Deciphering the molecular basis of memory failure in Alzheimer's disease.

TL;DR: LX2343 is demonstrated to be a non-ATP competitive GSK-3β inhibitor with IC50 of 1.84±0.07 μmol/L, and it potently inhibited tau hyperphosphorylation in the neuronal cells.

TL;DR: The fluorescence of functionalized NDs is more stable than that of fluorescent markers commonly used to stain Aβ aggregates such as Thioflavin T. These results pave the way for performing ultrasensitive and reliable detection of A β aggregates involved in the pathogenesis of the Alzheimer disease.

TL;DR: It is found that inflammation signaling pathways including Toll-like receptors and inflammasomes NOD-, LRR-, and pyrin domain-containing protein 3 are involved in the initiation of apoptosis by the Aβ fibrils, and these inflammation-related molecules are promising targets for the prevention of apoptotic cell death induced by Aβ.

TL;DR: A general impairment of synaptic function and learning and memory in young AβPP23tg mice with Aβ oligomers but no amyloid plaques is indicated.

TL;DR: The APOE-epsilon 4 allele is associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD) in 42 families with late onset AD.

TL;DR: A purified protein derived from the twisted beta-pleated sheet fibrils in cerebrovascular amyloidosis associated with Alzheimer's disease has been isolated and Amino acid sequence analysis and a computer search reveals this protein to have no homology with any protein sequenced thus far.

TL;DR: An apparently full-length complementary DNA clone coding for the A4 polypeptide is isolated and sequenced and suggests that the cerebral amyloid deposited in Alzheimer's disease and aged Down's syndrome is caused by aberrant catabolism of a cell-surface receptor.

TL;DR: The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy of Alzheimer disease and Down syndrome.