Electrophysiological Changes Underlying Lapses in Memory Consolidation
In this study we explore the electrophysiological changes associated with lapses in memory consolidation.
Preclinical drug screening in new generation Alzheimer’s disease mouse models: The MODEL-AD Consortium Strategy
A brief overview of the Preclinical Testing Core of the MODEL-AD consortium.
www.thebraindomain.org: Science Writing for Public Engagement
The Brain Domain is a blog and article focused public engagement website, geared towards helping young neuroscientists improve their skills in science writing and communication.
MEG Resting State Functional Connectivity and Network Topology in Dyslexia Related Genotype
Studying resting state neuro-functional interactions and their network distribution may tell us more about differences in typical and a typical brain development.
Analysis of the Effect of Aggregated β-Amyloid on Cellular Signaling Pathways Critical for Memory in Alzheimer’s Disease
Here we evaluate the ability to detect changes in phosphorylation levels of ERK and CREB following treatment with Aβ using the SH-SY5Y neuroblastoma cell line.
Assessment of Oral LISPRO Treatment in Ameliorating Amyloid and Tau Pathology in Transgenic Alzheimer’s Mice Model
Ionic co-crystals of lithium salicylate with organic proline (LISPRO) showed better safety and pharmacokinetic profile of lithium in plasma and brain of wild-type and transgenic Alzheimer mice model compared to lithium salts.
CiPA Phase 2 Study: validation of an automated microelectrode array (MEA) assay of hiPSC-derived cardiomyocyte electrophysiology for cardiac safety evaluation
These results support the use of hSC-CM and MEA technology for preclinical assessment of proarrhythmic risk within the proposed CiPA paradigm, and, more generally, demonstrate that automation of the CM-MEA assay can achieve high reliability and throughput for cardiac risk assessment in vitro.
Modulation of GPRC6A Signaling to Mitigate Tauopathies
Overall, our data suggest that decreased GPRC6A signaling reduces tau pathology. Further studies is required to warrant the role of GPRC6A in amino acid sensing associated autophagy or other protein degradation mechanisms. GPRC6A allosteric antagonists may potentially find utility as novel drugs to treat tauopathies and related disorders.
Amyloid Beta Nano Particle used to Sensitize Dendritic Cells as a Therapeutic Vaccine against Alzheimer's disease
This project researches the use of immunotherapy to combat Alzheimer's disease. This is achieved by exposing dendritic cells, antigen presenting cells, to amyloid beta in order to sensitize the cell. The results indicate that a mutant form of amyloid beta was successful in producing anti-amyloid-beta antibodies and in improving behavior in the mice.
Neuronal Mislocalization of Mutant DHHC9 in X-Linked Intellectual DIsability
DHHC9 is a protein acyltransferase (PAT) that adds a palmitate to specific protein substrates. In the neuron, palmitoylation of various proteins by DHHC9 facilitates proper neuronal function. Recently, a DHHC9 nonsense mutation (R298*), resulting in a truncation of the last 67 amino acids of the protein, has been associated with X-Linked Intellectual Disability (XLID). Here, we compare neuronal localization of the wild-type (WT) and R298* mutant DHHC9.