Session Information
Date: Tuesday, June 21, 2016
Session Title: Parkinson's disease: Pathophysiology
Session Time: 12:30pm-2:00pm
Location: Exhibit Hall located in Hall B, Level 2
Objective: Looking through the Kaiser Permanente National Parkinson’s disease Registry, generated through the electronic medical records (EMR), we took a first step in looking at “big data” to assess the possible association with B-ATKI and PD.
Background: Recent reports suggest that Bcr-Abl tyrosine-kinase inhibiting chemotherapeutic agents used in treating chronic myelogenous leukemia (CML) may play a possible protective role or improve symptoms of PD. B-ATKI are used in treating CML and are known to enhance clearance of Alpha synuclein (α-syn) from striatal neurons. This accumulation of pathologic proteins is thought to be a major contributor the PD pathology.
Methods: Using data collected from the EMR at Kaiser Permanente Northern California (NCAL), Southern California (SCAL) and Mid-Atlantic States (MAS)), we assessed (1) the number of people diagnosed with PD by a neurologist, (2) the number of patients diagnosed with PD who received B-ATKI, and (3) total number of patients who received B-ATKI.
Results: A total of 21,783 patients from NCAL, SCAL and MAS received a diagnosis of PD by a neurologist from 2004 to 2014. During this time period, 2224 patients received a B-ATKI (Imatinib, Dasatinib, Bosutinib, Ponatinib, Bafetinib, and Nilotinib). Of those who received B-ATKI, 11 patients had a diagnosis of PD also. Eight of these patients received B-ATKI on average 2.4 years prior to the diagnosis of PD (range 0.25-5.5 years). Three patients received B-ATKI on average 1.7 years after the diagnosis of PD (range 0.5-2.8 years) and it is not clear if there was any improvement following B-ATKI administration. Imatinib and Dasatinib were the two that are represented in our cohort of 11 patients with PD. All B-ATKI were represented in the 2224 patients, but Bosutinib, Ponatinib, Bafetinib, and Nilotinib were not seen in patients who had a diagnosis of PD.
Conclusions: Although a closer and more thorough epidemiological study is planned to better assess the neuroprotective or therapeutic role of B-ATKI in relation to PD, this is a first step in looking at a large population to better understand this possible association. It is possible that B-ATKIs like Bosutinib, Ponatinib, Bafetinib and Nilotinib may have a protective role in PD and as a result are not present in the PD cohort. In the era of “big data”, large data sets like this will be instrumental in understanding the pathology and therapies for complex neurological conditions like PD.
To cite this abstract in AMA style:
E.A. Shamim, S.F. Baker, F.F. Liu, K.K. Mane, J.G. Layug, S. Vupputuri, C.C. DiStasio, S.M. Khandhar, C. Neff, S. Van Den Eeden, C. Lungu, R. Cooley, H.S. Martel, C. Chen, J. Dorman, M.A. Sinkiewicz, J. Klingman. Bcr-Abl tyrosine-kinase inhibitors (B-ATKI) and Parkinson’s disease (PD) [abstract]. Mov Disord. 2016; 31 (suppl 2). https://www.mdsabstracts.org/abstract/bcr-abl-tyrosine-kinase-inhibitors-b-atki-and-parkinsons-disease-pd/. Accessed June 14, 2025.« Back to 2016 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/bcr-abl-tyrosine-kinase-inhibitors-b-atki-and-parkinsons-disease-pd/