MA Reger, GS Watson, PS Green, CW Wilkinson, LD … - Neurology, 2008 - AAN Enterprises From the Departments of Psychiatry and Behavioral Science (MAR, GSW, CWW, LDB, BC,
JCSB, SC), Medicine (PSG, SRP), and Neurology (MAF), University of Washington School of
Medicine, Seattle; Geriatric Research, Education, and Clinical Center (GSW, CWW, LDB, ... Cited by 64 - Related articles - All 8 versions
- ►nih.gov L Plum, X Ma, B Hampel, N Balthasar, R … - Journal of Clinical …, 2006 - Am Soc Clin Investig 1 Department of Mouse Genetics and Metabolism, Institute for Genetics, University of Cologne
and Center of Molecular Medicine Cologne (CMMC), Cologne, Germany. 2 Klinik II und Poliklinik
für Innere Medizin, University of Cologne and CMMC, Cologne, Germany. 3 University ... Cited by 52 - Related articles - BL Direct - All 16 versions
AI Duarte, P Santos, CR Oliveira, MS Santos, AC … - BBA-Molecular Cell …, 2008 - Elsevier Previously we demonstrated that insulin protects against neuronal oxidative stress by restoring
antioxidants and energy metabolism. In this study, we analysed how insulin influences
insulin- (IR) and insulin growth factor-1 receptor (IGF-1R) intracellular signaling pathways ... Cited by 12 - Related articles - All 3 versions
I Torres-Aleman - Expert opinion on therapeutic targets, 2007 - Informa Pharma Science The 'amyloid cascade hypothesis' proposes that disturbances in amyloid metabolism cause Alzheimer's
disease (AD). However, a comprehensive explanation of the mechanisms leading to brain amyloidosis
is still pending. Building on previous findings with insulin, and recent observations with ... Cited by 11 - Related articles - BL Direct - All 5 versions
JR Babu, ML Seibenhener, J Peng, AL Strom, R … - J …, 2008 - interscience.wiley.com The signaling adapter p62 plays a coordinating role in mediating phosphorylation and
ubiquitin-dependent trafficking of interacting proteins. However, there is little known about the
physiologic role of this protein in brain. Here, we report age-dependent constitutive ... Cited by 10 - Related articles - All 4 versions
V Meske, F Albert, TG Ohm - Journal of Biological Chemistry, 2008 - ASBMB Tau is an important microtubule-stabilizing protein in neurons. In its hyperphosphorylated
form, Tau protein loses its ability to bind to microtubules and then accumulates and is part of
pathological lesions characterizing tauopathies, eg Alzheimer disease. Glycogen ... Cited by 8 - Related articles - All 5 versions
CA Dickey, L Petrucelli - Expert Opin. Ther. Targets, 2006 - informahealthcare.com The pathological hallmarks of Alzheimer's disease (AD) include abnormal intra- and extraneuronal
tau and amyloid accumulation, respectively, accompanied by gliosis, oxidative stress and neuron
loss. The discovery of mutations within the tau gene itself that cause clinical dementia (ie, ... Cited by 7 - Related articles - BL Direct - All 5 versions
X Zhu, SL Siedlak, Y Wang, G Perry, RJ … - Neuropathology and …, 2008 - interscience.wiley.com Aims: The literature and teachings instruct that neurones in the adult brain are fully
differentiated, quiescent cells that never divide. Somewhat surprisingly, and counter to such
dogma, susceptible neurones in Alzheimer disease display an activated cell cycle ... Cited by 7 - Related articles - All 4 versions
B Sabayan, F Foroughinia, A Mowla, A … - American Journal of …, 2008 - aja.sagepub.com Recently, a considerable amount of studies have been focused on impairment in insulin metabolism
in the brain as a new pathogenic process for AD. Individuals suffering from AD had been shown
to have lower cerebrospinal fluid (CSF) and higher plasma insulin concentration. 5 In ... Cited by 6 - Related articles - BL Direct - All 3 versions
