Sentences with phrase «ad model mice»

In addition, we have identified signaling pathways that are activated as part of the integrated stress response in response to soluble amyloid - beta and in AD model mice.

Notably, we have found that prolonged activation of these pathways results in altered translational control, which contributes to synaptic dysfunction and memory deficits in AD model mice.

Both the patients and AD model mice were significantly impaired in terms of the distance traveled and the time it took for them to locate the hidden object.

Although genetic deletion of BACE1 results in abolished amyloid pathology in AD model mice, it also results in neurodevelopmental phenotypes such as hypomyelination and synaptic loss, observed in schizophrenia and autism - like phenotype.

These were: AD model mice; AD model mice that lacked PERK; and AD model mice that lacked GCN2.

In recent years, researchers have found that both humans with Alzheimer's Disease and AD model mice have relatively high levels of eIF2alpha phosphorylation.

To explore this question, the researchers examined the neurological impact of two enzymes that phosphorylate eIF2alpha, kinases termed PERK and GCN2, in different populations of AD model mice — all of which expressed genetic mutations akin to those carried by humans with AD.

By contrast, the other AD model mice lagged significantly in performing these tasks.

Here, the AD model mice lacking PERK were able to successfully maneuver through the mazes at rates achieved by normal mice.

Here, they found both increased levels of phosphorylated eIF2alpha in the hippocampus of both AD patients and the AD model mice.

Not exact matches

In a novel animal study design that mimicked human clinical trials, researchers at University of California, San Diego School of Medicine report that long - term treatment using a small molecule drug that reduces activity of the brain's stress circuitry significantly reduces Alzheimer's disease (AD) neuropathology and prevents onset of cognitive impairment in a mouse model of the neurodegenerative condition.

First author Antonio Di Meco and colleagues used a triple transgenic (3xTg) mouse model that displays an AD - like phenotype, including cognitive decline, and Aβ and tau neuropathology characteristic of the disease in humans.

The phosphorylation of eIF2alpha, which decreases protein synthesis, was previously found at elevated levels in both humans diagnosed with Alzheimer's and in Alzheimer's Disease (AD) model mice.

In addition, we have provided recommendations for selecting performance measures and sample sizes to make these assays sensitive to learning and memory deficits in humans with MCI - AD and in mouse models.

Engram cell in AD mouse — This image depicts a single memory engram cell (green) in the hippocampal dentate gyrus (DG) region of a mouse model of early Alzheimer's disease.

In some ways, hAPP mice better model the earlier mild cognitive impairment stage of AD (MCI - AD) than the dementia stage (10).

Interestingly, sleep deprivation markedly increased the buildup of Aβ in the brain of a mouse model of AD; whereas a drug that block orexin actions markedly decreased the buildup of Aβ.

Discovered that mouse models of AD (APP mice) develop aberrant patterns of neuronal network activity, including network hypersynchrony, epileptiform activity, and seizures.

We discovered that impaired inhibitory interneurons lead to altered oscillatory activity, network hypersynchrony, and cognitive deficits in mouse models of AD.

My goal is to use these mice as in vivo models to investigate AD - associated pathology and behavior deficits so that we can learn how BIN1 functions as a risk factor in AD.

The project described in this proposal will help us to extend the findings from other genetics research, including GWAS (genome - wide association studies) and in vitro studies, into an in vivo investigation using mouse models in order to establish BIN1 as a potential new candidate in AD pathophysiology.

I am currently exploring functions of BIN1 by generating mouse models to modify the levels of BIN1 expression in the brain, and investigating how altering the levels of this protein can modify AD - related pathophysiology.

Discovered that aberrant patterns of neuronal network activity result in profound anatomical and physiological alterations of learning and memory centers and may contribute to cognitive deficits in humans with AD and related mouse models.

We are also dissecting the circuit and neuron alterations in behaving mouse models of AD using single - unit recordings and optogenetic approaches.

We are currently profiling inhibitory interneuron cell types in mouse models of AD to identify potential molecular mechanisms of interneuron dysfunction and potential targets of intervention.

Temporal disorganization of hippocampal networks may lead to cognitive and memory dysfunction commonly observed in AD mouse models.

Importantly, cognitive performance in AD mouse models was improved when interneuron - dependent oscillatory brain activity was enhanced by restoration of Nav1.1 levels in endogenous inhibitory interneurons.

These use a high - throughput screening approach combined with MALDI - IMS to assess the specificity of those drugs on a transgenic mouse model of AD.

Discovered that deficits in inhibitory interneurons lead to reduced gamma oscillatory activity, network hypersynchrony, and memory deficits in mouse models of AD.

Her laboratory has successfully combined electrophysiological expertise with molecular and cell biology approaches to better understand complex mechanisms underlying the memory process in mouse models of AD.

We measured Vc in axons of Schaffer collaterals in CA1 area of hippocampus in two transgenic mouse models of AD that over-express β - amyloid, line 41 (6mo) and APP / PS1 (24mo).

Second, we propose to test the effect of chronic or acute treatment with ApoA - I - Milano in a transgenic mouse model of AD.

Previously, other researchers reported that ApoE4 seemed to reduce the clearance of amyloid - β, the protein that clumps together to form the hallmark plaques of AD, from the brain in a mouse model.

This study used the well characterized APPswe / PS1ΔE9 mouse model that exhibits a subset of behavioral and pathological features of AD, including age - dependent accumulation of beta - amyloid (Aβ) as well as learning and memory deficits [10].

In her translational research program, Dr. Duff has created several transgenic mouse models for Alzheimer's disease (AD) to explore disease mechanisms and test therapeutic approaches.

This argument was recently put forward in a study by Winton and colleagues who further concluded that the intraneuronal material in the well - established 3xTg - AD mouse model is not Aβ but in fact, solely APP [30].

To test the efficacy of J147 in a much more rigorous preclinical AD model, we treated mice using a therapeutic strategy more accurately reflecting the human symptomatic stage.

In a transgenic mouse model of AD, aducanumab is shown to enter the brain, bind parenchymal Aβ, and reduce soluble and insoluble Aβ in a dose - dependent manner.

Identifying the molecular triggers for the onset of AD - related cognitive decline presently requires the use of suitable animal models, such as the 3xTg - AD mice, which develop both amyloid and tangle pathology.

The current project utilized an array of immunochemical and molecular tools to perform a characterization of retinal pathology in the early stages of disease progression using a well - validated mouse model of AD (APPSWE / PS1ΔE 9).

Findings (i)- (iii) strongly resemble the changes seen after Abeta immunotherapy in mouse models of AD and suggest that the immune response generated against the peptide elicited clearance of Abeta plaques in this patient.

We present a nonpharmacological approach for removing Aβ and restoring memory function in a mouse model of AD in which Aβ is deposited in the brain.

This duration of wheel running is in the range of wheel running protocols that have produced improvements in mouse models of AD (Stranahan et al., 2012; Intlekofer and Cotman, 2013).

Our recent study has demonstrated that peripheral amylin treatment reduces the amyloid pathology in the brain of Alzheimer's disease (AD) mouse models, and improves their learning and memory.

Abstract: Our recent study has demonstrated that peripheral amylin treatment reduces the amyloid pathology in the brain of Alzheimer's disease (AD) mouse models, and improves their learning and memory.

Abstract: We previously reported that neuroinflammation contributes to the amnesia of AβPPswe / PSEN1dE9 Alzheimer's disease model mice fed a high - fat diet to induce type - 2 diabetes (T2DM - AD mice), but the underlying mechanism for the memory decline remained unclear.

Dmitry: as the paper itself notes, the most likely mechanism for the ability of hydroxypropyl - β - cyclodextrin to lower Aβ burden in the mouse model is AD finding is by normalizing membrane cholesterol content and reducing the appearance of abnormal cathepsin D - positive lysosomes, leading to reduced beta - secretase cleavage of APP and an upregulation of genes involved in cholesterol trafficking and Aβ clearance.