👤 Isabelle Pin

🔍 Search 📋 Browse 🏷️ Tags ❤️ Favourites ➕ Add 🧬 Extraction
2
Articles
2
Name variants
Also published as: G Pin,
articles
G Pin, T Horowitz, E Guedj +3 more · 2026 · Revue neurologique · Elsevier · added 2026-04-24
Medial temporal lobe amnestic syndrome (MTLA) is classically considered a hallmark of Alzheimer's disease (AD). However, emerging evidence suggests etiological heterogeneity, challenging the assumptio Show more
Medial temporal lobe amnestic syndrome (MTLA) is classically considered a hallmark of Alzheimer's disease (AD). However, emerging evidence suggests etiological heterogeneity, challenging the assumption that MTLA universally reflects AD pathology. To determine the prevalence of amyloid pathology in isolated MTLA, identify phenotypic and genetic risk factors, and characterize associated network vulnerabilities in amnestic mild cognitive impairment (aMCI). This retrospective observational study analyzed 55 patients with isolated MTLA at the aMCI stage. Participants underwent neuropsychological testing, cerebrospinal fluid (CSF) biomarker analysis, amyloid PET, and 18FDG-PET. Patients were stratified by amyloid status (positive/negative) and compared for APOE genotype, clinical features, and metabolic patterns. Statistical analyses included the Kruskal-Wallis test for non-parametric group comparisons and chi-square tests for categorical genetic associations. Amyloid pathology was observed in only 67% (37/55) of MTLA patients, dissociating the syndrome from AD in one-third of cases. Amyloid-positive patients demonstrated a significantly higher APOE ɛ4 carrier rate compared to amyloid-negative peers (χ MTLA syndrome is not homogeneous on the biological level and amyloid pathology and APOE ɛ4 genotype stratify patients into distinct subgroups. Amyloid-positive cases demonstrate inferotemporal hypometabolism, suggesting AD-related network vulnerability. By contrast, amyloid-negative MTLA group shows no systemic brain network vulnerabilities, likely due to its heterogeneous etiological origins. These findings advocate for a precision medicine framework integrating biomarkers to guide therapeutic strategies, moving beyond syndromic diagnoses to target underlying mechanisms. Show less
no PDF DOI: 10.1016/j.neurol.2026.02.149
APOE
Daan W Loth, María Soler Artigas, Sina A Gharib +157 more · 2014 · Nature genetics · Nature · added 2026-04-24
Daan W Loth, María Soler Artigas, Sina A Gharib, Louise V Wain, Nora Franceschini, Beate Koch, Tess D Pottinger, Albert Vernon Smith, Qing Duan, Chris Oldmeadow, Mi Kyeong Lee, David P Strachan, Alan L James, Jennifer E Huffman, Veronique Vitart, Adaikalavan Ramasamy, Nicholas J Wareham, Jaakko Kaprio, Xin-Qun Wang, Holly Trochet, Mika Kähönen, Claudia Flexeder, Eva Albrecht, Lorna M Lopez, Kim de Jong, Bharat Thyagarajan, Alexessander Couto Alves, Stefan Enroth, Ernst Omenaas, Peter K Joshi, Tove Fall, Ana Viñuela, Lenore J Launer, Laura R Loehr, Myriam Fornage, Guo Li, Jemma B Wilk, Wenbo Tang, Ani Manichaikul, Lies Lahousse, Tamara B Harris, Kari E North, Alicja R Rudnicka, Jennie Hui, Xiangjun Gu, Thomas Lumley, Alan F Wright, Nicholas D Hastie, Susan Campbell, Rajesh Kumar, Isabelle Pin, Robert A Scott, Kirsi H Pietiläinen, Ida Surakka, Yongmei Liu, Elizabeth G Holliday, Holger Schulz, Joachim Heinrich, Gail Davies, Judith M Vonk, Mary Wojczynski, Anneli Pouta, Asa Johansson, Sarah H Wild, Erik Ingelsson, Fernando Rivadeneira, Henry Völzke, Pirro G Hysi, Gudny Eiriksdottir, Alanna C Morrison, Jerome I Rotter, Wei Gao, Dirkje S Postma, Wendy B White, Stephen S Rich, Albert Hofman, Thor Aspelund, David Couper, Lewis J Smith, Bruce M Psaty, Kurt Lohman, Esteban G Burchard, André G Uitterlinden, Melissa Garcia, Bonnie R Joubert, Wendy L McArdle, A Bill Musk, Nadia Hansel, Susan R Heckbert, Lina Zgaga, Joyce B J van Meurs, Pau Navarro, Igor Rudan, Yeon-Mok Oh, Susan Redline, Deborah L Jarvis, Jing Hua Zhao, Taina Rantanen, George T O'Connor, Samuli Ripatti, Rodney J Scott, Stefan Karrasch, Harald Grallert, Nathan C Gaddis, John M Starr, Cisca Wijmenga, Ryan L Minster, David J Lederer, Juha Pekkanen, Ulf Gyllensten, Harry Campbell, Andrew P Morris, Sven Gläser, Christopher J Hammond, Kristin M Burkart, John Beilby, Stephen B Kritchevsky, Vilmundur Gudnason, Dana B Hancock, O Dale Williams, Ozren Polasek, Tatijana Zemunik, Ivana Kolcic, Marcy F Petrini, Matthias Wjst, Woo Jin Kim, David J Porteous, Generation Scotland, Blair H Smith, Anne Viljanen, Markku Heliövaara, John R Attia, Ian Sayers, Regina Hampel, Christian Gieger, Ian J Deary, H Marike Boezen, Anne Newman, Marjo-Riitta Jarvelin, James F Wilson, Lars Lind, Bruno H Stricker, Alexander Teumer, Timothy D Spector, Erik Melén, Marjolein J Peters, Leslie A Lange, R Graham Barr, Ken R Bracke, Fien M Verhamme, Joohon Sung, Pieter S Hiemstra, Patricia A Cassano, Akshay Sood, Caroline Hayward, Josée Dupuis, Ian P Hall, Guy G Brusselle, Martin D Tobin, Stephanie J London Show less
Forced vital capacity (FVC), a spirometric measure of pulmonary function, reflects lung volume and is used to diagnose and monitor lung diseases. We performed genome-wide association study meta-analys Show more
Forced vital capacity (FVC), a spirometric measure of pulmonary function, reflects lung volume and is used to diagnose and monitor lung diseases. We performed genome-wide association study meta-analysis of FVC in 52,253 individuals from 26 studies and followed up the top associations in 32,917 additional individuals of European ancestry. We found six new regions associated at genome-wide significance (P < 5 × 10(-8)) with FVC in or near EFEMP1, BMP6, MIR129-2-HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease. Show less
📄 PDF DOI: 10.1038/ng.3011
HSD17B12