Glucagon-like peptide-2 rescues memory impairments and neuropathological changes in a mouse model of dementia induced by the intracerebroventricular administration of streptozotocin

Abstract Glucagon-like peptide 2 (GLP-2) is derived from the proglucagon gene expressed in the intestines, pancreas and brain. Our previous study showed that GLP-2 improved lipopolysaccharide-induced memory impairments. The current study was designed to further investigated the potential of GLP-2 in memory impairment induced by intracerebroventricular administration of streptozotocin (ICV-STZ) in mice, which have been used as an animal model of sporadic Alzheimer’s disease (AD). STZ was administered on alternate days (Day-1 and Day-3) in order to induce dementia in male ddY mice. ICV-STZ-treated mice were administered GLP-2 (0.6 μg/mouse, ICV) for 5 days from 14 days after the first ICV administration of STZ. In these mice, we examined spatial working memory, the biochemical parameters of oxidative stress, or neurogenesis. The GLP-2 treatment restored spatial working memory in ICV-STZ-treated mice. ICV-STZ-treated mice showed markedly increased thiobarbituric acid reactive species (TBARS) and decreased glutathione (GSH) levels, and GLP-2 significantly restored these ICV-STZ-induced changes. GLP-2 also significantly restored neurogenesis in the subgranular zone of the dentate gyrus in ICV-STZ-treated mice. We herein demonstrated that GLP-2 significantly restored ICV-STZ-induced memory impairments as well as biochemical and histopathological alterations, and accordingly, propose that the memory restorative ability of GLP-2 is due to its potential to reduce oxidative stress.

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Protective Effects of Pelargonium graveolens Essential Oil on Methomyl-Induced Oxidative Stress and Spatial Working Memory Impairment in Association with Histopathological Changes in the Hippocampus of Male Wistar Rats

Basic and Clinical Neuroscience Journal ◽

10.32598/bcn.11.4.1402.1 ◽

2020 ◽

Author(s):

Khene M’hammed Amin ◽

Chabane Kahina ◽

Habchi Nawel ◽

Zaida Faiza ◽

Giaimis Jean ◽

...

Keyword(s):

Oxidative Stress ◽

Working Memory ◽

Essential Oil ◽

Memory Impairment ◽

Wistar Rats ◽

Spatial Working Memory ◽

Protective Effects ◽

Histopathological Changes ◽

Pelargonium Graveolens ◽

Male Wistar Rats

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P2-603: MEAN ARTERIAL BLOOD PRESSURE (MABP) IS ASSOCIATED WITH SPATIAL WORKING MEMORY PERFORMANCE VIA AN EFFECT UPON FORNIX MICROSTRUCTURE IN OLDER ADULTS WITH AGE-ASSOCIATED MEMORY IMPAIRMENT (AAMI)

Alzheimer s & Dementia ◽

10.1016/j.jalz.2019.06.3013 ◽

2019 ◽

Vol 15 ◽

pp. P855-P856

Author(s):

Jeffery Michael Reddan ◽

David White ◽

Ajay S. Kurani ◽

Andrew Pipingas ◽

Helen Macpherson ◽

...

Keyword(s):

Blood Pressure ◽

Older Adults ◽

Working Memory ◽

Arterial Blood Pressure ◽

Mean Arterial Blood Pressure ◽

Memory Impairment ◽

Spatial Working Memory ◽

Memory Performance ◽

Arterial Blood

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A multifunctional compound ebselen reverses memory impairment, apoptosis and oxidative stress in a mouse model of sporadic Alzheimer's disease

Journal of Psychiatric Research ◽

10.1016/j.jpsychires.2018.11.021 ◽

2019 ◽

Vol 109 ◽

pp. 107-117 ◽

Cited By ~ 24

Author(s):

Franciele Martini ◽

Suzan Gonçalves Rosa ◽

Isabella Pregardier Klann ◽

Bruna Cruz Weber Fulco ◽

Fabiano Barbosa Carvalho ◽

...

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mouse Model ◽

Memory Impairment ◽

Sporadic Alzheimer’S Disease ◽

And Oxidative Stress

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Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

10.21203/rs.3.rs-1112319/v1 ◽

2021 ◽

Author(s):

Simone N. De Luca ◽

Kurt Brassington ◽

Stanley M. H. Chan ◽

Aleksandar Dobric ◽

Kevin Mou ◽

...

Keyword(s):

Working Memory ◽

Cognitive Dysfunction ◽

Memory Impairment ◽

Microglial Activation ◽

Pulmonary Inflammation ◽

Systemic Circulation ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Memory Impairments ◽

The Brain

Abstract Background: Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” of pulmonary inflammation into the systemic circulation may damage the brain, leading to cognitive dysfunction. Cessation of CS can improve pulmonary and neurocognitive outcomes, however, its benefit on the neuroinflammatory profile remains uncertain. Here, we investigate how CS exposure impairs neurocognition and whether this can be reversed with CS cessation or an antioxidant treatment. Methods: Male BALB/c mice were exposed CS (9 cigarettes/day for 8 weeks) followed by 4 weeks of CS cessation. Another cohort of CS-exposed mice were co-administrated with a glutathione peroxidase (Gpx) mimetic, ebselen (10mg/kg) or vehicle (5% CM-cellulose). We assessed pulmonary inflammation, spatial and working memory, and the hippocampal microglial, oxidative and synaptic profiles. Results: CS exposure increased lung inflammation which was reduced following CS cessation. CS caused spatial and working memory impairments which were attributed to hippocampal microglial activation and suppression of synaptophysin. CS cessation did not improve memory deficits or alter microglial activation. Ebselen completely prevented the CS-induced working and spatial memory impairments, which was associated with restored synaptophysin expression without altering microglial activation.Conclusion: We were able to model the CS-induced memory impairment and microglial activation seen in human COPD. The preventative effects of ebselen on memory impairment is likely to be dependent on a preserved synaptogenic profile. Cessation alone also appears to be insufficient in correcting the memory impairment, suggesting the importance of incorporating antioxidant therapy to help maximizing the benefit of cessation.

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