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Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease
Brain Atrophy in Type 2 Diabetes
T2DM was associated with poorer visuospatial construction, planning, visual memory, and speed independent of age, sex, education, and vascular risk factors and the strength of these associations was attenuated when adjusted for hippocampal and total gray volumes but was unchanged by adjustment for cerebrovascular lesions or white matter volume.
Determination of Advanced Glycation End Products in Serum by Fluorescence Spectroscopy and Competitive ELISA
An accurate and rapid assay for their determination would be useful for monitoring the removal of advanced glycation endproducts by novel dialysis membranes, as well as the effect of new drugs for the inhibition of their formation.
Characterization of advanced glycation end products for biochemical studies: side chain modifications and fluorescence characteristics.
High molecular weight hyaluronic acid inhibits advanced glycation endproduct‐induced NF‐κB activation and cytokine expression
Activated astroglia during chronic inflammation in Alzheimer's disease--do they neglect their neurosupportive roles?
Crosslinking of α-synuclein by advanced glycation endproducts — an early pathophysiological step in Lewy body formation?
Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer's disease.
Protein glycation, oxidation and nitration adduct residues and free adducts of cerebrospinal fluid in Alzheimer's disease and link to cognitive impairment
- N. Ahmed, U. Ahmed, Paul J Thornalley, K. Hager, G. Fleischer, G. Münch
- Biology, ChemistryJournal of neurochemistry
- 1 January 2005
Findings indicate that protein glycation, oxidation and nitration adduct residues and free adducts were increased in the CSF of subjects with Alzheimer's disease.
Alzheimer’s associated inflammation, potential drug targets and future therapies
The inflammatory pathways that are thought to be present in Alzheimer’s disease and some of the new therapies that have shown promise, via alteration or inhibition of these pathways are described.