For the first time, a team of researchers has shown a significant increase in the chemokine prokineticin 2 (PK2), a chemokine-like peptide, in the serum of patients with Parkinson’s disease. The results of this pilot study conducted by Cinzia Severini of the Institute of Biochemistry and Cell Biology of the National Research Council (Cnr-Ibbc), by Nicola Biagio Mercuri and Tommaso Schirinzi of the Neurological Clinic of the University of Rome Tor Vergata and by Roberta Lattanzi and Daniela Maftei from the Department of Physiology and Pharmacology of the Sapienza University of Rome have been published in Movement Disorders.
The study analyzed the blood of 31 patients with Parkinson’s disease and for the first time it was shown that serum levels of PK2 are significantly increased compared to healthy control subjects.
Cinzia Severini researcher of the CNR-Ibbc explains:
“PK2 is abundantly present in the central nervous system and is involved in various physiological and pathological functions including neuroinflammation. Experimental evidence has previously shown that PK2 is a factor that is activated early in nigrostriatal degeneration associated with Parkinson’s disease, suggesting its neuroprotective role through an action to restore mitochondrial damage.”
“The correlation between the increase in PK2 in serum and two markers of neurodegeneration in the cerebrospinal fluid (CSF or CSF) of the same patients was particularly interesting, such as the beta amyloid1-42 protein and lactate. In particular, the increase in serum of PK2, associated with the higher levels of beta amyloid1-42 found in the CSF, may indicate a protective effect of this chemokine against the pathology at the level of neuronal synapses and the deposition of plaques of amyloid, common events in both Parkinson’s disease and Alzheimer’s disease.”
“Furthermore, this increase in PK2 correlates with the decrease in lactate levels in the CSF, an index of oxidative stress and mitochondrial damage, confirming the hypothesis of an antioxidant action and restoration of mitochondrial damage “.
These results suggest that PK2 may represent not only a potential early biomarker of the disease, but also a pharmacological target for the creation of potentially useful therapies in Parkinson’s disease.
“These encouraging preliminary data now need to be confirmed in a larger study, including a larger and heterogeneous sample of patients, and to evaluate additional biological tissues. The ultimate goal is to fully understand the role of PK2 in Parkinson’s disease, thus opening the way to possible clinical developments centered on this peptide “, concludes Severini.