Nicotinamide mononucleotide inhibits JNK activation to reverse Alzheimer disease

Neuroscience Letters

Volumn 647, Issue , 2017, Pages 133-140

  Yao, Zhiwen ^a   Yang, Wenhao ^a   Gao, Zhiqiang ^b   Jia, Peng ^b  

^a Tongji University School of Medicine   (China)

^b THE SECOND AFFILIATED HOSPITAL OF NANJING MEDICAL UNIVERSITY   (China)

Author keywords

Alzheimer disease; Amyloid ; JNK activation; Nicotinamide mononucleotide

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID PRECURSOR PROTEIN; NICOTINAMIDE NUCLEOTIDE; SECRETASE; STRESS ACTIVATED PROTEIN KINASE;

ALZHEIMER DISEASE; AMYLOID PLAQUE; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BEHAVIOR CHANGE; COGNITIVE DEFECT; CONTROLLED STUDY; DRUG EFFECT; DRUG MECHANISM; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; INFLAMMATION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN CLEAVAGE; PROTEIN EXPRESSION; TRANSGENIC ANIMAL; ANIMAL; AVOIDANCE BEHAVIOR; BRAIN; COGNITION DISORDERS; DRUG EFFECTS; ENZYMOLOGY; MEMORY; METABOLISM; PATHOLOGY; PSYCHOLOGY; SPATIAL LEARNING; SYNAPSE; TRANSGENIC MOUSE;

ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN PRECURSOR; AMYLOID PRECURSOR PROTEIN SECRETASES; ANIMALS; AVOIDANCE LEARNING; BRAIN; COGNITION DISORDERS; ENZYME ACTIVATION; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MEMORY; MICE, TRANSGENIC; NICOTINAMIDE MONONUCLEOTIDE; PLAQUE, AMYLOID; SPATIAL LEARNING; SYNAPSES;

EID: 85016427924     PISSN: 03043940     EISSN: 18727972     Source Type: Journal    
DOI: 10.1016/j.neulet.2017.03.027     Document Type: Article

References (41)

1. [1] Kapogiannis, D., Mattson, M.P., Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and Alzheimer's disease. Lancet Neurol. 10:2 (2011), 187–198.
2. [2] Gong, Y., et al. Alzheimer's disease-affected brain: presence of oligomeric A beta ligands (ADDLs) suggests a molecular basis for reversible memory loss. Proc. Natl. Acad. Sci. U. S. A. 100:18 (2003), 10417–10422.
3. [3] Hardy, J., Selkoe, D.J., The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 297:5580 (2002), 353–356.
4. [4] Lesne, S., et al. A specific amyloid-beta protein assembly in the brain impairs memory. Nature 440:7082 (2006), 352–357.
5. [5] Tayeb, H.O., et al. Pharmacotherapies for Alzheimer's disease: beyond cholinesterase inhibitors. Pharmacol. Ther. 134:1 (2012), 8–25.
6. [6] Imai, S., Guarente, L., NAD+ and sirtuins in aging and disease. Trends Cell Biol. 24:8 (2014), 464–471.
7. [7] Long, A.N., et al. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer's disease-relevant murine model. BMC Neurol., 15, 2015, 19.
8. [8] Kristian, T., et al. Mitochondrial dysfunction and nicotinamide dinucleotide catabolism as mechanisms of cell death and promising targets for neuroprotection. J. Neurosci. Res. 89:12 (2011), 1946–1955.
9. [9] Owens, K., et al. Mitochondrial dysfunction and NAD(+) metabolism alterations in the pathophysiology of acute brain injury. Transl. Stroke Res. 4:6 (2013), 618–634.
10. [10] Liu, D., Pitta, M., Mattson, M.P., Preventing NAD(+) depletion protects neurons against excitotoxicity: bioenergetic effects of mild mitochondrial uncoupling and caloric restriction. Ann. N. Y. Acad. Sci. 1147 (2008), 275–282.
11. [11] Yamamoto, T.et al., Nicotinamide mononucleotide, an intermediate of NAD+ synthesis, protects the heart from ischemia and reperfusion. PLoS One, 9(6), 2014, e98972.
12. [12] Imai, S., Dissecting systemic control of metabolism and aging in the NAD World: the importance of SIRT1 and NAMPT-mediated NAD biosynthesis. FEBS Lett. 585:11 (2011), 1657–1662.
13. [13] Mehan, S., et al. JNK: a stress-activated protein kinase therapeutic strategies and involvement in Alzheimer's and various neurodegenerative abnormalities. J. Mol. Neurosci. 43:3 (2011), 376–390.
14. [14] Yarza, R., et al. c-Jun N-terminal kinase (JNK) signaling as a therapeutic target for alzheimer's disease. Front. Pharmacol., 6, 2015, 321.
15. [15] Kim, D., et al. SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis. EMBO J. 26:13 (2007), 3169–3179.
16. [16] Zhang, W., et al. Multiple inflammatory pathways are involved in the development and progression of cognitive deficits in APPswe/PS1dE9 mice. Neurobiol. Aging 33:11 (2012), 2661–2677.
17. [17] Ishrat, T., et al. Amelioration of cognitive deficits and neurodegeneration by curcumin in rat model of sporadic dementia of Alzheimer's type (SDAT). Eur. Neuropsychopharmacol. 19:9 (2009), 636–647.
18. [18] Li, J.G., et al. Homocysteine exacerbates beta-amyloid pathology: tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles. Ann. Neurol. 75:6 (2014), 851–863.
19. [19] Chu, J., Pratico, D., Involvement of 5-lipoxygenase activating protein in the amyloidotic phenotype of an Alzheimer's disease mouse model. J. Neuroinflammation, 9, 2012, p127.
20. [20] Vukic, V., et al. Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer's brain is mediated by the JNK-AP1 signaling pathway. Neurobiol. Dis. 34:1 (2009), 95–106.
21. [21] Querfurth, H.W., LaFerla, F.M., Alzheimer's disease. N. Engl. J. Med. 362:4 (2010), 329–344.
22. [22] Wang, X., et al. Exendin-4 antagonizes Abeta1-42-induced suppression of long-term potentiation by regulating intracellular calcium homeostasis in rat hippocampal neurons. Brain Res. 1627 (2015), 101–108.
23. [23] Braithwaite, S.P., et al. Inhibition of c-Jun kinase provides neuroprotection in a model of Alzheimer's disease. Neurobiol. Dis. 39:3 (2010), 311–317.
24. [24] Sclip, A., et al. c-Jun N-terminal kinase regulates soluble Abeta oligomers and cognitive impairment in AD mouse model. J. Biol. Chem. 286:51 (2011), 43871–43880.
25. [25] Thakur, A., et al. c-Jun phosphorylation in Alzheimer disease. J. Neurosci. Res. 85:8 (2007), 1668–1673.
26. [26] Guglielmotto, M., et al. Amyloid-beta(4)(2) activates the expression of BACE1 through the JNK pathway. J. Alzheimers Dis. 27:4 (2011), 871–883.
27. [27] Rahman, M., et al. Intraperitoneal injection of JNK-specific inhibitor SP600125 inhibits the expression of presenilin-1 and Notch signaling in mouse brain without induction of apoptosis. Brain Res. 1448 (2012), 117–128.
28. [28] Colombo, A., et al. JNK regulates APP cleavage and degradation in a model of Alzheimer's disease. Neurobiol. Dis. 33:3 (2009), 518–525.
29. [29] Yoon, S.O., et al. JNK3 perpetuates metabolic stress induced by Abeta peptides. Neuron 75:5 (2012), 824–837.
30. [30] Godoy, J.A., et al. Signaling pathway cross talk in Alzheimer's disease. Cell Commun. Signal., 12, 2014, 23.
31. [31] Killick, R., et al. Clusterin regulates beta-amyloid toxicity via Dickkopf-1-driven induction of the wnt-PCP-JNK pathway. Mol. Psychiatry 19:1 (2014), 88–98.
32. [32] Hong, H.S., et al. Interferon gamma stimulates beta-secretase expression and sAPPbeta production in astrocytes. Biochem. Biophys. Res. Commun. 307:4 (2003), 922–927.
33. [33] Liao, Y.F., et al. Tumor necrosis factor-alpha: interleukin-1beta, and interferon-gamma stimulate gamma-secretase-mediated cleavage of amyloid precursor protein through a JNK-dependent MAPK pathway. J. Biol. Chem. 279:47 (2004), 49523–49532.
34. [34] Morales, I., et al. Neuroinflammation in the pathogenesis of Alzheimer's disease: a rational framework for the search of novel therapeutic approaches. Front. Cell. Neurosci., 8, 2014, 112.
35. [35] Kim, S.H., Smith, C.J., Van Eldik, L.J., Importance of MAPK pathways for microglial pro-inflammatory cytokine IL-1 beta production. Neurobiol. Aging 25:4 (2004), 431–439.
36. [36] Waetzig, V., et al. c-Jun N-terminal kinases (JNKs) mediate pro-inflammatory actions of microglia. Glia 50:3 (2005), 235–246.
37. [37] Marcello, E., et al. Synaptic dysfunction in Alzheimer's disease. Adv. Exp. Med. Biol. 970 (2012), 573–601.
38. [38] El-Husseini, A.E., et al. PSD-95 involvement in maturation of excitatory synapses. Science 290:5495 (2000), 1364–1368.
39. [39] Janz, R., et al. Essential roles in synaptic plasticity for synaptogyrin I and synaptophysin I. Neuron 24:3 (1999), 687–700.
40. [40] Costello, D.A., Herron, C.E., The role of c-Jun N-terminal kinase in the A beta-mediated impairment of LTP and regulation of synaptic transmission in the hippocampus. Neuropharmacology 46:5 (2004), 655–662.
41. [41] Sclip, A., et al. c-Jun N-terminal kinase has a key role in Alzheimer disease synaptic dysfunction in vivo. Cell. Death. Dis., 5, 2014, pe1019.