Lara V. van Renssen
Research Subjects
Research Interests
Lara V. van Renssen has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Anna Castells-Nobau
Department of Human Genetics and
1 shared publication - Annette Schenck
Department of Human Genetics, Radboud University Medical Center, Nijmegen, The Netherlands
1 shared publication - Caitlin M. Hudac
Department of Psychology University of South Carolina Columbia South Carolina USA
1 shared publication - Ilse Eidhof
Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden
1 shared publication - Jie Han
Department of Human Genetics and
1 shared publication - Jordi Mayneris-Perxachs
Integrative Systems Medicine and Biology Group, Girona Biomedical Research Institute (IDIBGI-CERCA)
1 shared publication
Latest Publications
- Open Access
- 17 February 2026
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 136 (7)
Conserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling
Sleep disturbances are among the most prevalent clinical features of FOXP1 syndrome, yet their nature and underlying mechanisms remain unclear. Here, we report that individuals with FOXP1 syndrome suffer from insomnia with sleep maintenance problems and early waking. Consistently, common variants in FOXP genes were associated with insomnia symptoms and short sleep. These sleep disturbances were recapitulated in Drosophila FoxP mutants, which exhibit severely fragmented and reduced sleep. FoxP loss also led to circadian arrhythmicity and impaired the plasticity of neuropeptide pigment dispersing factor–secreting (PDF-secreting) neurons in a non-cell-autonomous manner. FoxP was required during development for adult sleep integrity, particularly in peptidergic neurons. Transcriptomic analyses revealed a dysregulation of genes involved in peptidergic signaling, including hugin . FoxP was expressed in hugin + neurons (afferent to PDF-secreting neurons) during development, and its knockdown in these cells was sufficient to induce sleep fragmentation. Our findings establish an evolutionarily conserved role for FOXP proteins in the peptidergic regulation of sleep.
- 17 February 2026
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 136 (7)
Open AccessConserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling
Sleep disturbances are among the most prevalent clinical features of FOXP1 syndrome, yet their nature and underlying mechanisms remain unclear. Here, we report that individuals with FOXP1 syndrome suffer from insomnia with sleep maintenance problems and early waking. Consistently, common variants in FOXP genes were associated with insomnia symptoms and short sleep. These sleep disturbances were recapitulated in Drosophila FoxP mutants, which exhibit severely fragmented and reduced sleep. FoxP loss also led to circadian arrhythmicity and impaired the plasticity of neuropeptide pigment dispersing factor–secreting (PDF-secreting) neurons in a non-cell-autonomous manner. FoxP was required during development for adult sleep integrity, particularly in peptidergic neurons. Transcriptomic analyses revealed a dysregulation of genes involved in peptidergic signaling, including hugin . FoxP was expressed in hugin + neurons (afferent to PDF-secreting neurons) during development, and its knockdown in these cells was sufficient to induce sleep fragmentation. Our findings establish an evolutionarily conserved role for FOXP proteins in the peptidergic regulation of sleep.