TY  - JOUR
A1  - Haberstumpf, Sophia
A1  - Leinweber, Jonas
A1  - Lauer, Martin
A1  - Polak, Thomas
A1  - Deckert, Jürgen
A1  - Herrmann, Martin J.
T1  - Factors associated with dropout in the longitudinal Vogel study of cognitive decline
JF  - The European Journal of Neuroscience
N2  - Dementia, including Alzheimer's disease, is a growing problem worldwide. Prevention or early detection of the disease or a prodromal cognitive decline is necessary. By means of our long-term follow-up ‘Vogel study’, we aim to predict the pathological cognitive decline of a German cohort (mean age was 73.9 ± 1.55 years at first visit) with three measurement time points within 6 years per participant. Especially in samples of the elderly and subjects with chronic or co-morbid diseases, dropouts are one of the biggest problems of long-term studies. In contrast to the large number of research articles conducted on the course of dementia, little research has been done on the completion of treatment. To ensure unbiased and reliable predictors of cognitive decline from study completers, our objective was to determine predictors of dropout. We conducted multivariate analyses of covariance and multinomial logistic regression analyses to compare and predict the subject's dropout behaviour at the second visit 3 years after baseline (full participation, partial participation and no participation/dropout) with neuropsychiatric, cognitive, blood and lifestyle variables. Lower performance in declarative memory, attention and visual–spatial processing predicted dropout rather than full participation. Lower performance in visual–spatial processing predicted partial participation as opposed to full participation. Furthermore, lower performance in mini-mental status examination predicted whether subjects dropped out or participated partially instead of full participation. Baseline cognitive parameters are associated with dropouts at follow-up with a loss of impaired participants. We expect a bias into a healthier sample over time.
KW  - dementia
KW  - prevention
KW  - cognitive decline
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-318945
VL  - 56
IS  - 9
SP  - 5587
EP  - 5600
ER  - 
TY  - JOUR
A1  - Karunakaran, Mohindar M.
A1  - Subramanian, Hariharan
A1  - Jin, Yiming
A1  - Mohammed, Fiyaz
A1  - Kimmel, Brigitte
A1  - Juraske, Claudia
A1  - Starick, Lisa
A1  - Nöhren, Anna
A1  - Länder, Nora
A1  - Willcox, Carrie R.
A1  - Singh, Rohit
A1  - Schamel, Wolfgang W.
A1  - Nikolaev, Viacheslav O.
A1  - Kunzmann, Volker
A1  - Wiemer, Andrew J.
A1  - Willcox, Benjamin E.
A1  - Herrmann, Thomas
T1  - A distinct topology of BTN3A IgV and B30.2 domains controlled by juxtamembrane regions favors optimal human γδ T cell phosphoantigen sensing
JF  - Nature Communications
N2  - Butyrophilin (BTN)–3A and BTN2A1 molecules control the activation of human Vγ9Vδ2 T cells during T cell receptor (TCR)-mediated sensing of phosphoantigens (PAg) derived from microbes and tumors. However, the molecular rules governing PAg sensing remain largely unknown. Here, we establish three mechanistic principles of PAg-mediated γδ T cell activation. First, in humans, following PAg binding to the intracellular BTN3A1-B30.2 domain, Vγ9Vδ2 TCR triggering involves the extracellular V-domain of BTN3A2/BTN3A3. Moreover, the localization of both protein domains on different chains of the BTN3A homo-or heteromers is essential for efficient PAg-mediated activation. Second, the formation of BTN3A homo-or heteromers, which differ in intracellular trafficking and conformation, is controlled by molecular interactions between the juxtamembrane regions of the BTN3A chains. Finally, the ability of PAg not simply to bind BTN3A-B30.2, but to promote its subsequent interaction with the BTN2A1-B30.2 domain, is essential for T-cell activation. Defining these determinants of cooperation and the division of labor in BTN proteins improves our understanding of PAg sensing and elucidates a mode of action that may apply to other BTN family members.
KW  - gammadelta T cells
KW  - immunosurveillance
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-358179
VL  - 14
ER  -