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Juha Lauren

Researcher at Yale University

Publications -  28
Citations -  3866

Juha Lauren is an academic researcher from Yale University. The author has contributed to research in topics: Neurotrophic factors & Myelin. The author has an hindex of 14, co-authored 28 publications receiving 3604 citations. Previous affiliations of Juha Lauren include Massachusetts Institute of Technology & University of Helsinki.

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Cellular prion protein mediates impairment of synaptic plasticity by amyloid-β oligomers

TL;DR: The cellular prion protein (PrPC) is identified as an amyloid-β-oligomer receptor by expression cloning, and PrPC-specific pharmaceuticals may have therapeutic potential for Alzheimer’s disease.
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Novel neurotrophic factor CDNF protects and rescues midbrain dopamine neurons in vivo

TL;DR: In vivo and in vivo, CDNF prevented the 6-hydroxydopamine (6-OHDA)-induced degeneration of dopaminergic neurons in a rat experimental model of Parkinson’s disease and suggest that CDNF might be beneficial for the treatment of Parkinson's disease.
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Memory Impairment in Transgenic Alzheimer Mice Requires Cellular Prion Protein

TL;DR: Examination of familial AD transgenes encoding APPswe and PSen1ΔE9 into Prnp−/− mice shows the necessity of PrPC for AD-related phenotypes, with cognitive deficits selectively requiring PrPC.
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An unbiased expression screen for synaptogenic proteins identifies the LRRTM protein family as synaptic organizers.

TL;DR: An unbiased expression screen for synaptogenic proteins in the coculture assay using custom-made cDNA libraries suggests a prevalence of LRR domain proteins in trans-synaptic signaling and provides a cellular basis for the reported linkage of LRRTM1 to handedness and schizophrenia.
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LRRTM1 on chromosome 2p12 is a maternally suppressed gene that is associated paternally with handedness and schizophrenia

TL;DR: It is shown that LRRTM1 is expressed during the development of specific forebrain structures, and thus could influence neuronal differentiation and connectivity, and the first putative genetic effect on variability in human brain asymmetry is found.