US EditionStudy Uncovers New Molecular Mechanisms Linked to Alzheimer's Cognitive Decline
- A University of Barcelona research team discovered that the RTP801 protein in astrocytes plays a critical role in Alzheimer's cognitive decline in animal models.
- Previous research established that RTP801 plays a role in neuronal stress responses and dysfunction, yet its functions within astrocytes had not been clearly defined before this study.
- The team used gene therapy to silence RTP801 expression in hippocampal astrocytes and observed improvements in spatial memory, GABA levels, and brain network connectivity.
- Researcher Almudena Chicote noted that reducing the activity of the RTP801 protein could potentially repair some harm sustained by PV+ interneurons in the hippocampus, which might contribute to restoring proper GABA levels and enhancing brain function.
- These findings open new therapeutic avenues targeting astrocyte-related neuroinflammation, though further studies are needed to confirm effectiveness in humans.
17 Articles
17 Articles
Study uncovers new molecular mechanisms linked to Alzheimer's cognitive decline
A research team at the University of Barcelona's Institute of Neurosciences (UBneuro) has discovered new molecular mechanisms related to the cognitive decline associated with Alzheimer's disease, the most common dementia.
Astrocyte protein RTP801 may contribute to cognitive decline in Alzheimer's disease
A research team at the University of Barcelona's Institute of Neurosciences (UBneuro) has discovered new molecular mechanisms related to the cognitive decline associated with Alzheimer's disease, the most common dementia. This study, carried out on animal models with the disease, describes for the first time the decisive role of the RTP801 protein in cells known as astrocytes during the progression of this neurodegenerative disease.
Transcriptomic signatures of oxytosis/ferroptosis are enriched in Alzheimer’s disease - BMC Biology
Oxytosis/ferroptosis is a form of non-apoptotic regulated cell death characterized by specific changes in the redox balance that lead to lethal lipid peroxidation. It has been hypothesized recently that aging predisposes the brain to the activation of oxytosis/ferroptosis in Alzheimer’s disease (AD), and consequently that inhibition of oxytosis/ferroptosis offers a path to develop a new class of therapeutics for the disease. The goal of the pres…
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