Abstract
Response to inflammation is a key determinant in many diseases and their outcomes. Diseases that commonly affect older people are frequently associated with altered inflammatory processes. Neuroinflammation has been described in Parkinson's disease (PD) brain. PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and at the sub-cellular level, mitochondrial dysfunction is a key feature. However, there is evidence that a different region of the brain, the cerebellum, is involved in the pathophysiology of PD. We report relative levels of 40 pro- and anti-inflammatory cytokines measured in PD and control cerebellar mitochondria. These data were obtained by screening cytokine antibody arrays. In parallel, we present concentrations of 29 oxylipins and 4 endocannabinoids measured in mitochondrial fractions isolated from post-mortem PD cerebellum with age and sex matched controls. Our oxylipin and endocannabinoid data were acquired via quantitation by LC-ESI—MS/MS. The separate sample sets both show there are clearly different inflammatory profiles between the sexes in control samples. Sex specific profiles were not maintained in cerebellar mitochondria isolated from PD brains.
Highlights
Though Parkinson’s disease (PD) is a single diagnosis, it presents as a heterogeneous disorder with some patients experiencing a more akinetic phenotype with prevailing rigidity where others may be less affected by rigidity but have a more tremor dominant disease [1]
Our study looked at molecular markers of inflammation measured in mitochondrial fractions derived from cerebellum to reveal whether there is a disease related process that connects with PD in this part of the human brain
Epigenetic changes in PD cerebellum have been investigated and give good reason to anticipate that regulatory pathways are changed during the disease course [6, 38]
Summary
Though Parkinson’s disease (PD) is a single diagnosis, it presents as a heterogeneous disorder with some patients experiencing a more akinetic phenotype with prevailing rigidity where others may be less affected by rigidity but have a more tremor dominant disease [1]. Our study looked at molecular markers of inflammation measured in mitochondrial fractions derived from cerebellum to reveal whether there is a disease related process that connects with PD in this part of the human brain. Measurements of mean levels identified proinflammatory cytokines RANTES (p=0.007) and GMCSF (p=0.0418) as significantly higher in female controls when compared with age-matched male control cerebellar mitochondria (Figure 1C).
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