Exosome reduction in vivo is associated with lower amyloid plaque load in the 5XFAD mouse model of Alzheimer's disease.
AuthorsDinkins MB, Dasgupta S, Wang G, Zhu G, Bieberich E,
Journal
PubMed ID24650793
We present evidence here that exosomes stimulate aggregation of amyloid beta (Aß)1-42 in vitro and in vivo and interfere with uptake of Aß by primary cultured astrocytes and microglia in vitro. Exosome secretion is prevented by the inhibition of neutral sphingomyelinase 2 (nSMase2), a key regulatory enzyme generating ceramide from sphingomyelin, with GW4869. ... More
Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aß42 accumulation and Caspase-3 activation.
AuthorsEimer WA, Vassar R,
JournalMol Neurodegener
PubMed ID23316765
Although the mechanism of neuron loss in Alzheimer's disease (AD) is enigmatic, it is associated with cerebral accumulation of Aß42. The 5XFAD mouse model of amyloid deposition expresses five familial AD (FAD) mutations that are additive in driving Aß42 overproduction. 5XFAD mice exhibit intraneuronal Aß42 accumulation at 1.5 months, amyloid ... More
Hypoxia due to cardiac arrest induces a time-dependent increase in serum amyloid ß levels in humans.
AuthorsZetterberg H, Mörtberg E, Song L, Chang L, Provuncher GK, Patel PP, Ferrell E, Fournier DR, Kan CW, Campbell TG, Meyer R, Rivnak AJ, Pink BA, Minnehan KA, Piech T, Rissin DM, Duffy DC, Rubertsson S, Wilson DH, Blennow K,
JournalPLoS One
PubMed ID22194817
Amyloid ß (Aß) peptides are proteolytic products from amyloid precursor protein (APP) and are thought to play a role in Alzheimer disease (AD) pathogenesis. While much is known about molecular mechanisms underlying cerebral Aß accumulation in familial AD, less is known about the cause(s) of brain amyloidosis in sporadic disease. ... More