Publications by authors named "Ashley Bernardo"

Reduced somatostatin (SST) and SST-expressing GABAergic neurons are well-replicated findings in Alzheimer's disease (AD) and are associated with cognitive deficits. SST cells inhibit pyramidal cell dendrites through α5-GABA-A receptors (α5-GABAA-R). α5-GABAAR positive allosteric modulation (α5-PAM) has procognitive and neurotrophic effects in stress and aging models.

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Article Synopsis
  • Chronic stress increases the risk of Major Depressive Disorder (MDD) and leads to neuronal dysfunctions and impaired GABA signaling, affecting anxiety, cognition, and sedation.
  • A therapy boosting activity at α2- and α5-GABAA receptors while avoiding α1 activity shows promise for alleviating depression symptoms without sedative side effects.
  • The study demonstrated that two drug enantiomers, GL-I-54 and GL-II-73, modulate specific GABAA receptors, improve cognitive function in stressed rodents, and help reverse structural neuronal damage due to chronic stress.
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Article Synopsis
  • Laboratory animals, especially mice, experience stress from manipulations by humans, which can affect their well-being and skew experimental data, particularly anxiety measures.
  • Handling techniques that reduce stress have primarily focused on rats, but new methods, like the 3D-handling technique, show that mice can also be habituated to handling, leading to improved well-being and more reliable results.
  • The study demonstrates that this 3D-handling technique decreases anxiety-like behaviors and stress levels in mice, enhancing interaction with experimenters and suggesting it could replace more stressful methods like tail-pick up.
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Schizophrenia is a mental disorder characterized by positive symptoms, negative symptoms, and cognitive dysfunction. Phencyclidine (PCP)-a N-methyl-D-aspartate (NMDA) receptor antagonist-induces symptoms indistinguishable from those of schizophrenia. A reduction of the phosphoprotein synapsin II has also been implicated in schizophrenia and has a well-known role in the maintenance of the presynaptic reserve pool and vesicle mobilization.

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