Paul Coleman on Free radicals and superoxide dismutase in blood of patients with Alzheimer's disease and vascular dementia.
COMMENT These data are consistent with the hypothesis that AD has a significant systemic component. 0 Paul_Coleman
SEARCH RESULTS
270 RESULTS
Paul Coleman on Cyclooxygenase 2 RNA message abundance, stability, and hypervariability in sporadic Alzheimer neocortex.
COMMENT The role of the COX genes may be quite important in AD, not only from the point of view of an inflammatory cascade, but also in relation to synaptic activation. It would be of interest to determine whether the signal was neuronal, glial or both. Additiona
Paul Coleman on Isoform-specific effect of apolipoprotein E on cell survival and beta-amyloid-induced toxicity in rat hippocampal pyramidal neuronal cultures.
COMMENT Another bit of the puzzle that adds experimental analysis of a potential interaction- a neccessary consideration in view of the large number of potential interactions of APO E and in the AD brain. 0 Paul_Coleman
Paul Coleman on Circulating autoantibodies to neuronal and glial filament proteins in autism.
COMMENT No quantitative data in the abstract to allow any reasonable comment. 0 Paul_Coleman
Paul Coleman on Chronic (-) deprenyl administration increases dendritic arborization in CA3 neurons of hippocampus and AChE activity in specific regions of the primate brain.
COMMENT If this work can be replicated it would provide an interesting insight into a mechanism of action of deprenyl. 0 Paul_Coleman
Paul Coleman on Expression of the alpha3 nicotinic receptor subunit mRNA in aging and Alzheimer's disease.
COMMENT No significant difference in the expression of the alpha 3 mRNA, either qualitative or quantitative, was found between Alzheimer's individuals and controls in any of the analysed areas 0 Paul_Coleman
Paul Coleman on Ubiquitin, cellular inclusions and their role in neurodegeneration.
COMMENT On the basis of the abstract of this article it appears the authors assume that inclusions of ubiquitinated proteins is harmful rather than innocent by-products or attempts of the cell to deal with pathological processes. The assumption that seem to be ma
Paul Coleman on An immunohistochemical study of centenarian brains: a comparison.
COMMENT The abstract for this paper states 'the relative mildness of the age-related morphological changes in the cnetenarians compared with the AD patients suppors the idea that AD would not be the ultimate condition of the aging process'. This conclus
Paul Coleman on Arecoline via miniosmotic pump improves AF64A-impaired radial maze performance in rats: a possible model of Alzheimer's disease.
COMMENT Proposing AF64A treated animals as a model of AD is too long a stretch. 0 Paul_Coleman
Paul Coleman on Differential regional dysfunction of the hippocampal formation among elderly with memory decline and Alzheimer's disease.
COMMENT It appears that the results of this fMRI study may be roughly consistent with the stereological hippocampal regional cell counting study of M.J. West et al. in Lancet. 0 Paul_Coleman
Paul Coleman on Examination of the validity of the hierarchical model of neuropathological staging in normal aging and Alzheimer's disease.
COMMENT A useful exploration of the validity of a widely used approach to neuropathological staging of AD. 0 Paul_Coleman
Paul Coleman on Cortical load of PHF-tau in Alzheimer's disease is correlated to cholinergic dysfunction.
COMMENT It appears the data of this paper may be interpreted in several classes of ways. One class might involve directly causative mechanisms. The other might simply be that as disease progresses the load of PHF-tau increases and the cholinergic deficit also inc
Paul Coleman on Elevated neuronal Cdc2-like kinase activity in the Alzheimer disease brain.
COMMENT This paper appears to be based on the premise that 'tau hyperphosphorylation in AD may result in part from deregulation of Ndlk' (neuronal cdc2-like kinase). Ratio of this kinase activity in prefrontal vs. cerebellare cortex was found to be high
Paul Coleman on Two-dimensional map of human brain proteins.
COMMENT This study utilized 2D gels with Coomassie staining to identify 400 'spots' from parietal lobe sample(s?). The authors conclude 'The two-dimensional map may be useful as a reference database to study changes in the protein level caused by V
Paul Coleman on Mitochondrial DNA mutations in Alzheimer's disease.
COMMENT An important area with a number of findings of uncertain value. A recent paper in PNAS (Hirano et al., 1997, 94:14894-14899) indicates that some of the mt mutations previously described may be due to PCR amplification of nuclear mt DNA pseudogenes consequ