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Peter Cain

Researcher at University of Colorado Boulder

Publications -  6
Citations -  203

Peter Cain is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Neurodegeneration & Sleep in non-human animals. The author has an hindex of 6, co-authored 6 publications receiving 159 citations. Previous affiliations of Peter Cain include Excelsior College.

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Tau pathology induces loss of GABAergic interneurons leading to altered synaptic plasticity and behavioral impairments

TL;DR: It is shown for the first time that hippocampal GABAergic function is impaired by pathological tau protein, leading to altered synaptic plasticity and severe memory deficits in aged JNPL3 (BL6) mice.
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RCAN1 overexpression promotes age-dependent mitochondrial dysregulation related to neurodegeneration in Alzheimer's disease.

TL;DR: It is proposed that chronic RCAN1 overexpression during aging alters DRP1-mediated mitochondrial fission and thus acts to promote AD-related progressive neurodegeneration.
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Regulator of Calcineurin 1 Modulates Expression of Innate Anxiety and Anxiogenic Responses to Selective Serotonin Reuptake Inhibitor Treatment

TL;DR: The study suggests that RCAN1 plays an important role in the expression of anxiety-related and SSRI-related behaviors through CaN-dependent signaling pathways and identifies RCAN 1 as a mediator of innate emotional states and possible therapeutic target for anxiety.
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Sleep Behavior and EEG Oscillations in Aged Dp(16)1Yey/+ Mice: A Down Syndrome Model.

TL;DR: Sleep and EEG data reflect underlying differences in neuronal activity at the network level and thus are causative agents rather than merely symptoms of DS, and the abnormal EEG oscillations in aged Dp16 mice suggest a potential role for GABAergic activity in these sleep and EEG abnormalities.
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Isoform-specific rcan1 overexpression promotes age-dependent mitochondrial dysregulation related to neurodegeneration in Alzheimer’s disease

TL;DR: O2-12-05 ISOFORM-SPECIFIC RCAN1 OVEREXPRESSION PROMOTES AGE-DEPENDENTMITOCHONDRIAL DYSREGULATION RELATED to NEURODEGENERATION in ALZHEIMER’s DISEASE.