Alzheimer’s disease pathology

Neuroanatomical and neuropathological basis of Alzheimer s disease Histological features of Alzheimer s disease include neuritic plaques and neurofibrillary tangles (Boiler and Duyckaerts 1997). Neuritic plaques are composed of extracellular deposits of j8-amyloid protein and apolipoprotein E and are found primarily in neocortex. j8-amyloid is derived from an amyloid precursor protein, and is suspected to be a chief causal factor in Alzheimer s disease pathology (Samuel et al. 1997). Neurofibrillary tangles are clusters of protein fibers found in the cell body and composed of tau protein, which normally serves as a cytoskeletal element. Neurofibrillary tangles progress from entorhinal cortex to hippocampus, and then to neocortical areas. [Pg.147]

Konishi, Y., Beach, T., Sue, L.I., et al. (2003) The temporal localization of frame-shift ubiq-uitin-B and amyloid precursor protein, and complement proteins in the brain of non-demented control patients with increasing Alzheimer s disease pathology. Neurosci. Lett., 348, 46-50. [Pg.338]

Wang HY, Lee DH, D Andrea MR, Peterson PA, Shank RP, Reitz AB. 2000b. beta-Amyloid(1 12) binds to alpha7 nicotinic acetylcholine receptor with high affinity. Implications for Alzheimer s disease pathology. J Biol Chem 275(8) 5626-5632. [Pg.136]

Hoozemans JJ, O Banion MK (2005) The role of COX-1 and COX-2 in Alzheimer s disease pathology and the therapeutic potentials of non-steroidal anti-inflammatory drugs. Curr. Drug Targets CNSNeurol. Disord. 4 307-315. [Pg.38]

Subcortical infarcts, Alzheimer s disease pathology, and memory function in older persons. Annals of Neurology 62 59-66... [Pg.371]

Wilson RS, Arnold SE, Schneider JA, Tang Y, Bennett DA (2007) The relationship between cerebral Alzheimer s disease pathology and odour identification in old age. 1 Neurol Neurosurg Psychiatry 78(l) 30-35... [Pg.292]

Mishizen-Eherz, A.J., Rissman, R.A., Carter, T.L., Ikonomovic, M.D., Wolfe, B.B., Armstrong, D.M. (2004). Biochemical and molecular studies of NMDA receptor subunits NR1/2A/2B in hippocampal subregions throughout progression of Alzheimer s disease pathology. Neurobiol. Dis. 15 80-92. [Pg.648]

Emmerling MR, Watson MD, Raby CA, Spiegel K (2000) The role of complement in Alzheimer s disease pathology. Biochim Bio-phys Acta 1502 158-171. [Pg.103]

As (3-amyloidi 42 is a neurotoxic agent, the hypothesis that this is a key molecule in the pathology of Alzheimer s disease is now widely accepted (see Selkoe 2001, for review). The theory is controversial since the correlation between the concentrations and distribution of amyloid depositions in the brain and parameters of Alzheimer s disease pathology, such as the degree of dementia, loss of synapses, and loss of neurons, is poor (Neve and Robakis 1998). [Pg.92]

Zou F, Belbin O, Carrasquillo MM, Culley OJ, Hunter TA, Ma L et al (2013) Linking protective GAB2 variants, increased cortical GAB2 expression and decreased Alzheimer s disease pathology. PLoS One 8 e64802. doi 10.1371/journal.pone.0064802... [Pg.521]

Frisardi V, Panza F, Seripa D, Farooqui T, Farooqui AA (2011) Glycerophospholipids and glycerophospholipid-derived lipid mediators A complex meshwork in Alzheimer s disease pathology. Prog Lipid Res 50 313-330... [Pg.522]

Paban V, Manrique C, Filali M, Maunoir-Regimbal S, Fauvelle F, Alescio-Lautier B et al (2014) Therapeutic and preventive effects of methylene blue on Alzheimer s disease pathology in a transgenic mouse model. Neuropharmacology 76(Pt A) 68-79... [Pg.544]

Among the structural proteins which are subject to GSK-3 regulation, the microtubule-associated protein tau is a prime target in Alzheimer s disease pathology. Tau binds to tubulin and promotes microtubule assembly and stability in a phosphorylation-dependent manner. The phosphorylation status of tau is balanced by antagonistic kinase and phosphate activities. Inappropriate hyperphosphorylation of tau is a key event in contributing to cytoskeletal abnormalities and tau pathology in Alzheimer s disease. When hyperphos-phorylated, tau s affinity for the microtubule is reduced and as a consequence tau dissociates from the microtubules. This leads to abnormal accumulation... [Pg.140]

Styren, S.D., Hamilton, R. L., Styren, G.C., and Klunk, W. E. (2000) X-34, a fluorescent derivative of Congo red a novel histochem-ical stain for Alzheimer s disease pathology,... [Pg.1298]

Gomez-Pinilla, F., Cummings, B.J. and Cotman, C.W. (1990) Induction of basic fibroblast growth factor in Alzheimer s disease pathology. NeuroReport 1 211-214. [Pg.366]

Shi, Y., Kirwan, P., Smith, J., et al. A Human Stem Cell Model of Early Alzheimer s Disease Pathology in Down Syndrome. Sci. Transl. Med. 4, 1-9 (2012)... [Pg.319]

Skoch, J., et al. Development of an optical approach for noninvasive imaging of Alzheimer s disease pathology. Journal of Biomedical Optics 10(1), 011007-0110077 (2005)... [Pg.353]

There is no evidence to support a primary causative role for aluminium in Alzheimer s disease and aluminium does not induce Alzheimer s disease pathology in vivo in any species, including humans [12]. [Pg.581]

Lessons from the genetic control of translation of ferritin mRNAS and transferrin receptor mRNA stability can be applied to the control of APP expression by iron. This information will be relevant to Alzheimer s disease pathology after applying these models of post-transcriptional control to APP gene expression. [Pg.219]

ERp57 and improves Alzheimer s disease pathologies in 5XFAD mice. Sci Rep 2 535... [Pg.298]

Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...