Kavli Affiliate: Terry Jernigan
| Authors: Amirhossein Modabbernia, Didac Vidal-Pineiro, Ingrid Agartz, Ole A Andreassen, Rosa Ayesa-Arriola, Alessandro Bertolino, Dorret I Boomsma, Josiane Bourque, Alan Breier, Rachel M Brouwer, Jan K Buitelaar, Erick J Canales-Rodriguez, Xavier Caseras, Patricia J Conrod, Benedicto Crespo-Facorro, Fabrice Crivello, Eveline A Crone, Greig I de Zubicaray, Erin W Dickie, Danai Dima, Stefan Frenzel, Simon E. Fisher, Barbara Franke, David C Glahn, Hans-Jorgen Grabe, Dominik Grotegerd, Oliver Gruber, Amalia Guerrero-Pedraza, Raquel E Gur, Ruben C Gur, Catharina A Hartman, Pieter J Hoekstra, Hilleke E Hulshoff Pol, Neda Jahanshad, Terry L Jernigan, Jiyang Jiang, Andrew J Kalnin, Nicole A Kochan, Bernard Mazoyer, Brenna C McDonald, Katie L McMahon, Lars Nyberg, Jaap Oosterlaan, Edith Pomarol-Clotet, Joaquim Radua, Perminder S Sachdev, Theodore D Satterthwaite, Raymond Salvador, Salvador Sarro, Andrew J Saykin, Gunter Schumann, Jordan W Smoller, Iris E Sommer, Thomas Espeseth, Sophia I Thomopoulos, Julian N Trollor, Dennis van ‘t Ent, Aristotle Voineskos, Yang Wang, Bernd Weber, Wei Wen, Lars T Westlye, Heather C Whalley, Steven CR Williams, Katharina Wittfeld, Margaret J Wright, Paul M Thompson, Thomas Paus and Sophia Frangou
| Summary:
Mechanisms underpinning age-related variations in cortical thickness in the human brain remain poorly understood. We investigated whether inter-regional age-related variations in cortical thinning (in a multicohort neuroimaging dataset from the ENIGMA Lifespan Working Group totalling 14,248 individuals, aged 4-89 years) depended on cell-specific marker gene expression levels. We found differences amidst early-life (<20 years), mid-life (20-60 years), and late-life (>60 years) in the patterns of association between inter-regional profiles of cortical thickness and expression profiles of marker genes for CA1 and S1 pyramidal cells, astrocytes, and microglia. Gene ontology and enrichment analyses indicated that each of the three life-stages was associated with different biological processes and cellular components: synaptic modeling in early life, neurotransmission in mid-life, and neurodegeneration in late-life. These findings provide mechanistic insights into age-related cortical thinning during typical development and aging.