cells. This was true in both normal and Alzheimer’s disease brain sections.We also demonstrate that RCAN1-1 mRNA levels are approximately two-fold higher in neurons from Alzheimer’s disease patients versus non-Alzhei-mer’s disease[r]
association study identifies variants at CLU and PICALM associated withAlzheimer’s disease. Nat Genet 2009, 41:1088-1093.6. Lambert JC, Heath S, Even G, Campion D, Sleegers K, Hiltunen M,Combarros O, Zelenika D, Bullido MJ, Tavernier B, et al: Genome-wideassociation study identi[r]
whereby osteoarthritis resulted in neuroinflammation as well as exacerbation and acceleration of AD pathology.Results: Induction of osteoarthritis exacerbated and accelerated the development of neuroinflammation, asassessed by glial cell activation and quantification o[r]
17. Kamer A, Craig R, Dasanayake A, Brys M, Glodzik-Sobanska L, de Leon M:Inflammation and Alzheimer’s disease: Possible role of periodontaldiseases. Alzheimers Dement 2008, 4:242-250.18. Pepys M, Hirschfield G: C-reactive protein: a critical update. J Clin Invest2003, 11[r]
nal degeneration marker tau. More importantly, cogni-tively healthy elderly individuals, with increased risk ofdeveloping AD in the future, had elevated CSF MMP-3and MMP-9 levels and an increased CSF MMP-3/TIMP-1 ratio, indicating that MMP-3 and MMP-9might be involved in early pathogen[r]
cc107, Universite´de Montpellier II, place E.Bataillon, 34095 Montpellier cedex 5, FranceFax: +33 0467144727Tel: +33 0467144775E-mail: marcilhac@univ-montp2.fr(Received 23 March 2006, accepted 31 May2006)doi:10.1111/j.1742-4658.2006.05352.xApoptotic neuronal cell death is the cardinal feature of<[r]
Tanzi R, Jones K, Hyman BT, Albert MS. 2000. Use of structuralmagnetic resonance imaging to predict who will get Alzheimer’sdisease [see comments]. Ann Neurol 47(4):430–9.[34] Kleinbaum DG, KLL, MKE. 1988. Applied Regression Analysis andOther Multivariable Methods, p. 601–31, second ed[r]
with tau in homogenates of the medial temporal cortex from 20 AD and10 control brains. We found that levels of p-mTOR (Ser2481), and p-4E-BP1 (Thr70 and Ser65) dramatically increase in AD, and are positively sig-nificantly correlated with total tau and p-tau. Levels of<[r]
2006). The active form of IL-18 induces signal transduction by binding to itsreceptor, IL-18α/β receptor (IL1Rrp/IL1RAPL) expressed by diverse cell types,including neurons and glia cells. In adult brains of untreated BALB/c mice, IL-18 isconstitutively the most highly expressed[r]
Modulation of a-synuclein aggregation by dopamine in thepresence of MPTP and its metabolitePrashant N. Jethva, Jay R. Kardani and Ipsita RoyDepartment of Biotechnology, National Institute of Pharmaceutical Education and Research (NIPER), S.A.S. Nagar,[r]
cursor to amyloidosis: a discussion of the occurrence, role, andimplications. In Molecular Chaperones in the Cell (Lund, P., ed.),Frontiers in Molecular Biology Series, pp. 257–278. OxfordUniversity Press, Oxford.63. Carrel, R.W. & Gooptu, B. (1998) Conformational[r]
, J. MAROCO4, M.R. SIMOES5,D. GALASKO6, A. DE MENDONCA1,71. Dementia Clinics, Institute of Molecular Medicine and Faculty of Medicine of Lisbon, Lisbon, Portugal; 2. Neurology Clinics, Hospital of Santo André, Leiria, Portugal; 3. Laboratoryof Language, Institute of
then demonstrate how crosses of TGF-β1 mutant mice with mouse models of Alzheimer's disease(AD) produced important new information on the role of inflammation in AD and on theexpression of different neuropathological phenotypes that characteriz[r]
Advances,” Annual Reviews of Public Health 23 (2002): 213-231. 14. See National Alzheimer’s Association, supra note 10.15. M. Kivipelto, E. Helkala, M. Laakso, T. Hänninen, M. Hal-likainen, and K. Alhainen et al., “Midlife Vascular Risk Factors and Alzheimer’s D[r]
suggests that prefibrillar soluble Ab oligomers induce AD-related synapticdysfunction. The size of Ab oligomers is distributed over a wide molecularweight range (from < 10 kDa to > 100 kDa), with structural polymor-phism in Ab oligomers of similar sizes. Recent stud[r]
Non-hydrolytic functions of T-AChE peptides S. A. Greenfield et al.606 FEBS Journal 275 (2008) 604–611 ª 2008 The Authors Journal compilation ª 2008 FEBST30 within its C-terminus (Fig. 1A). However, preli-minary data from our laboratory suggest that glialcells will express a7-nAChR i[r]
Author 4 (W.S.T.G.) provided the RNA samples fromcharacterized human cases and controls. Author 5 (A.S.B.)performed the HPLC measurements and participated inthe design of the study. Author 6 (S.W.B.) conceived of thestudy, participated in its design and coor[r]
M, Mathews PM, Jucker M: Cerebral hemorrhage after passiveanti-Abeta immunotherapy. Science 2002, 298:1379.89. Nicoll JA, Wilkinson D, Holmes C, Steart P, Markham H, Weller RO:Neuropathology of human Alzheimer disease after immuni-zation with amyloid-beta peptide: a case report.[r]
Hogg RC, Bertrand D (2004) Nicotinic acetylcholine receptors as drug targets. Curr Drug TargetsCNS Neurol Disord 3:123–130Holzman PS (2000) Eye movements and the search for the essence of schizophrenia. Brain ResBrain Res Rev 31:350–356Howson AL, Batth S, Ilivitsky V, Boisjoli A, Jawor[r]