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Your search keyword '"Schiöth, Helgi"' showing total 183 results
Start Over Author "Schiöth, Helgi" Publisher elsevier b.v.
183 results on '"Schiöth, Helgi"'

3. Identifying proteomic risk factors for overall, aggressive, and early onset prostate cancer using Mendelian Randomisation and tumour spatial transcriptomics

Author

Desai, Trishna A., Hedman, Åsa K., Dimitriou, Marios, Koprulu, Mine, Figiel, Sandy, Yin, Wencheng, Johansson, Mattias, Watts, Eleanor L., Atkins, Joshua R., Sokolov, Aleksandr V., Schiöth, Helgi B., Gunter, Marc J., Tsilidis, Konstantinos K., Martin, Richard M., Pietzner, Maik, Langenberg, Claudia, Mills, Ian G., Lamb, Alastair D., Mälarstig, Anders, Key, Tim J., Travis, Ruth C., and Smith-Byrne, Karl

Published
2024
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48. Intranasal insulin in Alzheimer's disease: Food for thought.

Author

Chapman, Colin D., Schiöth, Helgi B., Grillo, Claudia A., and Benedict, Christian

Subjects
*INTRANASAL medication, *INSULIN, *ALZHEIMER'S disease, *NEURODEGENERATION, *HYPOGLYCEMIC agents, *PROGNOSIS
Abstract

Accumulating evidence suggests that disrupted brain insulin signaling promotes the development and progression of Alzheimer's disease (AD), driving clinicians to target this circuitry. While both traditional and more modern antidiabetics show promise in combating insulin resistance, intranasal insulin appears to be the most efficient method of boosting brain insulin. Furthermore, intranasal delivery elegantly avoids adverse effects from peripheral insulin administration. However, there remain significant open questions regarding intranasal insulin's efficacy, safety, and potential as an adjunct or mono-therapy. Thus, this review aims to critically evaluate the present evidence and future potential of intranasal insulin as a meaningful treatment for AD. This article is part of the Special Issue entitled ‘Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.’ [ABSTRACT FROM AUTHOR]

Published
2018
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49. IL-1β reduces GluA1 phosphorylation and its surface expression during memory reconsolidation and α-melanocyte-stimulating hormone can modulate these effects.

Author

Machado, Ivana, Schiöth, Helgi B., Lasaga, Mercedes, and Scimonelli, Teresa

Subjects
*INTERLEUKIN-1, *PHOSPHORYLATION, *MSH (Hormone), *HIPPOCAMPUS physiology, *COGNITIVE psychology
Abstract

Pro-inflammatory cytokines can affect cognitive processes such as learning and memory. Particularly, interleukin-1β (IL-1β) influences hippocampus-dependent memories. We previously reported that administration of IL-1β in dorsal hippocampus impaired contextual fear memory reconsolidation. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (α-MSH). Our results also demonstrated that IL-1β produced a significant decrease in glutamate release from dorsal hippocampus synaptosomes after reactivation of the fear memory. Therefore, we investigated whether IL-1β administration can affect GluA1 AMPA subunit phosphorylation, surface expression, and total expression during reconsolidation of a contextual fear memory. Also, we studied the modulatory effect of α-MSH. We found that IL-1β reduced phosphorylation of this subunit at Serine 831 and Serine 845 60 min after contextual fear memory reactivation. The intrahippocampal administration of IL-1β after memory reactivation also induced a decrease in surface expression and total expression of GluA1. α-MSH prevented the effect of IL-1β on GluA1 phosphorylation in Serine 845, but not in Serine 831. Moreover, treatment with α-MSH also prevented the effect of the cytokine on GluA1 surface and total expression after memory reactivation. Our results demonstrated that IL-1β regulates phosphorylation of GluA1 and may thus play an important role in modulation of AMPAR function and synaptic plasticity in the brain. These findings further illustrate the importance of IL-1β in cognition processes dependent on the hippocampus, and also reinforced the fact that α-MSH can reverse IL-1β effects on memory reconsolidation. [ABSTRACT FROM AUTHOR]

Published
2018
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50. Candidate mechanisms underlying the association between sleep-wake disruptions and Alzheimer's disease.

Author

Cedernaes, Jonathan, Osorio, Ricardo S., Varga, Andrew W., Kam, Korey, Schiöth, Helgi B., and Benedict, Christian

Abstract

During wakefulness, extracellular levels of metabolites in the brain increase. These include amyloid beta (Aβ), which contributes to the pathogenesis of Alzheimer's disease (AD). Counterbalancing their accumulation in the brain, sleep facilitates the removal of these metabolites from the extracellular space by convective flow of the interstitial fluid from the para-arterial to the para-venous space. However, when the sleep-wake cycle is disrupted (characterized by increased brain levels of the wake-promoting neuropeptide orexin and increased neural activity), the central nervous system (CNS) clearance of extracellular metabolites is diminished. Disruptions to the sleep-wake cycle have furthermore been linked to increased neuronal oxidative stress and impaired blood-brain barrier function - conditions that have also been proposed to play a role in the development and progression of AD. Notably, recent human and transgenic animal studies have demonstrated that AD-related pathophysiological processes that occur long before the clinical onset of AD, such as Aβ deposition in the brain, disrupt sleep and circadian rhythms. Collectively, as proposed in this review, these findings suggest the existence of a mechanistic interplay between AD pathogenesis and disrupted sleep-wake cycles, which is able to accelerate the development and progression of this disease. [ABSTRACT FROM AUTHOR]

Published
2017
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