Ghrelin and Memory

Kunath, Nicolas; Dresler, Martin

doi:10.1007/978-1-4939-0823-3_10

Cited by 3 publications

(2 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While pharmacological enhancers are typically designed to affect or mimic certain neurotransmitters, also neural signaling molecules themselves such as adrenaline, 39 GABA, 40 glucocorticoids, 41 ovarian hormones, 42 and different neuropeptides 43 − 45 have been suggested as cognitive enhancers.…”

Section: Mode Of Actionmentioning

confidence: 99%

Hacking the Brain: Dimensions of Cognitive Enhancement

Dresler¹,

Sandberg

Bublitz

et al. 2018

ACS Chem. Neurosci.

Self Cite

View full text Add to dashboard Cite

In an increasingly complex information society, demands for cognitive functioning are growing steadily. In recent years, numerous strategies to augment brain function have been proposed. Evidence for their efficacy (or lack thereof) and side effects has prompted discussions about ethical, societal, and medical implications. In the public debate, cognitive enhancement is often seen as a monolithic phenomenon. On a closer look, however, cognitive enhancement turns out to be a multifaceted concept: There is not one cognitive enhancer that augments brain function per se, but a great variety of interventions that can be clustered into biochemical, physical, and behavioral enhancement strategies. These cognitive enhancers differ in their mode of action, the cognitive domain they target, the time scale they work on, their availability and side effects, and how they differentially affect different groups of subjects. Here we disentangle the dimensions of cognitive enhancement, review prominent examples of cognitive enhancers that differ across these dimensions, and thereby provide a framework for both theoretical discussions and empirical research.

show abstract

Section: Mode Of Actionmentioning

confidence: 99%

Hacking the Brain: Dimensions of Cognitive Enhancement

Dresler¹,

Sandberg

Bublitz

et al. 2018

ACS Chem. Neurosci.

Self Cite

View full text Add to dashboard Cite

show abstract

“…In rodents, ghrelin improves performance on different memory tasks, like fear conditioning, object recognition and spatial memory retention (Carlini et al 2002;Diano et al 2006;Kent et al 2015). To explain these results, Kunath and Dresler used the analogy of a wild squirrel awakening from hibernation, whose only way to survive from starvation is to remember exactly where it hid the food before winter (Kunath and Dresler 2014). In this example, memory retention is intended as a survival mechanism to cope with metabolic changes like hunger, of which ghrelin represents part of the molecular signature.…”

Section: Figure 11 Ghrelin Activity Engages the Whole Organismmentioning

confidence: 99%

Characterisation of the ghrelinergic system in human models of neurodegenerative diseases

Carisi¹

View full text Add to dashboard Cite

Calorie restriction (CR) has well established neuroprotective properties across species and is known to prevent cognitive deficits in several mouse models and in aged humans. Our group and others have shown that CR beneficial effects are dependent on the circulating hormone acyl-ghrelin (AG), that promotes hippocampal memory function and protects against neurodegeneration in rodents. Indeed, ghrelin knockout (KO) mice show defects in memory task performance and plasma ghrelin levels are significantly reduced in aged humans. Because of its connection to memory and ageing, AG has been studied in mouse models of Alzheimer’s disease (AD) and Parkinson’s disease (PD), the two most common causes of dementia in the aged population. However, very few of these studies have been performed in human models. This project aimed to determine the expression of key regulatory proteins of the ghrelin pathway in the young and aged healthy human brain, as well as brain of AD and PD patients, combining immunohistochemistry, RNA in situ hybridization, and molecular biology. My findings show that the key enzymes of the ghrelinergic axis – GHS-R1a, GOAT and APT1 – are highly expressed in the aged healthy human hippocampus, but their expression level is impaired in PD with dementia . Further studies are needed to determine a potential correlation between the activity of ghrelin in the brain and the level of cognitive impairment and dementia. On the contrary, very little difference is observed between early and late stage of AD, suggesting that the ghrelinergic system may not be impaired in these patients. The second aim was to characterize the effects of AG on a human neuronal cell line treated with rotenone or amyloid-β oligomers (AβOs) to simulate oxidative stress from PD and AD, respectively. Using confocal microscopy and molecular biology techniques, I assessed neuronal cell death and mitochondrial function and reported significant mitochondrial toxicity in these models, that worsen by chronic pre-treatment with the inactive form of AG, unacylated ghrelin (UAG). Ultimately, this project supports the ghrelinergic axis as a potential target for future studies aiming to identify treatments to limit the progression of dementia in humans.

show abstract