The goal of this study was to assess the threshold of disruption and subsequent time-course of acoustic response of four experimental nitrogen-filled polymer-shelled microbubbles. Using an in vitro measurement system, a sequence of low-amplitude detection pulses measured the change in echo caused by a high-amplitude disruption pulse on a dilute suspension of bubbles. Detection pulses were transmitted 0.5 ms before disruption and between 1 and 200 ms after disruption. Separate transducers, aligned confocally and orthogonally, were used to transmit and receive bubble echoes. After disruption, all agents demonstrated a transient increase in scattered power. Above the disruption threshold, highly echogenic, nonlinear scatterers were observed. Their echoes slowly disappeared after disruption with median decay times from 7.4 to 13.6 ms, calculated by fitting to a mono-exponential decay. This is consistent with a process wherein the shell is disrupted, releasing the gas and generating free gas bubbles, which cause high-amplitude nonlinear scattering followed by relatively slow diffusion of the gas into solution. This picture has been observed optically with single bubbles and differs from the concept of "stimulated acoustic emission" from disrupted bubbles.
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http://dx.doi.org/10.1016/j.ultrasmedbio.2007.05.013 | DOI Listing |
Background: Alzheimer's disease (AD) is the most common cause of dementia worldwide. It is characterized by dysfunction in the U1 small nuclear ribonucleoproteins (snRNPs) complex, which may precede TAU aggregation, enhancing premature polyadenylation, spliceosome dysfunction, and causing cell cycle reentry and death. Thus, we evaluated the effects of a synthetic single-stranded cDNA, called APT20TTMG, in induced pluripotent stem cells (iPSC) derived neurons from healthy and AD donors and in the Senescence Accelerated Mouse-Prone 8 (SAMP8) model.
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December 2024
Columbia University Irving Medical Center, New York, NY, USA.
Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.
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December 2024
Department of Bioengineering, University of California, Los Angeles, CA, USA, Los Angeles, CA, USA.
Background: The initiation of amyloid plaque deposition signifies a crucial stage in Alzheimer's disease (AD) progression, which often coincides with the disruption of neural circuits and cognitive decline. While the role of excitatory-inhibitory balance is increasingly recognized in AD pathophysiology, targeted therapies to modulate this balance remain underexplored. This study investigates the effect of perampanel, a selective non-competitive AMPA receptor antagonist, in modulating neurophysiological changes in hAPP-J20 transgenic Alzheimer's mice.
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December 2024
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Background: Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder with limited treatment options. As it progresses, synapse degeneration is the most important feature contributing to cognitive dysfunction. Mitochondria supply synapses with ATP for neurotransmitter release and vesicle recycling and buffer calcium concentrations.
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December 2024
Mashhad University of Medical Sciences, Mashhad, Razavi Khorasan, Iran (Islamic Republic of).
Background: Microbiota of the distal part of the intestine produces Urolithin A (Uro A) as a derivative of ellagitannins hydrolysis. Recently, the mitophagy, anti-inflammatory, and antioxidant properties of Uro A have focused more attention on its probable beneficial effects on neurodegenerative states. The purpose of this research was to study the impact of Uro A on the histopathology of the cerebellum in a rat model of streptozotocin-induced Alzheimer's disease.
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