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4 Chapter 1 Introduction .β.α .γ . .APP .α-secretase .β-secretase .APPsα .α-stub .APPsβ .β-stub .γ-secretase Figure 1.2: Generation of amyloid-β from the amyloid precursor protein (APP). Adapted from Goedert and Spillantini (2006). identified to be amyloid-β (Aβ), and the tangle is made of tau. The current amyloid cascade hypothesis suggests the disease is caused by excessive deposition of Aβ which will be briefly summarized as follows (for an up-to-date review of the current development in the pathogenesis and related issues of Alzheimer’s disease, see Blennow et al., 2006; Goedert and Spillantini, 2006; Murphy and LeVine, 2010; Ballard et al., 2011). Amyloid-β is the secreted peptide of 40 or 42 amino acids from larger transmem- brane amyloid precursor protein (APP), with the physiological function still un- known. During the amyloidogenic cleavage, APP is processed by β- and γ-secretase subsequently, releasing Aβ peptide. In the alternative pathway, APP is cleaved by α-secretase within the Aβ domain first, which is therefore non-amyloidogenic. The Aβ product is degraded and cleared in normal metabolism. Observing in the familial Alzheimer’s disease that the mutations in the APP gene causes preference of β-secretase, and that the mutations in presenilin genes associated with the secretase enzymes increase the production of Aβ42, being more ready to aggregate to plaque, the current amyloid cascade hypothesis suggests that synaptic dysfunction and neuronal death are triggered by the Aβ deposition and oligomers aggregated from Aβ. In sporadic AD, the ε4 allele of apolipoprotein E (APOE-ε4) associated with the failure of Aβ clearance has been identified as the main genetic factor that increases the risk of AD 3.8 times (Alzgene database, see Bertram et al., 2007). .Aβ
Chapter 1 Introduction 5 The intracellular neurofibrillary tangle is composed of the hyperphosphorylated tau. Tau is a microtubule-associated protein, which promotes tubulin assembly and microtubule stability. The abnormal hyperphosphorylation of tau leads to the disassembly of microtubules inhibiting and disrupting the axonal transport. The aggregation of tau into paired helical filaments forms the neurofibrillary tangles. As the consequence, neuronal and synaptic function is impaired with neurotrans- mitter deficit, and the growth of tangles results in the neuron death. According to the amyloid cascade hypothesis, the alternation in tau and the tangle formation result from the Aβ deposition, though the link between Aβ and tau is still not fully understood. The load of plaque and tangles starts to accumulate before the clinical onset of the AD. Non-demented patients in the transitional stage with memory complaints are usually diagnosed with mild cognitive impairment (MCI), which is a heterogeneous entity including memory decline due to normal aging, or prodrome of other forms of dementia and disorders. Approximately 10–15% of the MCI cases convert into AD every year, while the rate is 1–2% in general population (Petersen et al., 1999). In research and clinical practices, the diagnosis of the disease commonly follows the criteria of ‘probable’ AD developed by National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA, McKhann et al., 1984), and that of Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV, American Psy- chiatric Association, 1994; Text Revision, DSM-IV-TR, American Psychiatric As- sociation and Task Force on DSM-IV, 2000). The definitive diagnosis requires post mortem histopathological examination. Revisions of the NINCDS-ADRDA have been proposed to keep it update with new findings in the biomarkers, and the growth of knowledge about the disease since its first publication, especially the advancement in the neuroimaging with structural MRI, molecular imaging with PET, and cerebrospinal fluid analysis of Aβ and tau (Dubois et al., 2007).
Page 1: UNIVERSITE DE BOURGOGNE U.F.R. SCIE
Page 5 and 6: Résumé L’objectif de cette thè
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Page 9 and 10: TABLE DES MATIÈRES Acknowledgement
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Chapter 6 Conclusions 139 Given the
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144 LIST OF PUBLICATIONS using dive
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146 BIBLIOGRAPHY Alzheimer, A. (191
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148 BIBLIOGRAPHY Baillard, C., Hell
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150 BIBLIOGRAPHY of post mortem mag
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152 BIBLIOGRAPHY B. (2008). Three-d
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154 BIBLIOGRAPHY Cootes, T. F., Tay
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156 BIBLIOGRAPHY head in MR images
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158 BIBLIOGRAPHY Evans, A. C., Coll
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BIBLIOGRAPHY 161 Ghanei, A., Soltan
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BIBLIOGRAPHY 163 Heckemann, R. A.,
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BIBLIOGRAPHY 165 R. C. (2003). MRI
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BIBLIOGRAPHY 167 Konrad, C., Ukas,
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BIBLIOGRAPHY 169 Mahony, R. and Man
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BIBLIOGRAPHY 171 disease, mild cogn
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BIBLIOGRAPHY 173 Petersen, R. C., S
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BIBLIOGRAPHY 175 Rorden, C. and Bre
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BIBLIOGRAPHY 177 Shen, K., Bourgeat
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BIBLIOGRAPHY 179 Barillot, C., Hayn
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BIBLIOGRAPHY 181 Tzourio-Mazoyer, N
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BIBLIOGRAPHY 183 Vos, F. M., de Bru
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BIBLIOGRAPHY 185 Woolrich, M. W., J
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