Mice Lacking Full Length Adgrb1 (bai1) Exhibit Social Deficits, Increased Seizure Susceptibility, and Altered Brain Development

The adhesion G protein-coupled receptor BAI1/ADGRB1 plays an important role in suppressing angiogenesis, mediating phagocytosis, and acting as a brain tumor suppressor. BAI1 is also a critical regulator of dendritic spine and excitatory synapse development and interacts with several autism-relevant proteins. However, little is known about the relationship between altered BAI1 function and clinically relevant phenotypes. Therefore, we studied the effect of reduced expression of full length Bai1 on behavior, seizure susceptibility, and brain morphology in Adgrb1 mutant mice. We compared homozygous (Adgrb1−/−), heterozygous (Adgrb1+/−), and wild-type (WT) littermates using a battery of tests to assess social behavior, anxiety, repetitive behavior, locomotor function, and seizure susceptibility. We found that Adgrb1−/− mice showed significant social behavior deficits and increased vulnerability to seizures. Adgrb1−/− mice also showed delayed growth and reduced brain weight. Furthermore, reduced neuron density and increased apoptosis during brain development were observed in the hippocampus of Adgrb1−/− mice, while levels of astrogliosis and microgliosis were comparable to WT littermates. These results show that reduced levels of full length Bai1 is associated with a broader range of clinically relevant phenotypes than previously reported

Gpr37 Modulates Progenitor Cell Dynamics in a Mouse Model of Ischemic Stroke

The generation of neural stem and progenitor cells following injury is critical for the function of the central nervous system, but the molecular mechanisms modulating this response remain largely unknown. We have previously identified the G protein-coupled receptor 37 (GPR37) as a modulator of ischemic damage in a mouse model of stroke. Here we demonstrate that GPR37 functions as a critical negative regulator of progenitor cell dynamics and gliosis following ischemic injury. In the central nervous system, GPR37 is enriched in mature oligodendrocytes, but following injury we have found that its expression is dramatically increased within a population of Sox2-positive progenitor cells. Moreover, the genetic deletion of GPR37 did not alter the number of mature oligodendrocytes following injury but did markedly increase the number of both progenitor cells and injury-induced Olig2-expressing glia. Alterations in the glial environment were further evidenced by the decreased activation of oligodendrocyte precursor cells. These data reveal that GPR37 regulates the response of progenitor cells to ischemic injury and provides new perspectives into the potential for manipulating endogenous progenitor cells following stroke

A brief assessment of object semantics in primary progressive aphasia

Aims: We developed a cross-culturally valid short form of the Pyramids and Palm Trees Test to assess object semantic memory. We investigated its clinical utility in differentiating the semantic variant of primary progressive aphasia, from the logopenic and nonfluent agrammatic variants. Areas of atrophy associated with poor performance were identified.Fil: Breining, Bonnie L.. University Johns Hopkins; Estados UnidosFil: Lala, Trisha. University Johns Hopkins; Estados UnidosFil: Martínez Cuitiño Carricaburo, María Macarena. Universidad de Buenos Aires; Argentina. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Manes, Facundo Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Australian Research Council Centre Of Excellence In Cognition And Its Disorders; Australia. Universidad Diego Portales; Chile. Universidad Favaloro; Argentina. Instituto de Neurología Cognitiva; ArgentinaFil: Peristeri, Eleni. Aristotle University Of Thessaloniki. Thessaloniki; GreciaFil: Tsapkini, Kyrana. University Johns Hopkins; Estados UnidosFil: Faria, Andreia V.. University Johns Hopkins; Estados UnidosFil: Hillis, Argye E.. University Johns Hopkins; Estados Unido