The UN Security Council's involvement in the area of international criminal justice raises concerns about judicial independence. Of primary concern in this study is the degree to which this political organ has come to determine and restrict jurisdiction of international criminal tribunals, with the effect of excluding cases involving alleged grave crimes by actors whose presence in situations of w

Denna sammanläggningsavhandling består av fyra artiklar, som alla berör olika utvidgningar av Standardmodellen (SM). De första två artiklarna behandlar en specifik, supersymmetrisk, storförenad teori (GUT), medan de senare två klassificerar alla anomali-fria instanser av 2-Higgs-dubblett modeller (2HDMs) med en gauge:ad abelsk symmetri. Artikel I. I denna artikel presenterar vi en alternativ lösniThis thesis is composed of four papers, which all treat various extensions to the Standard Model (SM). The first two papers concern a particular supersymmetric, grand-unified theory (GUT), while in the latter two, we classify anomaly-free implementations of two-Higgs doublet models (2HDM) with a gauged abelian symmetry. Paper I. In this paper, we present an alternative solution for avoiding GUT-sc

Although β-amyloid (Aβ) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Aβ and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precur

A central question in Alzheimer's disease research is what role synaptic activity plays in the disease process. Synaptic activity has been shown to induce β-amyloid peptide release into the extracellular space, and extracellular β-amyloid has been shown to be toxic to synapses. We now provide evidence that the well established synaptotoxicity of extracellular β-amyloid requires β-secretase process

Increasing evidence links intraneuronal β-amyloid (Aβ 42) accumulation with the pathogenesis of Alzheimer's disease (AD). In Aβ precursor protein (APP) mutant transgenic mice and in human AD brain, progressive intraneuronal accumulation of Aβ42 occurs especially in multivesicular bodies (MVBs). We hypothesized that this impairs the MVB sorting pathway. We used the trafficking of the epidermal grow

Amyloid-β peptide is elevated in the brains of patients with Alzheimer disease and is believed to be causative in the disease process. Amyloid-β reduces glutamatergic transmission and inhibits synaptic plasticity, although the underlying mechanisms are unknown. We found that application of amyloid-β promoted endocytosis of NMDA receptors in cortical neurons. In addition, neurons from a genetic mou

Multiple lines of evidence implicate β-amyloid (Aβ) in the pathogenesis of Alzheimer's disease (AD), but the mechanisms whereby Aβ is involved remain unclear. Addition of Aβ to the extracellular space can be neurotoxic. Intraneuronal Aβ42 accumulation is also associated with neurodegeneration. We reported previously that in Tg2576 amyloid precursor protein mutant transgenic mice, brain Aβ42 locali

Molecular chaperones and their functions in protein folding have been implicated in several neurodegenerative diseases, including Parkinson's disease and Huntington's disease, which are characterized by accumulation of protein aggregates (e.g., α-synuclein and huntingtin, respectively). These aggregates have been shown in various experimental systems to respond to changes in levels of molecular ch

Early events in Alzheimer's disease (AD) pathogenesis implicate the accumulation of β-amyloid (Aβ) peptide inside neurons in vulnerable brain regions. However, little is known about the consequences of intraneuronal Aβ on signaling mechanisms. Here, we demonstrate, using an inducible viral vector system to drive intracellular expression of Aβ42 peptide in primary neuronal cultures, that this accum

The issue of Critical Raw Materials (CRMs) and potential interruptions to their availability due to shortages, trade restrictions or other factors in their supply are topics that are relatively unknown to the general public. For this reason, education has been promoted as a key enabler of a circular economy. One key intervention point is the movement of electronic repair events. Repair events alre

The excessive generation and accumulation of 40- and 42-aa β-amyloid peptides (Aβ40/Aβ42) in selectively vulnerable brain regions is a major neuropathological feature of Alzheimer's disease. Aβ, derived by proteolytic cleavage from the β-amyloid precursor protein (βAPP), is normally secreted. However, recent evidence suggests that significant levels of Aβ also may remain inside cells. Here, we hav