[1]
Uc EY, Rizzo M. Driving and neurodegenerative diseases. Curr Neurol Neurosci Rep 2008; 8: 377-83.
[2]
Ziegler-Graham K, Brookmeyer R, Johnson E, Arrighi HM. Worldwide variation in the doubling time of Alzheimer’s disease incidence rates. Alzheimers Dement 2008; 4: 316-23.
[3]
Haass C, Selkoe DJ. Soluble protein oligomers in neurodegeneration: Lessons from the Alzheimer’s amyloid beta-peptide. Nat Rev Mol Cell Biol 2007; 8: 101-12.
[4]
Lacor PN, Buniel MC, Chang L, et al. Synaptic targeting by Alzheimer’s-related amyloid beta oligomers. J Neurosci 2004; 24: 10191-200.
[5]
Parodi J, Sepulveda FJ, Roa J, Opazo C, Inestrosa NC, Aguayo LG. Beta-amyloid causes depletion of synaptic vesicles leading to neurotransmission failure. J Biol Chem 2010; 285: 2506-14.
[6]
Parodi J, Ormeno D, Paz LD. Amyloid pore-channel hypothesis: Effect of ethanol on aggregation state using frog oocytes for an Alzheimer’s disease study. BMB Rep 2015; 48(1): 13-8.
[7]
Mattson MP, Chan SL. Dysregulation of cellular calcium homeostasis in Alzheimer’s disease: Bad genes and bad habits. J Mol Neurosci 2001; 17: 205-24.
[8]
Arispe N, Pollard HB, Rojas E. The ability of amyloid beta-protein [A beta P (1-40)] to form Ca2+ channels provides a mechanism for neuronal death in Alzheimer’s disease. Ann N Y Acad Sci 1994; 747: 256-66.
[9]
Arispe N, Diaz JC, Simakova O. Abeta ion channels. Prospects for treating Alzheimer’s disease with Abeta channel blockers. Biochim Biophys Acta 2017; 1768: 1952-65.
[10]
Arispe N. Architecture of the Alzheimer’s A beta P ion channel pore. J Membr Biol 2004; 197: 33-48.
[11]
Kawahara M, Kuroda Y, Arispe N, Rojas R. Alzheimer’s beta-amyloid, human islet amylin, and prion protein fragment evoke intracellular free calcium elevations by a common mechanism in a hypothalamic GnRH neuronal cell line. J Biol Chem 2000; 275: 14077-83.
[12]
Connelly L, Jang H, Arce FT, et al. Atomic force microscopy and MD simulations reveal pore-like structures of all-D-enantiomer of Alzheimer’s beta-amyloid peptide: Relevance to the ion channel mechanism of AD pathology. J Phys Chem B 2012; 116: 1728-35.
[13]
Prangkio P, Yusko EC, Sept D, Yang J, Mayer M. Multivariate analyses of amyloid-beta oligomer populations indicate a connection between pore formation and cytotoxicity. PLoS One 2012; 7e47261
[14]
Kourie JI, Henry CL, Farrelly P. Diversity of amyloid beta protein fragment [1-40]-formed channels. Cell Mol Neurobiol 2001; 21: 255-84.
[15]
Sepulveda FJ, Parodi J, Peoples RW, Opazo C, Aguayo LG. Synaptotoxicity of Alzheimer beta amyloid can be explained by its membrane perforating property. PLoS One 2010; 5e11820
[16]
Alarcon JM, Brito JA, Hermosilla T, Atwater I, Mears D, Rojas E. Ion channel formation by Alzheimer’s disease amyloid beta-peptide (Abeta40) in unilamellar liposomes is determined by anionic phospholipids. Peptides 2006; 27: 95-104.
[17]
Parodi J, Ormeño D, Ochoa-de la Paz LD. Amyloid pore-channel hypothesis: Effect of ethanol on aggregation state using frog oocytes for an Alzheimer’s disease study. BMB Rep 2015; 48: 13-8.
[18]
Peters C, Fernandez-Perez EJ, Burgos CF, et al. Inhibition of amyloid beta-induced synaptotoxicity by a pentapeptide derived from the glycine zipper region of the neurotoxic peptide. Neurobiol Aging 2013; 34: 2805-14.
[19]
Zurita MP, Munoz G, Sepulveda FJ, et al. Ibuprofen inhibits the synaptic failure induced by the amyloid-beta peptide in hippocampal neurons. J Alzheimers Dis 2013; 35: 463-73.
[20]
Gonzalez-Ramirez M, Gavilan J, Silva-Grecchi T, et al. A natural benzofuran from the patagonic aleurodiscus vitellinus fungus has potent neuroprotective properties on a cellular model of amyloid-beta peptide toxicity. J Alzheimers Dis 2018; 61: 1463-75.
[21]
Peters C, Bascunan D, Opazo C, Aguayo LG. Differential membrane toxicity of amyloid-beta fragments by pore forming mechanisms. J Alzheimers Dis 2016; 51: 689-99.
[22]
Parodi J, Ochoa-de la Paz L, Miledi R, Martinez-Torres A. Functional and structural effects of amyloid-beta aggregate on Xenopus laevis oocytes. Mol Cells 2012; 34: 349-55.
[23]
Demuro A, Parker I. Cytotoxicity of intracellular abeta42 amyloid oligomers involves Ca2+ release from the endoplasmic reticulum by stimulated production of inositol trisphosphate. J Neurosci 2013; 33: 3824-33.
[24]
Sepulveda FJ, Fierro H, Fernandez E, et al. Nature of the neurotoxic membrane actions of amyloid-beta on hippocampal neurons in Alzheimer’s disease. Neurobiol Aging 2014; 35: 472-81.
[25]
Scarmeas N, Luchsinger JA, Mayeux R, Stern Y. Mediterranean diet and Alzheimer disease mortality. Neurology 2007; 69: 1084-93.
[26]
Sun AY, Simonyi A, Sun GY. The “French Paradox” and beyond: Neuroprotective effects of polyphenols. Free Radic Biol Med 2002; 32: 314-8.
[27]
Anstey KJ, Mack HA, Cherbuin N. Alcohol consumption as a risk factor for dementia and cognitive decline: Meta-analysis of prospective studies. Am J Geriatr Psychiatry 2009; 17: 542-55.
[28]
Peters R, Peters J, Warner J, Beckett N, Bulpitt C. Alcohol, dementia and cognitive decline in the elderly: A systematic review. Age Ageing 2008; 37: 505-12.
[29]
Russo A, Palumbo M, Aliano C, Lempereur L, Scoto G, Renis M. Red wine micronutrients as protective agents in Alzheimer-like induced insult. Life Sci 2003; 72: 2369-79.
[30]
Orgogozo JM, Dartigues JF, Lafont S, et al. Wine consumption and dementia in the elderly: A prospective community study in the Bordeaux area. Rev Neurol 1997; 153: 185-92.
[31]
Wang J, Ho L, Zhao Z, et al. Moderate consumption of Cabernet Sauvignon attenuates Abeta neuropathology in a mouse model of Alzheimer’s disease. FASEB J 2006; 20: 2313-20.
[32]
Kang IJ, Jeon YE, Yin XF, et al. Butanol extract of Ecklonia cava prevents production and aggregation of beta-amyloid, and reduces beta-amyloid mediated neuronal death. Food Chem Toxicol 2011; 49: 2252-9.
[33]
Noor H, Cao P, Raleigh DP. Morin hydrate inhibits amyloid formation by islet amyloid polypeptide and disaggregates amyloid fibers. Protein Sci 2012; 21: 373-82.
[34]
Luhrs T, Ritter C, Adrian M, et al. 3D structure of Alzheimer’s amyloid-beta(1-42) fibrils. Proc Natl Acad Sci USA 2005; 102: 17342-7.
[35]
Zhao J, Wang Q, Liang G, Zheng J. Molecular dynamics simulations of low-ordered alzheimer beta-amyloid oligomers from dimer to hexamer on self-assembled monolayers. Langmuir 2011; 27: 14876-87.
[36]
Edelstein-keshet L, Spiros A. Exploring the formation of Alzheimer’s disease senile plaques in silico. J Theor Biol 2002; 216: 301-26.
[37]
Ormeño D, Romero F, Lopez-Fenner J, Avila A, Martinez-Torres A, Parodi J. Ethanol reduces amyloid aggregation in vitro and prevents toxicity in cell lines. Arch Med Res 2013; 44: 1-7.
[38]
Hassing LB. Light alcohol consumption does not protect cognitive function: A longitudinal prospective study. Front Aging Neurosci 2018; 10: 81.
[39]
Piumatti G, Moore SC, Berridge DM, Sarkar C, Gallacher J. The relationship between alcohol use and long-term cognitive decline in middle and late life: A longitudinal analysis using UK Biobank. J Public Health 2018; 40(2): 304-11.
