Mark Paul Mattson, Ph.D.
Laboratory of Neurosciences
251 Bayview Boulevard
Baltimore, MD 21224
Accumulating evidence suggests that telomere integrity depends on the ability to maintain telomere length and/or the ability to mask telomeres from being recognized as damaged DNA. In mammals, telomeres normally exist in a loop structure with 3' single stranded telomeric DNA overhang concealed within the telomere double helix. This t-loop configuration is believed to protect chromosome ends from being recognized as broken DNA. Disruption of the telomere loop and subsequent exposure of the 3' overhang represents the uncapped state of telomeres. Telomerase and telomere associated proteins play essential roles in telomere length maintenance and telomere capping functions. Telomerase replenishes telomere loss due to incomplete DNA replication in almost all eukaryotes. Loss of telomerase activity leads to attrition of telomeric DNA, which, in turn, is known to trigger chromosome end-to-end fusions, genomic instability, and cell arrest or death. Recent studies have shown that uncapped telomeres directly associate with many DNA damage response proteins in telomere-initiated cellular senescence, indicating that DNA damage repair proteins interact with telomere as a DNA damage check-point response during cellular senescence. Several DNA damage repair proteins are also critical in protecting telomere and chromosome integrity.
Dr. Mattson received his Ph.D. in Biology from the University of Iowa in 1986. After 3 years of postdoctoral studies in Developmental Neuroscience at Colorado State University, Dr. Mattson took a faculty position at the Sanders-Brown Research Center on Aging at the University of Kentucky Medical Center where he was promoted to Full Professor in 1997. Dr. Mattson is currently Chief of the Laboratory of Neurosciences at the National Institute on Aging, and Professor of Neuroscience at Johns Hopkins University. He is Editor-in-Chief of Ageing Research Reviews and NeuroMolecular Medicine, a Section Editor for Neurobiology of Aging, and an Associate Editor for Trends in Neurosciences. In addition, he has edited 10 volumes in the areas of mechanisms of brain function, stress responses, aging and age-related neurodegenerative disorders. Dr. Mattson is a Fellow of the American Association for the Advancement of Science, and has received numerous awards including the Metropolitan Life Foundation Medical Research Award and the Alzheimer's Association Zenith Award. He is considered a leader in the area of cellular and molecular mechanisms underlying neuronal plasticity and neurodegenerative disorders, and has made major contributions to understanding of the pathogenesis of Alzheimer's disease, and to its prevention and treatment. Dr. Mattson has published more than 400 original research articles and more than 200 review articles and commentaries.
Sykora P, Misiak M, Wang Y, Ghosh S, Leandro GS, Liu D, Tian J, Baptiste BA, Cong WN, Brenerman BM, Fang E, Becker KG, Hamilton RJ, Chigurupati S, Zhang Y, Egan JM, Croteau DL, Wilson DM 3rd, Mattson MP, Bohr VA. DNA polymerase β deficiency leads to neurodegeneration and exacerbates Alzheimer disease phenotypes. Nucleic Acids Res. 2015;43(2):943-59.
Nigam SM, Xu S, Kritikou JS, Marosi K, Brodin L, Mattson MP. Exercise and BDNF reduce Aβ production by enhancing α-secretase processing of APP. J Neurochem. 2017;142(2):286-296.
Cheng A, Yang Y, Zhou Y, Maharana C, Lu D, Peng W, Liu Y, Wan R, Marosi K, Misiak M, Bohr VA, Mattson MP. Mitochondrial SIRT3 Mediates Adaptive Responses of Neurons to Exercise and Metabolic and Excitatory Challenges. Cell Metab. 2016;23(1):128-42.
Marosi K, Kim SW, Moehl K, Scheibye-Knudsen M, Cheng A, Cutler R, Camandola S, Mattson MP. 3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons. J Neurochem. 2016;139(5):769-781.
Cheng A, Wan R, Yang JL, Kamimura N, Son TG, Ouyang X, Luo Y, Okun E, Mattson MP. Involvement of PGC-1α in the formation and maintenance of neuronal dendritic spines. Nat Commun. 2012;3:1250.