Publications by authors named "P Canas"
Article Synopsis
- Astrocytes help clear proteins and waste in the brain using aquaporin-4 (AQP4), which can be disrupted in stress-related disorders.
- Dexamethasone (Dexa), a glucocorticoid used to model stress, was found to reduce the activity of AQP4 and its associated proteins in astrocytes, leading to impaired protein clearance.
- The study suggests that blocking adenosine A receptors (AR) can restore AQP4 function and clearance, indicating a potential therapeutic strategy to address neurological disorders linked to stress and protein accumulation.
Adenosine A receptor (AR) antagonists are the leading nondopaminergic therapy to manage Parkinson's disease (PD) since they afford both motor benefits and neuroprotection. PD begins with a synaptic dysfunction and damage in the striatum evolving to an overt neuronal damage of dopaminergic neurons in the substantia nigra. We tested if AR antagonists are equally effective in controlling these two degenerative processes.
View Article and Find Full Text PDFIncreasing evidence implicates astrocytic dysfunction in Alzheimer's disease (AD), a neurodegenerative disorder characterised by progressive cognitive loss. The accumulation of amyloid-β (Aβ) plaques is a histopathological hallmark of AD and associated with increased astrocyte reactivity. In APP/PS1 mice modelling established AD (9 months), we now show an altered astrocytic morphology and enhanced activity of astrocytic hemichannels, mainly composed by connexin 43 (Cx43).
View Article and Find Full Text PDFArticle Synopsis
- Fear learning is crucial for survival, but traumatic experiences can lead to excessive fear responses, as seen in PTSD, through abnormal fear consolidation and overgeneralization.* -
- Research examined the role of adenosine A receptors (AR) in fear memory; blocking these receptors after fear conditioning increased fear generalization, while activating them reduced it.* -
- Findings indicate that ARs influence long-term potentiation in key brain areas during fear consolidation, suggesting they could be a target for treatments addressing fear-related disorders like PTSD.*
Article Synopsis
- The study investigates how amyloid peptide injections in mice mimic Alzheimer's disease symptoms, particularly focusing on memory loss and hippocampal plasticity changes.
- It was found that before significant memory deficits occur, there is an increase in adenosine A receptor (AR) density and excitability in hippocampal synapses.
- Blocking these receptors can prevent early changes in synaptic function, suggesting that overactive ARs might initiate memory deterioration associated with Alzheimer's disease.