

Background: Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases. We in vivo evaluated microglia activation in early dementia with Lewy bodies, still not reported, and compared with early Parkinson’s disease, to assess possible differential pathological patterns.

Methods: We measured the [11C]-PK11195 binding potentials with Positron Emission Tomography, using a simplified reference tissue model, as marker of microglia activation, and cerebral spinal fluid protein carbonylation levels, as marker of oxidative stress. Six dementia with Lewy bodies and 6 Parkinson’s disease patients within a year from the onset, and eleven healthy controls were included. Clinical diagnosis was confirmed at a 4-year follow-up.

Results: In dementia with Lewy bodies as well as in Parkinson’s disease, we found significant (p < 0.001) [11C]-PK11195 binding potential increases in the substantia nigra and putamen. Patients with Lewy bodies dementia had extensive additional microglia activation in several associative cortices. This was evident also at a single subject level. Significant increase of Cerebral Spinal Fluid protein carbonization was shown in both patients’ groups.

Conclusions: [11C]-PK11195 Positron Emission Tomography imaging revealed neuroinflammation in dementia with Lewy bodies and Parkinson’s disease, mirroring, even at a single subject level, the common and the different topographical distribution of neuropathological changes, yet in the earliest stages of the disease process. Focusing on those events that characterize parkinsonisms and Parkinson’s disease may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection.

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Funding

INMIND – Imaging of Neuroinflammation in Neurodegenerative Diseases 278850
European Commission