keyword
https://read.qxmd.com/read/29210673/detecting-beta-amyloid-aggregation-from-time-resolved-emission-spectra
#1
JOURNAL ARTICLE
A Alghamdi, V Vyshemirsky, D J S Birch, O J Rolinski
The aggregation of beta-amyloids is one of the key processes responsible for the development of Alzheimer's disease. Early molecular-level detection of beta-amyloid oligomers may help in early diagnosis and in the development of new intervention therapies. Our previous studies on the changes in beta-amyloid's single tyrosine intrinsic fluorescence response during aggregation demonstrated a four-exponential fluorescence intensity decay, and the ratio of the pre-exponential factors indicated the extent of the aggregation in the early stages of the process before the beta-sheets were formed...
January 22, 2018: Methods and Applications in Fluorescence
https://read.qxmd.com/read/19378813/-pathology-of-basal-ganglia-in-neurodegenerative-diseases
#2
REVIEW
Koichi Wakabayashi, Kunikazu Tanji, Fumiaki Mori
Intra- and/or extracellular proteinaceous inclusions in the brain tissue are characteristic pathological markers of many neurodegenerative diseases. Tau protein in neurofibrillary tangles and beta-amyloid in senile plaques are associated with Alzheimer's disease. Tau is associated with various neurological conditions, which are collectively referred to as tauopathies. Alpha-synucleinopathy is a term that collectively refers to a set of diseases in which neurodegeneration is accompanied by intracellular accumulation of alpha-synuclein in neurons or glial cells...
April 2009: Brain and Nerve, Shinkei Kenkyū No Shinpo
https://read.qxmd.com/read/12710947/the-mechanism-of-cytokeratin-aggresome-formation-the-role-of-mutant-ubiquitin-ubb-1
#3
JOURNAL ARTICLE
F Bardag-Gorce, N Riley, V Nguyen, R O Montgomery, B A French, J Li, F W van Leeuwen, W Lungo, L W McPhaul, S W French
Aggresome formation in cells involves the failure of the ubiquitin-proteasome pathway to dispose of proteins destined for degradation by the 26S proteasome. UBB(+1) is present in Mallory bodies in alcoholic liver disease and in aggresomes formed in Alzheimer's desease. The present investigation focuses on the role that UBB(+1) plays in cytokeratin aggresome formation in Mallory bodies (MBs) in vitro. Immunoprecipitation with a monoclonal antibody to cytokeratin-8 (CK-8) was used. The immunoprecipitate was incubated for 24 h in the presence of different constituents involved in aggresome formation including ubiquitin, UBB(+1), the proteasome inhibitor PS341, an ATP generating energy source, a deubiquitinating enzyme inhibitor, a purified proteasome fraction, and an E(1-3) conjugating enzyme fraction...
April 2003: Experimental and Molecular Pathology
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