[1]
Halliday M, Radford H, Sekine Y, Moreno J, Verity N, le Quesne J, et al. Partial restoration of protein synthesis rates by the small molecule ISRIB prevents neurodegeneration without pancreatic toxicity. Cell Death Dis 6: e1672. (2015)
[2]
Ma T, Klann E. PERK: a novel therapeutic target for neurodegenerative diseases? Alzheimers Res Ther 6(3): 30. (2014)
[3]
Kim I, Xu W, Reed JC. Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities. Nat Rev Drug Discov 7(12): 1013-30. (2008)
[4]
Ma Y, Hendershot LM. The role of the unfolded protein response in tumour development: friend or foe? Nat Rev Cancer 4(12): 966-77. (2004)
[5]
Rozpedek W, Markiewicz L, Diehl JA, Pytel D, Majsterek I. Unfolded protein response and PERK Kinase as a New Therapeutic Target in the Pathogenesis of Alzheimer’s Disease. Curr Med Chem 22(27): 3169-84. (2015)
[6]
Ma T, Trinh MA, Wexler AJ, Bourbon C, Gatti E, Pierre P, et al. Suppression of eIF2alpha kinases alleviates Alzheimer’s disease-related plasticity and memory deficits. Nat Neurosci 16(9): 1299-305. (2013)
[7]
Doyle KM, Kennedy D, Gorman AM, Gupta S, Healy SJ, Samali A. Unfolded proteins and endoplasmic reticulum stress in neurodegenerative disorders. J Cell Mol Med 15(10): 2025-39. (2011)
[8]
Duran-Aniotz C, Martinez G, Hetz C. Memory loss in Alzheimer’s disease: are the alterations in the UPR network involved in the cognitive impairment? Front Aging Neurosci 6: 8. (2014)
[9]
Teske BF, Wek SA, Bunpo P, Cundiff JK, McClintick JN, Anthony TG, et al. The eIF2 kinase PERK and the integrated stress response facilitate activation of ATF6 during endoplasmic reticulum stress. Mol Biol Cell 22(22): 4390-405. (2011)
[10]
Baird TD, Wek RC. Eukaryotic initiation factor 2 phosphorylation and translational control in metabolism. Adv Nutr 3(3): 307-21. (2012)
[11]
Vassar R, Kovacs DM, Yan R, Wong PC. The beta-secretase enzyme BACE in health and Alzheimer’s disease: regulation, cell biology, function, and therapeutic potential. J Neurosci 29(41): 12787-94. (2009)
[12]
Endres K, Reinhardt S. ER-stress in Alzheimer’s disease: turning the scale? Am J Neurodegener Dis 2(4): 247-65. (2013)
[13]
Chow VW, Mattson MP, Wong PC, Gleichmann M. An overview of APP processing enzymes and products. Neuromolecular Med 12(1): 1-12. (2010)
[14]
B'Chir W, Maurin AC, Carraro V, Averous J, Jousse C, Muranishi Y, et al. The eIF2alpha/ATF4 pathway is essential for stress-induced autophagy gene expression. Nucleic Acids Res 41(16): 7683-99. (2013)
[15]
Li Y, Guo Y, Tang J, Jiang J, Chen Z. New insights into the roles of CHOP-induced apoptosis in ER stress. Acta Biochim Biophys Sin (Shanghai) 47(2): 146-7. (2015)
[16]
Pytel D, Seyb K, Liu M, Ray SS, Concannon J, Huang M, et al. Enzymatic characterization of er stress-dependent kinase, PERK, and development of a high-throughput assay for identification of PERK inhibitors. J Biomol Screen 19(7): 1024-34. (2014)
[17]
Bobrovnikova-Marjon E, Hatzivassiliou G, Grigoriadou C, Romero M, Cavener DR, Thompson CB, et al. PERK-dependent regulation of lipogenesis during mouse mammary gland development and adipocyte differentiation. Proc Natl Acad Sci USA 105(42): 16314-9. (2008)
[18]
Rodriguez-Arellano JJ, Parpura V, Zorec R, Verkhratsky A. Astrocytes in physiological aging and Alzheimer’s disease. Neuroscience 323: 170-82. (2016)
[19]
Verkhratsky A, Olabarria M, Noristani HN, Yeh CY, Rodriguez JJ. Astrocytes in Alzheimer’s disease. Neurotherapeutics 7(4): 399-412. (2010)
[20]
Allaman I, Gavillet M, Belanger M, Laroche T, Viertl D, Lashuel HA, et al. Amyloid-beta aggregates cause alterations of astrocytic metabolic phenotype: impact on neuronal viability. J Neurosci 30(9): 3326-38. (2010)
[21]
Phatnani H, Maniatis T. Astrocytes in neurodegenerative disease. Cold Spring Harb Perspect Biol 7(6) (2015)
[22]
Kimelberg HK, Nedergaard M. Functions of astrocytes and their potential as therapeutic targets. Neurotherapeutics 7(4): 338-53. (2010)
[23]
Halliday M, Mallucci GR. Targeting the unfolded protein response in neurodegeneration: A new approach to therapy. Neuropharmacology 76 Pt A:: 169-74. (2014)
[24]
Chang RC, Wong AK, Ng HK, Hugon J. Phosphorylation of eukaryotic initiation factor-2alpha (eIF2alpha) is associated with neuronal degeneration in Alzheimer’s disease. Neuroreport 13(18): 2429-32. (2002)
[25]
Hoozemans JJ, Veerhuis R, Van Haastert ES, Rozemuller JM, Baas F, Eikelenboom P, et al. The unfolded protein response is activated in Alzheimer’s disease. Acta Neuropathol 110(2): 165-72. (2005)
[26]
Ohno M. PERK as a hub of multiple pathogenic pathways leading to memory deficits and neurodegeneration in Alzheimer’s disease. Brain Res Bull 141: 72-8. (2018)
[27]
Baird TD, Palam LR, Fusakio ME, Willy JA, Davis CM, McClintick JN, et al. Selective mRNA translation during eIF2 phosphorylation induces expression of IBTKalpha. Mol Biol Cell 25(10): 1686-97. (2014)
[28]
Chang RC, Yu MS, Lai CS. Significance of molecular signaling for protein translation control in neurodegenerative diseases. Neurosignals 15(5): 249-58. (2006)
[29]
O’Connor T, Sadleir KR, Maus E, Velliquette RA, Zhao J, Cole SL, et al. Phosphorylation of the translation initiation factor eIF2alpha increases BACE1 levels and promotes amyloidogenesis. Neuron 60(6): 988-1009. (2008)
[30]
Finnie JW, Manavis J, Blumbergs PC, Kuchel TR. Axonal and neuronal amyloid precursor protein immunoreactivity in the brains of guinea pigs given tunicamycin. Vet Pathol 37(6): 677-80. (2000)
[31]
Stone S, Lin W. The unfolded protein response in multiple sclerosis. Front Neurosci 9: 264. (2015)
[32]
Axten JM, Medina JR, Feng Y, Shu A, Romeril SP, Grant SW, et al. Discovery of 7-methyl-5-(1-[3-(trifluoromethyl)phenyl]acetyl-2,3-dihydro-1H-indol-5-yl)-7H-p yrrolo[2,3-d]pyrimidin-4-amine (GSK2606414), a potent and selective first-in-class inhibitor of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK). J Med Chem 55(16): 7193-207. (2012)
[33]
Moreno JA, Halliday M, Molloy C, Radford H, Verity N, Axten JM, et al. Oral treatment targeting the unfolded protein response prevents neurodegeneration and clinical disease in prion-infected mice. Sci Transl Med 5(206): 206ra138. (2013)
[34]
Raghubir R, Nakka VP, Mehta SL. Endoplasmic reticulum stress in brain damage. Methods Enzymol 489: 259-75. (2011)
[35]
Benavides A, Pastor D, Santos P, Tranque P, Calvo S. CHOP plays a pivotal role in the astrocyte death induced by oxygen and glucose deprivation. Glia 52(4): 261-75. (2005)
[36]
Gu X, Li K, Laybutt DR, He ML, Zhao HL, Chan JC, et al. Bip overexpression, but not CHOP inhibition, attenuates fatty-acid-induced endoplasmic reticulum stress and apoptosis in HepG2 liver cells. Life Sci 87(23-26): 724-32. (2010)
[37]
Logsdon AF, Lucke-Wold BP, Nguyen L, Matsumoto RR, Turner RC, Rosen CL, et al. Salubrinal reduces oxidative stress, neuroinflammation and impulsive-like behavior in a rodent model of traumatic brain injury. Brain Res 1643: 140-51. (2016)
[38]
Smith WW, Jiang H, Pei Z, Tanaka Y, Morita H, Sawa A, et al. Endoplasmic reticulum stress and mitochondrial cell death pathways mediate A53T mutant alpha-synuclein-induced toxicity. Hum Mol Genet 14(24): 3801-11. (2005)
[39]
Huang X, Chen Y, Zhang H, Ma Q, Zhang YW, Xu H. Salubrinal attenuates beta-amyloid-induced neuronal death and microglial activation by inhibition of the NF-kappaB pathway. Neurobiol Aging 33(5): 1007 e9--. (2012)
[40]
Radford H, Moreno JA, Verity N, Halliday M, Mallucci GR. PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia. Acta Neuropathol 130(5): 633-42. (2015)
[41]
Mimori S, Okuma Y, Kaneko M, Kawada K, Hosoi T, Ozawa K, et al. Protective effects of 4-phenylbutyrate derivatives on the neuronal cell death and endoplasmic reticulum stress. Biol Pharm Bull 35(1): 84-90. (2012)
[42]
Marwarha G, Claycombe K, Schommer J, Collins D, Ghribi O. Palmitate-induced endoplasmic reticulum stress and subsequent C/EBPalpha Homologous Protein activation attenuates leptin and Insulin-like growth factor 1 expression in the brain. Cell Signal 28(11): 1789-805. (2016)
[43]
Sidrauski C, Acosta-Alvear D, Khoutorsky A, Vedantham P, Hearn BR, Li H, et al. Pharmacological brake-release of mRNA translation enhances cognitive memory. Elife 2: e00498. (2013)
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