Gamma entrainment using sensory stimuli alleviate chemo brain pathology and cognitive impairment induced by chemotherapy agents
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE216146 | GEO | 2024/12/04
REPOSITORIES: GEO
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Project description:Gamma entrainment using sensory stimuli alleviate chemo brain pathology and cognitive impairment induced by chemotherapy agents
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Project description:Meaningful social interactions modify behavioral responses to sensory stimuli. The neural mechanisms underlying the entrainment of neutral sensory stimuli to salient social cues to produce social learning remain unknown. We used odor-driven behavioral paradigms to ask if oxytocin, a neuropeptide implicated in various social behaviors, plays a crucial role in the formation of learned associations between odor and socially significant cues. Through genetic, optogenetic, and pharmacological manipulations, we show that oxytocin receptor signaling is crucial for entrainment of odor to social cues but is dispensable for entrainment to nonsocial cues. Furthermore, we demonstrate that oxytocin directly impacts the piriform, the olfactory sensory cortex, to mediate social learning. Lastly, we provide evidence that oxytocin plays a role in both appetitive and aversive social learning. These results suggest that oxytocin conveys saliency of social stimuli to sensory representations in the piriform cortex during odor-driven social learning.
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Project description:Cognitive impairment is a shared abnormality between type 2 diabetes mellitus (T2DM) and many neurodegenerative and neuropsychiatric disorders, such as Alzheimer's disease (AD) and schizophrenia. Emerging evidence suggests that brain insulin resistance plays a significant role in cognitive deficits, which provides the possibility of anti-diabetic agents repositioning to alleviate cognitive deficits. Both preclinical and clinical studies have evaluated the potential cognitive enhancement effects of anti-diabetic agents targeting the insulin pathway. Repurposing of anti-diabetic agents is considered to be promising for cognitive deficits prevention or control in these neurodegenerative and neuropsychiatric disorders. This article reviewed the possible relationship between brain insulin resistance and cognitive deficits. In addition, promising therapeutic interventions, especially current advances in anti-diabetic agents targeting the insulin pathway to alleviate cognitive impairment in AD and schizophrenia were also summarized.
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Project description:IntroductionSensory impairment (SI) is linked to cognitive decline, but its association with early cognitive impairment (ECI) is unclear.MethodsSensory functions (vision, hearing, vestibular function, proprioception, and olfaction) were measured between 2012 and 2018 in 414 Baltimore Longitudinal Study of Aging (BLSA) participants (age 74 ± 9 years; 55% women). ECI was defined as 1 standard deviation below age-, sex-, race-, and education-specific mean performance in Card Rotations or California Verbal Learning Test immediate recall. Log binomial models (cross-sectional analysis) and Cox regression models (time-to-event analysis) were used to examine the association between SI and ECI.ResultsCross-sectionally, participants with ≥3 SI had twice the prevalence of ECI (prevalence ratio = 2.10, p = 0.02). Longitudinally, there was no significant association between SI and incident ECI over up to 6 years of follow-up.DiscussionSI is associated with higher prevalence, but not incident ECI. Future studies with large sample sizes need to further elucidate the relationship between SI and ECI.HighlightsSensory impairment is associated with high prevalence of early cognitive impairmentMultisensory impairment may pose a strong risk of early changes in cognitive functionIdentifying multisensory impairment may help early detection of dementia.
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Project description:Neural oscillations have been categorized into various frequency bands that are mechanistically associated with different cognitive functions. Specifically, the gamma band frequency is widely implicated to be involved in a wide range of cognitive processes. As such, decreased gamma oscillation has been associated with cognitive declines in neurological diseases, such as memory dysfunction in Alzheimer's disease (AD). Recently, studies have attempted to artificially induce gamma oscillations by using 40 Hz sensory entrainment stimulation. These studies reported attenuation of amyloid load, hyper-phosphorylation of tau protein, and improvement in overall cognition in both AD patients and mouse models. In this review, we discuss the advancements in the use of sensory stimulation in animal models of AD and as a therapeutic strategy in AD patients. We also discuss future opportunities, as well as challenges, for using such strategies in other neurodegenerative and neuropsychiatric diseases.
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Project description:A size and shape tuned, multifunctional metal chalcogenide, Cu2S-based nanotheranostic agent is developed for trimodal imaging and multimodal therapeutics against brain cancer cells. This theranostic agent was highly efficient in optical, photoacoustic and X-ray contrast imaging systems. The folate targeted NIR-responsive photothermal ablation in synergism with the chemotherapeutic action of doxorubicin proved to be a rapid precision guided cancer-killing module. The multi-stimuli, i.e., pH-, thermo- and photo-responsive drug release behavior of the nanoconjugates opens up a wider corridor for on-demand triggered drug administration. The simple synthesis protocol, combined with the multitudes of interesting features packed into a single nanoformulation, clearly demonstrates the competing role of this Cu2S nanosystem in future cancer treatment strategies.
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Project description:Chemo-senolytic therapeutic potential against angiosarcoma
| PRJNA1030406 | ENA
Project description:IntroductionThe relationship between oscillatory activity in hippocampus and cognitive impairment in traumatic brain injury (TBI) remains unclear. Although TBI decreases gamma oscillations and 40 Hz light flicker improves TBI prognosis, the effects and mechanism of rhythmic flicker on TBI remain unclear.AimsIn this study, we aimed to explore whether light flicker could reverse cognitive deficits, and further explore its potential mechanisms in TBI mouse model.MethodsThe Morris water maze test (MWM), step-down test (SDT), and novel object recognition test (NOR) were applied to evaluate the cognitive ability. The local field potential (LFP) recording was applied to measure low gamma reduction of CA1 in hippocampus after TBI. And electrophysiological experiments were applied to explore effects of the gamma frequency entrainment on long-term potentiation (LTP), postsynaptic transmission, and intrinsic excitability of CA1 pyramidal cells (PCs) in TBI mice. Immunofluorescence staining and western blotting were applied to explore the effects of 40 Hz light flicker on the expression of PSD95 in hippocampus of TBI mice.ResultsWe found that 40 Hz light flicker restored low gamma reduction of CA1 in hippocampus after TBI. And 40 Hz, but not random or 80 Hz light flicker, reversed cognitive impairment after TBI in behavioral tests. Moreover, 40 Hz light flicker improved N-methyl-D-aspartate (NMDA) receptor-dependent LTP (LTPNMDAR ) and L-type voltage-gated calcium channel-dependent LTP (LTPL-VGCC ) after TBI treatment. And gamma frequency entrainment decreased excitatory postsynaptic currents (EPSCs) of CA1 PCs in TBI mice. Our results have illustrated that 40 Hz light flicker could decrease intrinsic excitability of PCs after TBI treatment in mice. Furthermore, 40 Hz light flicker decreased the expression of PSD95 in hippocampus of TBI mice.ConclusionThese results demonstrated that 40 Hz light flicker rescues cognitive impairment by decreasing postsynaptic transmission in PCs after TBI treatment in mice.
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Project description:The effect of music therapy on cognitive function has been widely reported; however, its clinical implications remain controversial. Performing therapeutic musical activities in groups using individualized instruments can help overcome the issues of engagement and compliance. We aimed to evaluate the effect of a cognitive intervention with musical stimuli using digital devices on mild cognitive impairment (MCI). In this prospective study, 24 patients with MCI (intervention group, 12; and control group, 12) were enrolled. We developed an electronic device with musical instruments and the Song-based Cognitive Stimulation Therapy protocol (SongCST). Patients in the intervention group underwent a 10-week cognitive intervention involving musical stimuli generated by our device. Effect of the intervention on cognitive function was evaluated by the Mini-Mental State Examination-Dementia Screening (MMSE-DS), Montreal Cognitive Assessment-Korean (MOCA-K), and Clinical Dementia Rating Scale Sum of Boxes (CDR-SOB). In the intervention group, MMSE-DS and MOCA-K scores improved significantly after the 10-week intervention. The changes in MOCA-K and CDR-SB scores were significantly different between the intervention and control groups. Our study showed that music therapy with digital devices has a positive effect on the executive function and overall disease severity in patients with MCI. Our study can facilitate individualization of music therapy using digital devices in groups.
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Project description:A decline in cognitive ability is a typical feature of the normal aging process, and of neurodegenerative disorders such as Alzheimer's, Parkinson's and Huntington's diseases. Although their etiologies differ, all of these disorders involve local activation of innate immune pathways and associated inflammatory cytokines. However, clinical trials of anti-inflammatory agents in neurodegenerative disorders have been disappointing, and it is therefore necessary to better understand the complex roles of the inflammatory process in neurological dysfunction. The dietary phytochemical curcumin can exert anti-inflammatory, antioxidant and neuroprotective actions. Here we provide evidence that curcumin ameliorates cognitive deficits associated with activation of the innate immune response by mechanisms requiring functional tumor necrosis factor ? receptor 2 (TNFR2) signaling. In vivo, the ability of curcumin to counteract hippocampus-dependent spatial memory deficits, to stimulate neuroprotective mechanisms such as upregulation of BDNF, to decrease glutaminase levels, and to modulate N-methyl-D-aspartate receptor levels was absent in mice lacking functional TNFRs. Curcumin treatment protected cultured neurons against glutamate-induced excitotoxicity by a mechanism requiring TNFR2 activation. Our results suggest the possibility that therapeutic approaches against cognitive decline designed to selectively enhance TNFR2 signaling are likely to be more beneficial than the use of anti-inflammatory drugs per se.
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