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Neuroprotective effect of alpha-asarone on spatial memory and nitric oxide levels in rats injected with amyloid-β(25–35)
TLDR
The results suggest that alpha-asarone may protect neurons against Abeta((25-35))-caused neurotoxicity by inhibiting the effects of NO overproduction in the hippocampus and temporal cortex. Expand
Alzheimer's disease and metabolic syndrome: A link from oxidative stress and inflammation to neurodegeneration
TLDR
Therapeutic efforts to achieve attenuation of oxidative stress could be beneficial in AD treatment, attenuating Aβ‐induced neurotoxicity and improve neurological outcomes in AD. Expand
Vanadium in Biological Action: Chemical, Pharmacological Aspects, and Metabolic Implications in Diabetes Mellitus
TLDR
This review examines the development of vanadium-containing compounds in biological systems regarding the role of the physiological environment, dosage, intracellular interactions, metabolic transformations, modulation of signaling pathways, toxicology, and transport and tissue distribution as well as therapeutic implications and sheds light on the prevailing gaps between primary scientific data and information from animal models and human studies. Expand
Antioxidant effects of epicatechin on the hippocampal toxicity caused by amyloid-beta 25-35 in rats.
TLDR
The results showed that Amyloid-beta 25-35-caused oxidative damage of the hippocampus was blocked by the administration of Epicatechin. Expand
Curcuma treatment prevents cognitive deficit and alteration of neuronal morphology in the limbic system of aging rats
TLDR
It is suggested that curcuma induces modification of dendritic morphology in neurons in the prefrontal cortex, the CA1 and CA3 regions of the dorsal hippocampus, the dentate gyrus, and the basolateral amygdala of aged rats, preventing deterioration in neuronal morphology of the limbic system and recognition memory. Expand
Amyloid-β25–35 impairs memory and increases NO in the temporal cortex of rats
TLDR
The data suggest that the fraction Abeta((25-35)) injected into the temporal cortex might contribute to understanding the role of nitric oxide on the biological changes related to the neuropathological progression and the memory impairment in AD. Expand
Aβ25-35 injection into the temporal cortex induces chronic inflammation that contributes to neurodegeneration and spatial memory impairment in rats.
TLDR
It is suggested that the chronic inflammatory reaction could contribute to the progression of Aβ25-35 toxicity and cause cognitive impairment. Expand
Aminoguanidine treatment ameliorates inflammatory responses and memory impairment induced by amyloid-beta 25–35 injection in rats
TLDR
Results suggest that AG treatment inhibited glia activation and cytokine release, which may help to counteract neurodegenerative events induced by the toxicity of Aβ. Expand
A high calorie diet causes memory loss, metabolic syndrome and oxidative stress into hippocampus and temporal cortex of rats
TLDR
It is demonstrated that HCD (90 day consumption) induces an alteration of the main energy metabolism markers, indicating the development of MS in rats, and the effect of the consumption of a high‐calorie diet on both neurodegeneration and spatial memory impairment in rats is evaluated. Expand
Unilateral injection of Aβ25–35 in the hippocampus reduces the number of dendritic spines in hyperglycemic rats
TLDR
The results suggest that hyperglycemia can trigger Aβ‐induced neurodegeneration and thus the appearance of AD symptoms would be accelerated. Expand
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