Mark R. Cookson, Ph.D.

Senior Investigator

Laboratory of Neurogenetics

NIA

Building 35, Room 1A116
35 Convent Drive
Bethesda, MD 20814

301-451-3870

cookson@mail.nih.gov

Research Topics

Parkinson's disease is one of the major age-related neurodegenerative disorders and is characterized by the progressive loss of neurons over time. Some of the major symptoms of Parkinson's relate to the ability of the patient to initiate or stop movement and these symptoms are related to loss of neurons that express the neurotransmitter dopamine in a region of the brain called the substantia nigra. One of the major mysteries about Parkinson's disease and other neurodegenerative disorders is that for most patients the root cause remains unidentified. However, in the last decade several rare families have been found where a disease is inherited whose symptoms overlap with typical Parkinson's disease. Our work is aimed at using this genetic information to understand the pathways involved that lead to neuronal damage and death.

Biography

Dr. Mark R. Cookson is a cell biologist whose current research interests include the effects of mutations in the genes associated with neurodegeneration at the cellular and molecular level. His laboratory efforts are directed at finding the underlying pathways that lead to Parkinson's disease and related disorders. Dr. Cookson received both his B.Sc. and Ph.D. degrees from the University of Salford, UK in 1991 and 1995, respectively. His postdoctoral studies included time spent at the Medical Research Council laboratories and at the University of Newcastle, Newcastle, UK. He joined the Mayo Clinic, Jacksonville, Florida, as an Assistant Professor in 2000 and moved to the NIA in February 2002. Within the Laboratory of Neurogenetics, Dr. Cookson's group works on the effects of mutations associated with Parkinson's disease on protein function.

Selected Publications

  1. Pellegrini L, Hauser DN, Li Y, Mamais A, Beilina A, Kumaran R, Wetzel A, Nixon-Abell J, Heaton G, Rudenko I, Alkaslasi M, Ivanina N, Melrose HL, Cookson MR, Harvey K. Proteomic analysis reveals co-ordinated alterations in protein synthesis and degradation pathways in LRRK2 knockout mice. Hum Mol Genet. 2018.

  2. Blauwendraat C, Reed X, Kia DA, Gan-Or Z, Lesage S, Pihlstrøm L, Guerreiro R, Gibbs JR, Sabir M, Ahmed S, Ding J, Alcalay RN, Hassin-Baer S, Pittman AM, Brooks J, Edsall C, Hernandez DG, Chung SJ, Goldwurm S, Toft M, Schulte C, Bras J, Wood NW, Brice A, Morris HR, Scholz SW, Nalls MA, Singleton AB, Cookson MR, COURAGE-PD (Comprehensive Unbiased Risk Factor Assessment for Genetics and Environment in Parkinson’s Disease) Consortium, the French Parkinson’s Disease Consortium, and the International Parkinson’s Disease Genomics Consortium (IPDGC).. Frequency of Loss of Function Variants in LRRK2 in Parkinson Disease. JAMA Neurol. 2018.

  3. Kluss JH, Conti MM, Kaganovich A, Beilina A, Melrose HL, Cookson MR, Mamais A. Detection of endogenous S1292 LRRK2 autophosphorylation in mouse tissue as a readout for kinase activity. NPJ Parkinsons Dis. 2018;4:13.

  4. Liu Z, Bryant N, Kumaran R, Beilina A, Abeliovich A, Cookson MR, West AB. LRRK2 phosphorylates membrane-bound Rabs and is activated by GTP-bound Rab7L1 to promote recruitment to the trans-Golgi network. Hum Mol Genet. 2018;27(2):385-395.

  5. Hauser DN, Mamais A, Conti MM, Primiani CT, Kumaran R, Dillman AA, Langston RG, Beilina A, Garcia JH, Diaz-Ruiz A, Bernier M, Fiesel FC, Hou X, Springer W, Li Y, de Cabo R, Cookson MR. Hexokinases link DJ-1 to the PINK1/parkin pathway. Mol Neurodegener. 2017;12(1):70.


This page was last updated on August 24th, 2018