[1]
Wouterlood FG, Vinkenoog M, van den Oever M. Tracing tools to resolve neural circuits. Network 2002; 13: 327-42.
[2]
Wang QH, Wang X, Bu XL, et al. Comorbidity burden of dementia: A hospital-based retrospective study from 2003 to 2012 in seven cities in china. Neurosci Bull 2017; 33: 703-10.
[3]
Masliah E, Mallory M, Deerinck T, et al. Re-evaluation of the structural organization of neuritic plaques in Alzheimer’s disease. J Neuropathol Exp Neurol 1993; 52: 619-32.
[4]
Spittaels K, Van den Haute C, Van Dorpe J, et al. Prominent axonopathy in the brain and spinal cord of transgenic mice overexpressing four-repeat human tau protein. Am J Pathol 1999; 155: 2153-65.
[5]
Spittaels K, Van den Haute C, Van Dorpe J, et al. Glycogen synthase kinase-3beta phosphorylates protein tau and rescues the axonopathy in the central nervous system of human four-repeat tau transgenic mice. J Biol Chem 2000; 275: 41340-9.
[6]
Dai J, Buijs RM, Kamphorst W, et al. Impaired axonal transport of cortical neurons in Alzheimer’s disease is associated with neuropathological changes. Brain Res 2002; 948: 138-44.
[7]
Higuchi M, Lee VM, Trojanowski JQ. Tau and axonopathy in neurodegenerative disorders. Neuromolecular Med 2002; 2: 131-50.
[8]
Bian F, Nath R, Sobocinski G, et al. Axonopathy, tau abnormalities, and dyskinesia, but no neurofibrillary tangles in p25-transgenic mice. J Comp Neurol 2002; 446: 257-66.
[9]
Stokin GB, Lillo C, Falzone TL, et al. Axonopathy and transport deficits early in the pathogenesis of Alzheimer’s disease. Science 2005; 307: 1282-8.
[10]
Yoon SY, Choi JE, Yoon JH, et al. BACE inhibitor reduces APP-beta-C-terminal fragment accumulation in axonal swellings of okadaic acid-induced neurodegeneration. Neurobiol Dis 2006; 22: 435-44.
[11]
Götz J, Ittner LM, Kins S. Do axonal defects in tau and amyloid precursor protein transgenic animals model axonopathy in Alzheimer’s disease? J Neurochem 2006; 98: 993-1006.
[12]
Wirths O, Weis J, Szczygielski J, et al. Axonopathy in an APP/PS1 transgenic mouse model of Alzheimer’s disease. Acta Neuropathol 2006; 111: 312-9.
[13]
Yang Y, Yang XF, Wang YP, et al. Inhibition of protein phosphatases induces transport deficits and axonopathy. J Neurochem 2007; 102: 878-86.
[14]
Smith KD, Kallhoff V, Zheng H, et al. In vivo axonal transport rates decrease in a mouse model of Alzheimer’s disease. Neuroimage 2007; 35: 1401-8.
[15]
Lazarov O, Morfini GA, Pigino G, et al. Impairments in fast axonal transport and motor neuron deficits in transgenic mice expressing familial Alzheimer’s disease-linked mutant presenilin 1. J Neurosci 2007; 27: 7011-20.
[16]
Minoshima S, Cross D. In vivo imaging of axonal transport using MRI: aging and Alzheimer’s disease. Eur J Nucl Med Mol Imaging 2008; 35: S89-92.
[17]
Adalbert R, Nogradi A, Babetto E, et al. Severely dystrophic axons at amyloid plaques remain continuous and connected to viable cell bodies. Brain 2008; 132: 402-16.
[18]
Vickers JC, King AE, Woodhouse A, et al. Axonopathy and cytoskeletal disruption in degenerative diseases of the central nervous system. Brain Res Bull 2009; 80: 217-23.
[19]
Zhang Q, Gao T, Luo Y, et al. Transient focal cerebral ischemia/reperfusion induces early and chronic axonal changes in rats: its importance for the risk of Alzheimer’s disease. PLoS One 2012; 7e33722
[20]
Zhou Y, Luo Y, Dai J. Axonal and dendritic changes are associated with diabetic encephalopathy in rats: An important risk factor for Alzheimer’s disease. J Alzheimers Dis 2013; 34: 937-47.
[21]
Dennissen FJ, Anglada-Huguet M, Sydow A, et al. Adenosine A1 receptor antagonist rolofylline alleviates axonopathy caused by human Tau ΔK280. Proc Natl Acad Sci USA 2016; 113: 11597-602.
[22]
Seehusen F, Kiel K, Jottini S, et al. Axonopathy in the central nervous system is the hallmark of mice with a novel intragenic null mutation of dystonin. Genetics 2016; 204: 191-203.
[23]
Gilley J, Ribchester RR, Coleman MP. Sarm1 deletion, but Not Wld(S), confers lifelong rescue in a mouse model of severe axonopathy. Cell Rep 2017; 21: 10-6.
[24]
Wang S, He B, Hang W, et al. Berberine alleviates tau hyperphosphorylation and axonopathy-associated with diabetic encephalopathy via restoring PI3K/Akt/GSK3β pathway. J Alzheimers Dis 2018; 65: 1385-400.
[25]
Xiao AW, He J, Wang Q, et al. The origin and development of plaques and phosphorylated tau are associated with axonopathy in Alzheimer’s disease. Neurosci Bull 2011; 27: 287-99.
[26]
Krstic D, Knuesel I. Deciphering the mechanism underlying late-onset Alzheimer disease. Nat Rev Neurol 2013; 9: 25-34.
[27]
Jankowsky JL, Fadale DJ, Anderson J, et al. Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. Hum Mol Genet 2004; 13: 159-70.
[28]
Ke ZJ, DeGiorgio LA, Volpe BT, et al. Reversal of thiamine deficiency-induced neurodegeneration. J Neuropathol Exp Neurol 2003; 62: 195-207.
[29]
Paxinos G, Watson C. The Rat Brain in Stereotaxic Coordinates, Third ed. People’s Medical Publishing House, Beijing. 2005.
[30]
Dai J, Swaab DF, Van der Vliet J, et al. Postmortem tracing reveals the organization of hypothalamic projections of the suprachiasmatic nucleus in the human brain. J Comp Neurol 1998; 400: 87-102.
[31]
Erisir A, Aoki C. A method of combining biocytin tract-tracing with avidin-biotin-peroxidase complex immunocytochemistry for pre-embedding electron microscopic labeling in neonatal tissue. J Neurosci Methods 1998; 81: 189-97.
[32]
Chen G, Chen KS, Knox J, et al. A learning deficit related to age and beta-amyloid plaques in a mouse model of Alzheimer’s disease. Nature 2000; 408: 975-9.
[33]
Wouterlood FG, Vinkenoog M, van den Oever M. Tracing tools to resolve neural circuits. Network 12002(3): 327-42.
[34]
Calingasan NY, Chun WJ, Park LC, et al. Oxidative stress is associated with region-specific neuronal death during thiamine deficiency. J Neuropathol Exp Neurol 1999; 58: 946-58.
[35]
Wang X, Wang B, Fan Z, et al. Thiamine deficiency induces endoplasmic reticulum stress in neurons. Neuroscience 2007; 144: 1045-56.
[36]
Gibson G, Barclay L, Blass J. The role of the cholinergic system in thiamin deficiency. Ann N Y Acad Sci 1982; 378: 382-403.
[37]
Ke ZJ, Gibson GE. Selective response of various brain cell types during neurodegeneration induced by mild impairment of oxidative metabolism. Neurochem Int 2004; 45: 361-9.
[38]
Yamamoto M, Kiyota T, Horiba M, et al. Interferon-gamma and tumor necrosis factor-alpha regulate amyloid-beta plaque deposition and beta-secretase expression in Swedish mutant APP transgenic mice. Am J Pathol 2007; 170: 680-92.
[39]
Chornyy S, Parkhomenko J, Chorna N. Thiamine deficiency caused by thiamine antagonists triggers upregulation of apoptosis inducing factor gene expression and leads to caspase 3-mediated apoptosis in neuronally differentiated rat PC-12 cells. Acta Biochim Pol 2007; 54: 315-22.
[40]
Karuppagounder SS, Xu H, Shi Q, et al. Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer’s mouse model. Neurobiol Aging 2009; 30: 1587-600.
[41]
Perry G. Neuritic plaques in Alzheimer disease originate from neurofibrillary tangles. Med Hypotheses 1993; 40: 257-8.
[42]
Schönheit B, Zarski R, Ohm TG. Spatial and temporal relationships between plaques and tangles in Alzheimer-pathology. Neurobiol Aging 2004; 25: 697-711.
[43]
Trojanowski JQ, Lee VM-Y. The Alzheimer’s brain binding out what’s broken tells us how to fix it. Am J Pathol 2005; 167: 1183-8.
[44]
Arai H, Schmidt ML, Lee VM, et al. Epitope analysis of senile plaque components in the hippocampus of patients with Parkinson’s disease. Neurology 1992; 42: 1315-22.
[45]
Steiner B, Mandelkow EM, Biernat J, et al. Phosphorylation of microtubule-associated protein tau: identification of the site for Ca2 (+)-calmodulin dependent kinase and relationship with tau hosphorylation in Alzheimer tangles. EMBO J 1990; 9: 3539-44.
[46]
Fleming LM, Johnson GV. Modulation of the phosphorylation state of tau in situ: the roles of calcium and cyclic AMP. Biochem J 1995; 309: 41-7.
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