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Topic: hyperglycemia

ePoster
5 ePosters

In Neuroscience

Effect of melatonin on blood-brain barrier disruption in the hippocampus of type 1 diabetic rats

Sunantha Yang-en, Chutikorn Nopparat, Ratchadaporn Pramong · FENS Forum 2024

Diabetes mellitus is characterized by hyperglycemia due to lack of insulin production or function. Chronic hyperglycemia leads to damage microvascular dysfunction, including in hippocampus. Previous studies found that diabetes can cause blood-brain barrier (BBB) dysfunction and implicate cognitive decline in the hippocampus. BBB comprises endothelial cells attached with tight junctions to protect pathogens in circulation through the brain parenchyma. Interestingly, melatonin, a neurohormone secreted from pineal gland, is a neuroprotective effect and plays a vital role in learning and memory. T

ePoster · Neuroscience

Hyperglycemia affects mitochondrial respiratory chain but not the hydrogen peroxide production in neurons during ischemic stroke

Kseniia Morozova, Daria Kotova, Aleksandra Ivanova, Matvei Pochechuev, Ilya Kelmanson, Yulia Khramova, Alisa Tiaglik, Mark Sudoplatov, Arina Trifonova, Anna Fedotova, Veronika Katrukha, Anastasia Sergeeva, Roman Raevskii, Mariia Pestriakova, Maxim Solotenkov, Evgeny Stepanov, Aleksandra Tsopina, Aleksandr Moshchenko, Milena Shestopalova, Anton Zalygin, Ilya Fedotov, Andrei Fedotov, Vladimir Oleinikov, Vsevolod Belousov, Alexey Semyanov, Nadezda Brazhe, Aleksei Zheltikov, Dmitry Bilan · FENS Forum 2024

Diabetes has a systemic effect on the metabolism and can be linked to higher risks of severe medical conditions, such as ischemic stroke. Hyperglycemia leads to more extensive cerebral damage during stroke and, as a result, to more severe consequences. One of the main damaging factors of the stroke is the reactive oxygen species generation occurring in mitochondrial respiratory chain (electron transport chain, ETC). We used in vivo Raman microspectroscopy with the chronic cranial windows implantation to assess the redox state of mitochondria ETC in neurons of awake mice under normal and hyperg

ePoster · Neuroscience

Prediabetes and type 2 diabetes affect tau phosphorylation patterns in murine models of Alzheimer’s disease

Maria Vargas Soria, Miriam Corraliza Gomez, Carmen Infante Garcia, Alan W. Stitt, Rafael Simó, Monica Garcia Alloza · FENS Forum 2024

Alzheimer’s disease (AD) is the most common cause of dementia. Metabolic disorders, including prediabetes (preDM) and type two diabetes (T2D) increase the risk to suffer AD, and may contribute to dysfunctional brain insulin signaling and abnormal tau phosphorylation. Thus, we measured cortical tau phosphorylation at Ser-199, Ser-202/Thr-205, Ser-396, Ser-404, Thr-217 and Thr-231 residues in animals reproducing PreDM and T2D, alone or with AD. We analyzed the relationship between tau phosphorylation and metabolic profile, Aβ levels, microglia activation, cytokines production and cognitive impai

ePoster · Neuroscience

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder marked by hyperglycemia, hyperinsulinemia, and altered insulin signaling. Current investigations propose that insulin not only participates in general metabolic processes but also exerts influence over brain functions. Also, altered insulin signaling is observed in conditions like Alzheimer's Disease and Obsessive-Compulsive Disorder. Despite evidence, current treatments targeting insulin signaling lack validation for mental disorders. Understanding insulin's role in concurrent mental and somatic disorders may reveal strategies fo

ePoster · Neuroscience

Type one diabetes modifies tau phosphorylation patterns and worsens cognitive impairment in the APP/PS1 mouse model of Alzheimer’s disease

Miriam Corraliza-Gomez, Maria Vargas-Soria, Carmen Infante-Garcia, Alan W. Stitt, Rafael Simó, Mónica García-Alloza · FENS Forum 2024

Alzheimer’s disease (AD) is the most common cause of dementia. Despite age being the main risk factor, previous studies have also reported that type 1 diabetes (T1D) may contribute to abnormal tau phosphorylation and worsen cognitive impairment in AD patients. However, the underlying mechanisms are not completely understood. Therefore, we have analyzed the effects of streptozotocin (STZ)-induced T1D in a mouse model of AD (APP/PS1) in terms of metabolic impairment, cortical tau phosphorylation and cognition at 26 weeks of age, when the pathology is fully established. When all groups under stud

ePoster · Neuroscience