Sentence examples for rescued memory from inspiring English sources

The in vivo results indicated that GR has efficiently reduced Aβ deposition, ameliorated neurologic changes and rescued memory loss, thus, enhancing the cognitive and spatial memory in a AD rat model.

BACE1+/− deletion rescued memory deficits as tested by the spontaneous alternation Y-maze task in 5XFAD mice at the earlier stage and prevented their septohippocampal cholinergic deficits associated with significant neuronal loss.

Assuming that enhanced inhibition of LTP mediates memory decline in APP/PS1 mice, we rescued memory deficits in adult APP/PS1 mice by treating them with another GABAA receptor antagonist, picrotoxin (PTX), at a non-epileptic dose for 10 days.

Increasing the expression of DNMT3a2 in the hippocampus of cognitively impaired aged mice rescued memory function (Oliveira et al, 2012).

Our study shows that 100 mg and 125 mg doses achieved CSF levels corresponding to brain levels that rescued memory deficits in transgenic AD mouse models.

Restoring the autophagy-lysosomal pathway by deletion of cystatinB in these AD mice reduced intracellular and extracellular amyloid load, and rescued memory performance.

In contrast, pretraining administration of levetiracetam was not able to rescue memory deficits in 5XFAD transgenic mice harboring amyloid plaque pathologies at moderate (6 8 months old) or massive (12 15 months old) levels, differentiating between normal aging- and AD-related memory impairments in the responsiveness to acute levetiracetam treatment.

Importantly, BACE1+/− deletion was no longer able to rescue memory deficits or cholinergic neurodegeneration in 5XFAD mice at the advanced stage.

Therefore, it seems plausible that failure of BACE1+/− deletion to rescue memory deficits in 5XFAD mice at the advanced phase may be attributable to the high residual levels of neurotoxic C99 fragments in addition to Aβ42 peptides in brain.

In contrast, BACE1+/− deletion is no longer sufficient to rescue memory impairments or affect Aβ42 levels in 5XFAD mice as disease progresses into the more severe pathological stage (15 18 months of age) that is accompanied by robust Aβ burden and BACE1 elevation.

Therefore, selective activation of β1-ADR may be used as a therapeutic approach to rescue memory deficits in AD.