| 1. |
|
|
| 2. |
- Garcia-Parrado, Alfonso, 2000-, et al.
(author)
-
Initial data sets for Schwarzschild spacetime
- 2007
-
In: Physical Review D. Particles and fields. - 0556-2821 .- 1089-4918. ; 75, s. 024027-024041
-
Journal article (peer-reviewed)abstract
- A characterization of initial data sets for the Schwarzschild spacetime is provided. This characterization is obtained by performing a 3+1 decomposition of a certain invariant characterization of the Schwarzschild spacetime given in terms of concomitants of the Weyl tensor. This procedure renders a set of necessary conditions -which can be written in terms of the electric and magnetic parts of the Weyl tensor and their concomitants -for an initial data set to be a Schwarzschild initial data set. Our approach also provides a formula for a static Killing initial data set candidate -a KID candidate. Sufficient conditions for an initial data set to be a Schwarzschild initial data set are obtained by supplementing the necessary conditions with the requirement that the initial data set possesses a stationary Killing initial data set of the form given by our KID candidate. Thus, we obtain an algorithmic procedure of checking whether a given initial data set is Schwarzschildean or not.
|
|
| 3. |
- Natunen, Teemu, et al.
(author)
-
Elucidation of the BACE1 Regulating Factor GGA3 in Alzheimer's Disease
- 2013
-
In: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 37:1, s. 217-232
-
Journal article (peer-reviewed)abstract
- Golgi-localized gamma-ear-containing ADP-ribosylation factor-binding protein (GGA3) is a central regulator of trafficking and degradation of BACE1 (beta-site A beta PP-cleaving enzyme), the rate-limiting enzyme in the production of amyloid-beta (A beta) in Alzheimer's disease (AD). Here, we assessed the potential role of GGA3 in AD pathogenesis using independent neuropathological, case-control, and family-based human sample cohorts. Increased BACE1 levels coincided with decreased GGA3 levels and with elevated phosphorylation status of eIF2 alpha-Ser51 in the temporal cortex of AD patients as compared to age-matched controls. Severity of the disease did not alter mRNA or protein levels of GGA3 in the inferior temporal cortex of AD patients, while a positive correlation between GGA3 and the levels of total, but not phosphorylated, tau was observed. Genetically, we did not observe consistent evidence for association between AD risk and common GGA3 polymorphisms across a number of independent sample cohorts. However, a nominally significant association was observed with rs2242230 (p < 0.05) among the Finnish case-control cohort. Accordingly, mRNA and protein levels of GGA3 in the inferior temporal cortex of AD patients did not significantly correlate with rs2242230 genotype status. While the present study indicates that GGA3 is involved in the cellular processes relevant for AD pathogenesis, the genetic data do not support the idea that common GGA3 polymorphisms would contribute to AD risk.
|
|
| 4. |
- Treusch, Sebastian, et al.
(author)
-
Functional links between Aβ toxicity, endocytic trafficking, and Alzheimer's disease risk factors in yeast
- 2011
-
In: Science. - Washington : American association of advancement in science. - 0036-8075 .- 1095-9203. ; 334:6060, s. 1241-1245
-
Journal article (peer-reviewed)abstract
- Aβ (beta amyloid peptide) is an important contributor to Alzheimer's disease (AD). We modeled Aβ toxicity in yeast by directing the peptide to the secretory pathway. A genome-wide screen for toxicity modifiers identified the yeast homolog of phosphatidylinositol binding clathrin assembly protein (PICALM) and other endocytic factors connected to AD whose relationship to Aβ was previously unknown. The factors identified in yeast modified Aβ toxicity in glutamatergic neurons of Caenorhabditis elegans and in primary rat cortical neurons. In yeast, Aβ impaired the endocytic trafficking of a plasma membrane receptor, which was ameliorated by endocytic pathway factors identified in the yeast screen. Thus, links between Aβ, endocytosis, and human AD risk factors can be ascertained using yeast as a model system.
|
|
