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Thalmann, M.

Publications and source records attributed to Thalmann, M..

3 recordsLinked to original sources

Night-time control of carbohydrate availability in grasses differs radically from that in Arabidopsis

Grass leaves reportedly accumulate sucrose during the day then export it to other organs at night. The control of export at night is not understood. In contrast, Arabidopsis leaves accumulate starch then convert it to sucrose for export at night. Control of starch mobilisation ensures a constant sucrose supply and exhaustion of starch around anticipated dawn. We found that that 41 species of pooid grasses differed widely in the ratio of sucrose to starch accumulation and night-time depletion (turnover) in leaf blades, regardless of growth conditions. Sucrose turnover exceeded starch turnover in most species, but in a minority of species the two were similar. In eight species spanning this diversity, the rate of sucrose depletion fell through the night. In six of the species, all with higher sucrose than starch turnover, starch depletion at night was initially slow. Later, it increased to a rate that exhausted starch around dawn. The initial lag was absent and starch depletion was linear throughout the night in the other two species, both of which had similar sucrose and starch turnover. We suggest that underlying control of starch mobilisation in grass leaf blades resembles that in Arabidopsis leaves. The initial lag in starch depletion in high-sucrose species may result from suppression of starch degradation by sucrose, acting via the sucrose signalling metabolite Tre6P. The large diel fluctuations in sucrose export from grass leaf blades may be dampened by exchange with dynamic pools of sucrose in leaf bases and sheaths prior to export to other organs.

plant biology↗

The hippocampus supports interpolation into new states during category abstraction

The hippocampus forms concepts by integrating multi-feature relations into a unified representation. A common yet unconfirmed assumption is that such cognitive maps afford interpolations to never-experienced states. We approach this question as a category-learning problem in which prototypes are omitted from training but guide category-based decisions in a subsequent feature-inference task. Consistent with behavior, missing inferred stimulus features were represented at prototypical values in neocortex. This cortical completion effect correlated with hippocampal responses, which in turn reflected the distance between imagined prototypes and experienced exemplars. This was paralleled by a learning-dependent grid-like representation of the underlying conceptual space in entorhinal cortex. Our results suggest that abstracted prototypes correspond to interpolated central states in a cognitive map that guide cortical pattern completion during category-based decisions.

neuroscience↗

Ageing-associated myelin dysfunction drives amyloid deposition in mouse models of Alzheimer's disease

The prevalence of Alzheimers disease (AD), the leading cause of dementia, shows a strict age-dependency, but why ageing constitutes the main risk factor for this disease is still poorly understood. Brain ageing affects oligodendrocytes1 and the structural integrity of myelin sheaths2, the latter associated with secondary neuroinflammation3. Since oligodendrocytes support axonal and neuronal health4-7, we hypothesised that ageing-associated loss of myelin integrity could be an upstream risk factor for neuronal amyloid-{beta} (A{beta}) deposition, the primary neuropathological hallmark of AD. Here, we show that in AD mouse models different genetically induced defects of myelin integrity or demyelinating injuries are indeed potent drivers of amyloid deposition in vivo, quantified by whole brain light sheet microscopy. Conversely, the lack of myelin in the forebrain provides protection against plaque deposition. Mechanistically, we find that myelin dysfunction causes the accumulation of the A{beta} producing machinery within axonal swellings and increases cortical amyloid precursor protein (APP) cleavage. Surprisingly, AD mice with dysfunctional myelin lack plaque-corralling microglia but show a disease-associated microglia (DAM)-like signature as revealed by bulk and single cell transcriptomics. These activated microglia, however, are primarily engaged with myelin, preventing the protective reactions of microglia to A{beta} plaques. Our data suggest a working model, in which age-dependent structural defects of myelin promote plaque formation, directly and indirectly, and are thus an upstream AD risk factor. Improving oligodendrocyte health and myelin integrity could be a promising target to delay AD.g

neuroscience↗