Arthurvick2095

The role of microglia and cytokines in sleep disturbances associated with these diseases is highlighted. The proposed sleep and inflammation-mediated link between TBI and AD presents an opportunity for a multifaceted approach to clinical intervention.Progressive supranuclear palsy (PSP) is a neurodegenerative disease based on four-repeat tauopathy pathology. Currently, this entity is not fully recognized in the context of pathogenesis or clinical examination. This review evaluates the association between neuroinflammation and microglial activation with the induction of pathological cascades that result in tauopathy pathology and the clinical manifestation of PSP. Multidimensional analysis was performed by evaluating genetic, biochemical, and neuroimaging biomarkers to determine whether neurodegeneration as an effect of neuroinflammation or neuroinflammation is a consequence of neurodegeneration in PSP. To the best of our knowledge, this review is the first to investigate PSP in this context.

This study examined the central auditory processing (CAP) assessment results of adults between 45 and 85 years of age with probable pre-clinical Alzheimer's disease - i.e., individuals with subjective memory complaints (SMCs) as compared to those who were not reporting significant levels of memory complaints (non-SMCs). It was hypothesized that the SMC group would perform significantly poorer on tests of central auditory skills compared to participants with non-SMCs (control group).

A total of 95 participants were recruited from the larger Western Australia Memory Study and were classified as SMCs (

= 61; 20 males and 41 females, mean age 71.47 ±7.18 years) and non-SMCs (

= 34; 10 males, 24 females, mean age 68.85 ±7.69 years). All participants completed a peripheral hearing assessment, a CAP assessment battery including Dichotic Digits, Duration Pattern Test, Dichotic Sentence Identification, Synthetic Sentence Identification with Ipsilateral Competing Message (SSI-ICM) and the Quick-Speech-in-Noise,ontrols. The poor CAP in SMC individuals may result in a higher cost to their finite pool of cognitive resources. The CAP results provide yet another biomarker that supports the hypothesis that SMCs may be a primary indication of neuropathological changes in the brain. Longitudinal follow up of individuals with SMCs, and decreased CAP abilities should inform whether this group is at higher risk of developing dementia as compared to non-SMCs and those SMC individuals without CAP difficulties.Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders characterized by deficits in communication, impaired social interaction, and repetitive or restricted interests and behaviors. We have recently shown that neuronal nitric oxide synthase (nNOS) expression was reduced in the basolateral amygdala of mice after postnatal valproic acid exposure. However, the specific role of nNOS downregulation in mice remains to be elucidated. Herein, we investigated the behavioral alternations of naive mice with a recombinant adeno-associated virus (rAAV)-mediated knockdown of nNOS in a comprehensive test battery, including the social interaction, marble burying, self-grooming, and open field tests. #link# Further, the electrophysiological and surface expression changes induced by nNOS deficiency of the basolateral amygdala in these animals were examined. Our results show that nNOS knockdown displayed typical symptoms of ASD-like behaviors, such as reduced social interaction and communication, elevated stereotypes, and anxiety in mice. Surprisingly, we found that nNOS knockdown exhibited greatly reduced excitatory synaptic transmission concomitant with the lower surface expression of GluN2B-containing N-methyl-D-aspartate receptors and postsynaptic density protein 95 in mice. These findings support a notion that dysregulation of nNOS might contribute to ASD-associated phenotypes, with disease pathogenesis most likely resulting from deficits in excitatory synaptic transmission.Simulation of large scale biologically plausible spiking neural networks, e.g., Bayesian Confidence Propagation Neural Network (BCPNN), usually requires high-performance supercomputers with dedicated accelerators, such as GPUs, FPGAs, or even Application-Specific Integrated Circuits (ASICs). Almost all of these computers are based on the von Neumann architecture that separates storage and computation. In Withaferin A datasheet , memory access is the dominant cost even for highly customized computation and memory architecture, such as ASICs. In this paper, we propose an optimization technique that can make the BCPNN simulation memory access friendly by avoiding a dual-access pattern. The BCPNN synaptic traces and weights are organized as matrices accessed both row-wise and column-wise. Accessing data stored in DRAM with a dual-access pattern is extremely expensive. A post-synaptic history buffer and an approximation function thus are introduced to eliminate the troublesome column update. The error analysis combining theoretical analysis and experiments suggests that the probability of introducing intolerable errors by such optimization can be bounded to a very small number, which makes it almost negligible. Derivation and validation of such a bound is the core contribution of this paper. Experiments on a GPU platform shows that compared to the previously reported baseline simulation strategy, the proposed optimization technique reduces the storage requirement by 33%, the global memory access demand by more than 27% and DRAM access rate by more than 5%; the latency of updating synaptic traces decreases by roughly 50%. Compared with the other similar optimization technique reported in the literature, our method clearly shows considerably better results. Although the BCPNN is used as the targeted neural network model, the proposed optimization method can be applied to other artificial neural network models based on a Hebbian learning rule.Preclinical models of cocaine use disorder are widely utilized to identify neuroadaptations underlying cocaine seeking and to screen medications to reduce seeking. However, while the majority of cocaine users engage in poly-substance use (PSU), a minority of preclinical studies employ PSU models. We previously reported that when rats consume alcohol after daily intravenous cocaine self-administration, nucleus accumbens (NA) core basal glutamate levels are reduced below those of rats that consumed only cocaine, and do not increase during cue + cocaine-primed reinstatement of cocaine-seeking. Here we used the same model of sequential cocaine and alcohol self-administration to test the hypothesis that a similar pattern of glutamate changes would be observed in the NA core prior to and during a cocaine-primed reinstatement test. Rats underwent intravenous cocaine self-administration followed by access to unsweetened alcohol in the home cage for 12 days. Rats underwent a minimum of 12 daily extinction sessions prior to a cocaine-primed reinstatement test conducted during microdialysis procedures.