between polymorphism in regulatory region of gene encod-ing tumour necrosis factor alpha and risk of Alzheimer's dis-ease and vascular dementia: a case-control study. Lancet 2001,357:436-439.8. Small GW, Scott WK, Komo S, Yamaoka LH, Farrer LA, AuerbachSH, S[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]
MINIREVIEWAmyloid–cholinesterase interactionsImplications for Alzheimer’s diseaseNibaldo C. Inestrosa, Margarita C. Dinamarca and Alejandra AlvarezCRCP Biomedical Center, Pontificia Universidad Cato´lica de Chile, Santiago, ChileAlzheimer’s disease is a progressive[r]
P-value of < 0.05) between the control and AD samples found wasin the RCAN1-1 protein in the Hc (marked with an asterisk). AsRCAN1-1 protein expression was approximately double that ofRCAN1-4 (Fig. 2B), the signal strength of the two isoforms h[r]
Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction ofcognitive decline in nondemented older adults. Arch Neurol 2007,64:343-349.75. Graff-Radford NR, Crook JE, Lucas J, Boeve BF, Knopman DS, Ivnik RJ,Smith GE, Younkin LH, Petersen RC, Younkin SG: Association of low plasmaAbeta42/A[r]
We report the development of a high-level bacterial expression system forthe Alzheimer’s disease-associated amyloid b-peptide (Ab), together with ascaleable and inexpensive purification procedure. Ab(1–40) and Ab(1–42)coding sequences together with added ATG codons[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[r]
HA DNA vaccine prime–inactivated influenza vaccine boost is moreeffective than using DNA or inactivated vaccine alone in elicitingantibody responses against H1 or H3 serotype influenza viruses. Vaccine2008, 26:3626-3633.30. Dickey CA, Morgan DG, Kudchodkar S, Weiner DB, Bai Y, Cao C,Gordon MN[r]
modulate metal bio-availability have the potential to ameliorate several ofthe dysfunctional events characteristic of Alzheimer’s disease. Metal-basedtherapeutics have already provided promising results for the treatment ofAlzheimer’s diseas[r]
Zinc and Zinc Transport in AD 691Rogaeva E, Meng Y, Lee JH, Gu Y, Kawarai T, Zou F, Katayama T, Baldwin CT, Cheng R,Hasegawa H, Chen F, Shibata N, Lunetta KL, Pardossi-Piquard R, Bohm C, Wakutani Y,Cupples LA, Cuenco KT, Green RC, Pinessi L, Rainero I, Sorbi S, Bruni A, Duara R, FriedlandRP,[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]
Abstract The first description of the inflammatory process appeared as early as thefirst century AD. Among the first things learned about inflammation is that vascu-lar permeability is increased and leukocyte extravasation occurs. It is now realizedthat the central nerv[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, IndiaI[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
ological effects of microglia on tau phosphorylation and onsynaptophysin synthesis in cortical neurons through a p38-MAPK pathway. J Neurosci 2003, 23:1605-1611.39. Klegeris A, McGeer PL: β-amyloid protein enhances macro-phage production of oxygen free radicals and glutamate. J.Neurosc[r]
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]