Adjust Text Size:change font sizechange font sizechange font sizechange font sizechange font sizechange font size

Featured Research

Can we predict who is at risk of facing cognitive issues in PD and address them earlier? These are the questions being pursued by Dr. Goldman of the PDF Research Center at Rush University Medical Center.

Learn More

PDF Grant Programs

Are you interested in furthering Parkinson's science? View PDF's open grant programs.

Learn More


The role of parkin in Parkinson's disease].

PDF's targeted PubMed search provides you with access to journal articles from the last 90 days that may be pertinent to Parkinson's disease research. 

Not what you're looking for? Do you need informational publications about Parkinson's targeted for people living with Parkinson's, caregivers and family members?  Please browse PDF's educational materials and programs - which are all available electronically or in print.  Order for yourself, a loved one or in bulk for your patients or support group.

Neuropsychopharmacol Hung 2014 Jun; 16(2):67-76

Authors: Ildiko Miklya, Patricia Goltl, Florencia Hafenscher, Noemi Pencz

Parkin (Parkinson juvenile disease protein 2) is a ~52 kDa (426 amino acid) enzyme protein, encoded by PARK2 gene and located on the 6q chromosome. It plays an important role in the ubiquitin-proteasome system and acts as a regulator of protein breakdown. Parkin is located in the cytoplasma until a sustained depolarization occurs as a result of which it is translocated to the mitochondrial surface and induces the degradation of various membrane proteins which are candidates for mitophagia. Parkin is essential for cellular mitochondrial integrity. Parkin mutation leads to the accumulation of missfolded, aggregated proteins and degenerated mitochondria. The role of these changes in the pathomechanism of neurodegenerative diseases is well-known. It was a general belief for a long time that Parkinson's disease is without genetic component a sporadic disease. In 1997 a point mutation was, however, discovered in the ?-synuclein gene, which caused dominantly inherited parkinsonism. At least 10 other genes were thereafter detected the mutation or deletion of which cause monogenic parkinsonism. Parkin mutation is responsible for about 50% of familial cases and for 10 to 20% of youth cases. According to the present views the improper regulation of protein aggregation and a dysfunction of the ubiquitin-proteasome system may be the common pathway of sporadic and hereditary Parkinson's disease. In the future it might have therapeutic value that parkin has versatile neuroprotective activity (against ?-synuclein toxicity, proteasomal dysfunction, oxidative stress, kainite-induced and dopamine-mediated toxicity) as a result of which any reduction of parkin level or activity may cause damage in neuronal integrity.

PMID: 24978049 [PubMed - as supplied by publisher]

See More

Back to PubMed Articles