Michael Hoos

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The assembly and deposition of amyloid β-protein (Aβ) in brain is a key pathological feature of Alzheimer's disease and related disorders. Factors have been identified that can either promote or inhibit Aβ assembly in brain. We previously reported that myelin basic protein (MBP) is a potent inhibitor of Aβ fibrillar assembly [Hoos, M. D., et al. (2007) J.(More)
Fibrillar amyloid plaques are largely composed of amyloid-beta (Aβ) peptides that are metabolized into products, including Aβ1-16, by proteases including matrix metalloproteinase 9 (MMP-9). The balance between production and degradation of Aβ proteins is critical to amyloid accumulation and resulting disease. Regulation of MMP-9 and its endogenous inhibitor(More)
Accumulation of amyloid β-protein (Aβ) into brain parenchymal plaques and the cerebral vasculature is a pathological feature of Alzheimer disease and related disorders. Aβ peptides readily form β-sheet-containing oligomers and fibrils. Previously, we reported a strong interaction between myelin basic protein (MBP) and Aβ peptides that resulted in potent(More)
Deposition of fibrillar amyloid -protein (A ) in the brain is a prominent pathological feature of Alzheimer disease and related disorders, including familial forms of cerebral amyloid angiopathy (CAA). Mutant forms of A , including Dutchand Iowa-type A , which are responsible for familial CAA, deposit primarily as fibrillar amyloid along the cerebral(More)
The deposition of amyloid beta-protein (Abeta) fibrils into plaques within the brain parenchyma and along cerebral blood vessels is a hallmark of Alzheimer's disease. Abeta peptides are produced through the successive cleavage of the Abeta precursor protein by beta- and gamma-secretase, producing peptides between 39 and 43 amino acids in length. The most(More)
Deposition of fibrillar amyloid beta-protein (Abeta) in the brain is a prominent pathological feature of Alzheimer disease and related disorders, including familial forms of cerebral amyloid angiopathy (CAA). Mutant forms of Abeta, including Dutch- and Iowa-type Abeta, which are responsible for familial CAA, deposit primarily as fibrillar amyloid along the(More)
Alzheimer's disease (AD) is a complex neurodegenerative process that involves altered brain immune, neuronal and metabolic functions. Understanding the underlying mechanisms has relied on mouse models that mimic components of AD pathology. We used gel-free, label-free LC-MS/MS to quantify protein and phosphopeptide levels in brains of APPSwDI/NOS2-/-(More)
Die Sicherheit ist tot, es lebe die Sicherheit – zugegeben, ein wenig abgekupfert von alter, französischer Tradition, doch auf die Belange heutiger IT gemünzt ein ungemein passender Ausspruch. Denn das derzeitige Modell, nach dem die meisten Firmen ihre Sicherheit organisieren, funktioniert nicht mehr! Es ist zu starr und unflexibel, zugleich zu löchrig und(More)
Mouse models are used in the study of human disease. Despite well-known homologies, the difference in immune response between mice and humans impacts the application of data derived from mice to human disease outcomes. Nitric oxide synthase-2 (NOS2) is a key gene that displays species-specific outcomes via altered regulation of the gene promoter and via(More)
INTRODUCTION Kunitz proteinase inhibitor (KPI) domain-containing forms of the amyloid β-protein precursor (AβPP) inhibit cerebral thrombosis. KPI domain-lacking forms of AβPP are abundant in brain. Regions of AβPP other than the KPI domain may also be involved with regulating cerebral thrombosis. To determine the contribution of the KPI domain to the(More)
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