Journal of Clinical Medicine Article Adiponectin Modulation by Genotype and Maternal Choline Supplementation in a Mouse Model of Down Syndrome and Alzheimer’s Disease Melissa J. Alldred 1,2,*, Sang Han Lee 3,4 and Stephen D. Ginsberg 1,2,5,6,* 1 Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY 10962, USA 2 Departments of Psychiatry, New York University Grossman School of Medicine, New York, NY 10016, USA 3 Center for Biomedical Imaging and Neuromodulation, Nathan Kline Institute, Orangeburg, NY 10962, USA;
[email protected] 4 Child & Adolescent Psychiatry, New York University Grossman School of Medicine, New York, NY 10016, USA 5 Neuroscience & Physiology, New York University Grossman School of Medicine, New York, NY 10016, USA 6 NYU Neuroscience Institute, New York University Grossman School of Medicine, New York, NY 10016, USA * Correspondence:
[email protected] (M.J.A.);
[email protected] (S.D.G.); Tel.: +1-(845)-398-2176 (M.J.A.); +1-(845)-398-2170 (S.D.G.) Abstract: Down syndrome (DS) is a genetic disorder caused by the triplication of human chromosome 21, which results in neurological and physiological pathologies. These deficits increase during aging and are exacerbated by cognitive decline and increase of Alzheimer’s disease (AD) neuropathology. A nontoxic, noninvasive treatment, maternal choline supplementation (MCS) attenuates cognitive decline in mouse models of DS and AD. To evaluate potential underlying mechanisms, laser capture microdissection of individual neuronal populations of MCS offspring was performed, followed Citation: Alldred, M.J.; Lee, S.H.; by RNA sequencing and bioinformatic inquiry. Results at ~6 months of age (MO) revealed DS Ginsberg, S.D.