publication . Other literature type . Article . 2017

Amyloid β-42 induces neuronal apoptosis by targeting mitochondria

Xiao-Jian Han; Yang-Yang Hu; Zhang-Jian Yang; Li-Ping Jiang; Sheng-Lan Shi; Ye-Ru Li; Miao-Yu Guo; Hong-Li Wu; Yu-Ying Wan;
  • Published: 01 Oct 2017
  • Publisher: Spandidos Publications
Abstract
Alzheimer's disease (AD), with a typical pathological hallmark of amyloid-beta (Aβ)-containing plaques and neurofibrillary tangles, is one of the most common types of chronic neurodegenerative diseases. Aβ oligomers serve a crucial role in the pathogenesis of AD, and lead to neuronal loss. However, the precise mechanism of Aβ oligomers in AD remains to be elucidated. The present study demonstrated that 10 µM Aβ-42 activated the caspase signaling pathway, and induced significant apoptosis in primary cultured mouse cerebral cortical neurons. The results of reverse transcription-quantitative polymerase chain reaction and western blotting demonstrated that Aβ-42 (10...
Subjects
free text keywords: Articles, Amyloid β-42, mitochondria, reactive oxygen species, mitophagy, apoptosis, Molecular Medicine, Genetics, Biochemistry, Cancer Research, Oncology, Molecular Biology, Amyloid, Cell cycle, Biology, Mitochondrion, Cell, medicine.anatomical_structure, medicine, Cell biology, Oncogene
Related Organizations
46 references, page 1 of 4

Mendiola-Precoma, J, Berumen, LC, Padilla, K, Garcia-Alcocer, G. Therapies for prevention and treatment of Alzheimer's disease. Biomed Res Int. 2016; 2016: 2589276 [OpenAIRE] [PubMed] [DOI]

Arbor, SC, LaFontaine, M, Cumbay, M. Amyloid-beta Alzheimer targets-protein processing, lipid rafts, and amyloid-beta pores. Yale J Biol Med. 2016; 89: 5-21 [OpenAIRE] [PubMed]

Glass, CK, Saijo, K, Winner, B, Marchetto, MC, Gage, FH. Mechanisms underlying inflammation in neurodegeneration. Cell. 2010; 140: 918-934 [OpenAIRE] [PubMed] [DOI]

Van Cauwenberghe, C, Van Broeckhoven, C, Sleegers, K. The genetic landscape of Alzheimer disease: Clinical implications and perspectivs. Genet Med. 2016; 18: 421-430 [OpenAIRE] [PubMed] [DOI]

Ingelsson, M, Fukumoto, H, Newell, KL, Growdon, JH, Hedley-Whyte, ET, Frosch, MP, Albert, MS, Hyman, BT, Irizarry, MC. Early Abeta accumulation and progressive synaptic loss, gliosis and tangle formation in AD brain. Neurology. 2004; 62: 925-931 [OpenAIRE] [PubMed] [DOI]

Li, Q, Liu, Y, Sun, M. Autophagy and Alzheimer's Disease. Cell Mol Neurobiol. 2017; 37: 377-388 [OpenAIRE] [PubMed] [DOI]

Barage, SH, Sonawane, KD. Amyloid cascade hypothesis: Pathogenesis and therapeutic strategies in Alzheimer's disease. Neuropeptides. 2015; 52: 1-18 [OpenAIRE] [PubMed] [DOI]

Dulin, F, Léveillé, F, Ortega, JB, Mornon, JP, Buisson, A, Callebaut, I, Colloc'h, N. P3 peptide, a truncated form of A beta devoid of synaptotoxic effect, does not assemble into soluble oligomers. FEBS Lett. 2008; 582: 1865-1870 [OpenAIRE] [PubMed] [DOI]

Holmes, C, Boche, D, Wilkinson, D, Yadegarfar, G, Hopkins, V, Bayer, A, Jones, RW, Bullock, R, Love, S, Neal, JW. Long-term effects of Abeta42 immunisation in Alzheimer's disease: Follow-up of arandomised, placebo-controlled phase I trial. Lancet. 2008; 372: 216-223 [PubMed] [DOI]

Saito, T, Suemoto, T, Brouwers, N, Sleegers, K, Funamoto, S, Mihira, N, Matsuba, Y, Yamada, K, Nilsson, P, Takano, J. Potent amyloidogenicity and pathogenicity of Aβ43. Nat Neurosci. 2011; 14: 1023-1032 [OpenAIRE] [PubMed] [DOI]

Kawahara, M, Ohtsuka, I, Yokoyama, S, Kato-Negishi, M, Sadakane, Y. Membrane incorporation, channel formation and disruption of calcium homeostasis by alzheimer's β-amyloid protein. Int J Alzheimers Dis. 2011; 2011: 304583 [OpenAIRE] [PubMed]

Kawahara, M. Neurotoxicity of β-amyloid protein: Oligomerization, channel formation and calcium dyshomeostasis. Curr Pharm Des. 2010; 16: 2779-2789 [OpenAIRE] [PubMed] [DOI]

Jarrett, JT, Lansbury, PT. Seeding ‘one-dimensional crystallization’ of amyloid: A pathogenic mechanism in Alzheimer's disease andscrapie?. Cell. 1993; 73: 1055-1058 [OpenAIRE] [PubMed] [DOI]

Jan, A, Adolfsson, O, Allaman, I, Buccarello, AL, Magistretti, PJ, Pfeifer, A, Muhs, A, Lashuel, HA. Abeta42 neurotoxicity is mediated by ongoing nucleated polymerization process rather than by discrete Abeta42 species. J Biol Chem. 2011; 286: 8585-8596 [OpenAIRE] [PubMed] [DOI]

Mirzabekov, T, Lin, MC, Yuan, WL, Marshall, PJ, Carman, M, Tomaselli, K, Lieberburg, I, Kagan, BL. Channel formation in planar lipid bilayers by a neurotoxic fragment of the beta-amyloid peptide. Biochem Biophys Res Commun. 1994; 202: 1142-1148 [OpenAIRE] [PubMed] [DOI]

46 references, page 1 of 4
Abstract
Alzheimer's disease (AD), with a typical pathological hallmark of amyloid-beta (Aβ)-containing plaques and neurofibrillary tangles, is one of the most common types of chronic neurodegenerative diseases. Aβ oligomers serve a crucial role in the pathogenesis of AD, and lead to neuronal loss. However, the precise mechanism of Aβ oligomers in AD remains to be elucidated. The present study demonstrated that 10 µM Aβ-42 activated the caspase signaling pathway, and induced significant apoptosis in primary cultured mouse cerebral cortical neurons. The results of reverse transcription-quantitative polymerase chain reaction and western blotting demonstrated that Aβ-42 (10...
Subjects
free text keywords: Articles, Amyloid β-42, mitochondria, reactive oxygen species, mitophagy, apoptosis, Molecular Medicine, Genetics, Biochemistry, Cancer Research, Oncology, Molecular Biology, Amyloid, Cell cycle, Biology, Mitochondrion, Cell, medicine.anatomical_structure, medicine, Cell biology, Oncogene
Related Organizations
46 references, page 1 of 4

Mendiola-Precoma, J, Berumen, LC, Padilla, K, Garcia-Alcocer, G. Therapies for prevention and treatment of Alzheimer's disease. Biomed Res Int. 2016; 2016: 2589276 [OpenAIRE] [PubMed] [DOI]

Arbor, SC, LaFontaine, M, Cumbay, M. Amyloid-beta Alzheimer targets-protein processing, lipid rafts, and amyloid-beta pores. Yale J Biol Med. 2016; 89: 5-21 [OpenAIRE] [PubMed]

Glass, CK, Saijo, K, Winner, B, Marchetto, MC, Gage, FH. Mechanisms underlying inflammation in neurodegeneration. Cell. 2010; 140: 918-934 [OpenAIRE] [PubMed] [DOI]

Van Cauwenberghe, C, Van Broeckhoven, C, Sleegers, K. The genetic landscape of Alzheimer disease: Clinical implications and perspectivs. Genet Med. 2016; 18: 421-430 [OpenAIRE] [PubMed] [DOI]

Ingelsson, M, Fukumoto, H, Newell, KL, Growdon, JH, Hedley-Whyte, ET, Frosch, MP, Albert, MS, Hyman, BT, Irizarry, MC. Early Abeta accumulation and progressive synaptic loss, gliosis and tangle formation in AD brain. Neurology. 2004; 62: 925-931 [OpenAIRE] [PubMed] [DOI]

Li, Q, Liu, Y, Sun, M. Autophagy and Alzheimer's Disease. Cell Mol Neurobiol. 2017; 37: 377-388 [OpenAIRE] [PubMed] [DOI]

Barage, SH, Sonawane, KD. Amyloid cascade hypothesis: Pathogenesis and therapeutic strategies in Alzheimer's disease. Neuropeptides. 2015; 52: 1-18 [OpenAIRE] [PubMed] [DOI]

Dulin, F, Léveillé, F, Ortega, JB, Mornon, JP, Buisson, A, Callebaut, I, Colloc'h, N. P3 peptide, a truncated form of A beta devoid of synaptotoxic effect, does not assemble into soluble oligomers. FEBS Lett. 2008; 582: 1865-1870 [OpenAIRE] [PubMed] [DOI]

Holmes, C, Boche, D, Wilkinson, D, Yadegarfar, G, Hopkins, V, Bayer, A, Jones, RW, Bullock, R, Love, S, Neal, JW. Long-term effects of Abeta42 immunisation in Alzheimer's disease: Follow-up of arandomised, placebo-controlled phase I trial. Lancet. 2008; 372: 216-223 [PubMed] [DOI]

Saito, T, Suemoto, T, Brouwers, N, Sleegers, K, Funamoto, S, Mihira, N, Matsuba, Y, Yamada, K, Nilsson, P, Takano, J. Potent amyloidogenicity and pathogenicity of Aβ43. Nat Neurosci. 2011; 14: 1023-1032 [OpenAIRE] [PubMed] [DOI]

Kawahara, M, Ohtsuka, I, Yokoyama, S, Kato-Negishi, M, Sadakane, Y. Membrane incorporation, channel formation and disruption of calcium homeostasis by alzheimer's β-amyloid protein. Int J Alzheimers Dis. 2011; 2011: 304583 [OpenAIRE] [PubMed]

Kawahara, M. Neurotoxicity of β-amyloid protein: Oligomerization, channel formation and calcium dyshomeostasis. Curr Pharm Des. 2010; 16: 2779-2789 [OpenAIRE] [PubMed] [DOI]

Jarrett, JT, Lansbury, PT. Seeding ‘one-dimensional crystallization’ of amyloid: A pathogenic mechanism in Alzheimer's disease andscrapie?. Cell. 1993; 73: 1055-1058 [OpenAIRE] [PubMed] [DOI]

Jan, A, Adolfsson, O, Allaman, I, Buccarello, AL, Magistretti, PJ, Pfeifer, A, Muhs, A, Lashuel, HA. Abeta42 neurotoxicity is mediated by ongoing nucleated polymerization process rather than by discrete Abeta42 species. J Biol Chem. 2011; 286: 8585-8596 [OpenAIRE] [PubMed] [DOI]

Mirzabekov, T, Lin, MC, Yuan, WL, Marshall, PJ, Carman, M, Tomaselli, K, Lieberburg, I, Kagan, BL. Channel formation in planar lipid bilayers by a neurotoxic fragment of the beta-amyloid peptide. Biochem Biophys Res Commun. 1994; 202: 1142-1148 [OpenAIRE] [PubMed] [DOI]

46 references, page 1 of 4
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publication . Other literature type . Article . 2017

Amyloid β-42 induces neuronal apoptosis by targeting mitochondria

Xiao-Jian Han; Yang-Yang Hu; Zhang-Jian Yang; Li-Ping Jiang; Sheng-Lan Shi; Ye-Ru Li; Miao-Yu Guo; Hong-Li Wu; Yu-Ying Wan;