Publications by authors named "F Motamedi"

Neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases, share key characteristics, notably cognitive impairment and significant cell death in specific brain regions. Cognition, a complex mental process allowing individuals to perceive time and place, is disrupted in these conditions. This consistent disruption suggests the possibility of a shared underlying mechanism across all neurodegenerative diseases.

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Directed differentiation of pluripotent stem cells into specialized cell types represents an invaluable tool for a wide range of applications. Here, we have exploited single-cell transcriptomic data to develop a stepwise in vitro differentiation system from mouse embryonic stem cells into adrenocortical cells. We show that during development, the adrenal primordium is embedded in an extracellular matrix containing tenascin and fibronectin.

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Synaptic plasticity is believed to underlie the cellular and molecular basis of memory formation. Mitochondria are one of the main organelles involved in metabolism and energy maintenance as plastic organelles that change morphologically and functionally in response to cellular needs and regulate synaptic function and plasticity through multiple mechanisms, including ATP generation, calcium homeostasis, and biogenesis. An increased neuronal activity enhances synaptic efficiency, during which mitochondria's spatial distribution and morphology change significantly.

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The neuropeptide relaxin-3 and its cognate receptor, relaxin family peptide-3 receptors (RXFP3), have been implicated in modulating learning and memory processes, but their specific roles remain unclear. This study utilized behavioral and molecular approaches to investigate the effects of putatively reversible blockade of RXFP3 in the ventral dentate gyrus (vDG) of the hippocampus on spatial and fear memory formation in rats. Male Wistar rats received bilateral vDG cannula implantation and injections of the RXFP3 antagonist, R3(BΔ23-27)R/I5 (400 ng/0.

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Article Synopsis
  • Peroxisomes are key organelles involved in lipid metabolism, specifically in the breakdown of very long-chain fatty acids that mitochondria cannot process; inhibition of the enzyme ACOX1 in young rats impacts brain fatty acid composition and neuronal activity, mirroring changes seen in aging.
  • ACOX1 was selectively inhibited using TDYA in male Wistar rats over 25 days, leading to notable changes in brain fatty acid levels, with increased levels of certain fatty acids and decreased levels of others, signifying an altered lipid profile.
  • The inhibition of ACOX1 resulted in reduced excitability of neuronal cells, as evidenced by changes in resting membrane potential and action potential properties, highlighting the importance of peroxisome
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