Feil Family Brain & Mind Research Institute

Publications

Found 10 results
Author Title Type [ Year(Asc)]
Filters: Keyword is Mitochondria  [Clear All Filters]
2025
Larrea D, Tamucci KA, Kabra K, Velasco KR, Yun TD, Pera M, Montesinos J, Agrawal RR, Paradas C, Smerdon JW et al..  2025.  Altered mitochondria-associated ER membrane (MAM) function shifts mitochondrial metabolism in amyotrophic lateral sclerosis (ALS).. Nat Commun. 16(1):379.
2024
Bennett NK, Lee M, Orr AL, Nakamura K.  2024.  Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production.. Proc Natl Acad Sci U S A. 121(3):e2307904121.
2017
Starkov AA, Chinopoulos C, Starkova NN, Konrad C, Kiss G, Stepanova A, Popov VN.  2017.  Divalent cation chelators citrate and EDTA unmask an intrinsic uncoupling pathway in isolated mitochondria.. J Bioenerg Biomembr. 49(1):3-11.
Kawamata H, Manfredi G.  2017.  Proteinopathies and OXPHOS dysfunction in neurodegenerative diseases.. J Cell Biol. 216(12):3917-3929.
Tapias V, Hu X, Luk KC, Sanders LH, Lee VM, J Greenamyre T.  2017.  Synthetic alpha-synuclein fibrils cause mitochondrial impairment and selective dopamine neurodegeneration in part via iNOS-mediated nitric oxide production.. Cell Mol Life Sci. 74(15):2851-2874.
2016
Stepanova A, Shurubor Y, Valsecchi F, Manfredi G, Galkin A.  2016.  Differential susceptibility of mitochondrial complex II to inhibition by oxaloacetate in brain and heart.. Biochim Biophys Acta. 1857(9):1561-8.
Chandra A, Sharma A, Calingasan NY, White JM, Shurubor Y, X Yang W, M Beal F, Johri A.  2016.  Enhanced mitochondrial biogenesis ameliorates disease phenotype in a full-length mouse model of Huntington's disease.. Hum Mol Genet. 25(11):2269-2282.
Manfredi G, Kawamata H.  2016.  Mitochondria and endoplasmic reticulum crosstalk in amyotrophic lateral sclerosis.. Neurobiol Dis. 90:35-42.
Chung SYoung, Kishinevsky S, Mazzulli JR, Graziotto J, Mrejeru A, Mosharov EV, Puspita L, Valiulahi P, Sulzer D, Milner TA et al..  2016.  Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation.. Stem Cell Reports. 7(4):664-677.
Esmaeili MA, Yadav S, Gupta RKr, Waggoner GR, DeLoach A, Calingasan NY, M Beal F, Kiaei M.  2016.  Preferential PPAR-α activation reduces neuroinflammation, and blocks neurodegeneration in vivo.. Hum Mol Genet. 25(2):317-27.