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ISSUE: Universal school lunches hold the potential to improve student nutritional intake and access to food, but to do so menus must be nutritionally adequate. There is growing interest in school lunch programs (SLPs) in Australia, and one is currently being trialled in Tasmania. No nutrition guidelines currently exist for menu development in Australian schools. METHODS: A desktop review of international SLPs was completed, and findings analysed in the context of Australian Nutrient Reference Values and Australian Dietary Guidelines to inform the development of Tasmanian SLP guidelines. DISCUSSION: Globally, SLPs are guided by portion sizes and/or nutrient criteria. SLPs (many of which address food insecurity) must provide children the opportunity to meet energy and nutrient needs, while minimising food waste. We propose energy-based nutrient criteria and qualitative recommendations for menu development. SO WHAT?: We have developed guidelines to inform the development of Tasmanian SLP menus. These guidelines may be applicable to other states and territories piloting similar programs.

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ISSUE ADDRESSED: Australian school canteen guidelines do not broadly incentivise procuring food from local producers, despite evidence of this occurring abroad. This scoping review aims to investigate what is known about local food procurement for school foodservice. METHODS: A scoping review of peer-reviewed articles published since 2000 was undertaken using MEDLINE, CINAHL and Scopus. RESULTS: Twenty-one studies met the inclusion criteria. Local food was generally perceived as fresher and more nutritious. Small, positive impacts on fruit and vegetable intake have been demonstrated when food is procured locally. Challenges identified included concerns around food safety, varied availability, time spent coordinating food supply, lack of incentive from regional or national guidelines, inadequate kitchen facilities and budget constraints. CONCLUSIONS: There is no universal definition or standard for procuring 'local food'. The main motivation for local food procurement was a sense of social responsibility, however there are barriers, including cost, facilities and food safety. Purchasing food locally holds potential to benefit the local economy but government funding and policy supporting local and small-scale producers is an important enabler. SO WHAT?: Government support to build stakeholder capacity is important in establishing and maintaining these programmes and would be crucial in achieving change in Australian schools. Investigating feasibility of a national school lunch service would be beneficial, as these programmes may have merit not just in feeding children but also in supporting the local economy. Further research is warranted in this area.

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Although ß-amyloid plaques are a well-recognized hallmark of Alzheimer's disease (AD) neuropathology, no drugs reducing amyloid burden have shown efficacy in clinical trials, suggesting that once AD symptoms emerge, disease progression becomes independent of Aß production. Reactive astrocytes are another neuropathological feature of AD, where there is an emergence of neurotoxic (A1) reactive astrocytes. We find that serine racemase (SR), the neuronal enzyme that produces the N-methyl-d-aspartate receptor (NMDAR) co-agonist d-serine, is robustly expressed in A1-reactive neurotoxic astrocytes in the hippocampus and entorhinal cortex of AD subjects and an AD rat model. Furthermore, we observe intracellular signaling changes consistent with increased extra-synaptic NMDAR activation, excitotoxicity and decreased neuronal survival. Thus, reducing neurotoxic d-serine release from A1 inflammatory astrocytes could have therapeutic benefit for mild to advanced AD, when anti-amyloid strategies are ineffective.

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Alzheimer's disease (AD) is a neurodegenerative disease that disproportionately impacts memory and the hippocampus. However, it is unclear how AD pathology influences the activity of surviving neurons in the hippocampus to contribute to the memory symptoms in AD. One well-understood connection between spatial memory and neuronal activity in healthy brains is the activity of place cells, neurons in the hippocampus that fire preferentially in a specific location of a given environment (the place field of the place cell). In the present study, place cells were recorded from the hippocampus in a recently-developed rat model of AD (Tg-F344 AD) at an age (12-20 months) at which the AD rats showed marked spatial memory deficits. Place cells in the CA2 and CA3 pyramidal regions of the hippocampus in AD rats showed sharply reduced spatial fidelity relative to wild-type (WT) rats. In contrast, spiking activity of place cells recorded in region CA1 in AD rats showed good spatial fidelity that was similar to CA1 place cells in WT rats. Oral administration of the M1 muscarinic acetylcholine receptor agonist VU0364572 impacted place cell firing rates in CA1 and CA2/3 hippocampal regions, but did not improve the spatial fidelity of CA2/3 hippocampal place cells in AD rats. The results indicated that, to the extent the spatial memory impairment in AD rats was attributable to hippocampal dysfunction, the memory impairment was more attributable to dysfunction in hippocampal regions CA2 and CA3 rather than CA1.

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Neuronal oscillations in the rat hippocampus relate to both memory and locomotion, raising the question of how these cognitive and behavioral correlates interact to determine the oscillatory network state of this region. Here, rats freely locomoted while performing an object-location task designed to test hippocampus-dependent spatial associative memory. Rhythmic activity in theta, beta, slow gamma, and fast gamma frequency ranges were observed in both action potentials and local field potentials (LFPs) across four main hippocampal subregions. Several patterns of LFP oscillations corresponded to overt behavior (e.g., increased dentate gyrus-CA3 beta coherence during stationary moments and CA1-subiculum theta coherence during locomotion). In comparison, slow gamma (∼40 Hz) oscillations throughout the hippocampus related most specifically to object-location associative memory encoding rather than overt behavior. The results help to untangle how hippocampal oscillations relate to both memory and motion and single out slow gamma oscillations as a distinguishing correlate of spatial associative memory.

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Recent research in humans has used formal models of temporal context, broadly defined as a lingering representation of recent experience, to explain a wide array of recall and recognition memory phenomena. One difficulty in extending this work to studies of experimental animals has been the challenge of developing a task to test temporal context effects on performance in rodents. The current study presents results from a novel object recognition memory paradigm that was adapted from a task used in humans and demonstrates a temporal context repetition effect in rats. Specifically, the findings indicate that repeating the first two objects from a once-encountered sequence of three objects incidentally cues memory for the third object, even in its absence. These results reveal that temporal context influences item memory in rats similar to the manner in which it influences memory in humans and also highlight a new task for future studies of temporal context in experimental animals.

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Acetylcholine signaling through muscarinic receptors has been shown to benefit memory performance in some conditions, but pan-muscarinic activation also frequently leads to peripheral side effects. Drug therapies that selectively target M1 or M4 muscarinic receptors could potentially improve memory while minimizing side effects mediated by the other muscarinic receptor subtypes. The ability of three recently developed drugs that selectively activate M1 or M4 receptors to improve recognition memory was tested by giving Long-Evans rats subcutaneous injections of three different doses of the M1 agonist VU0364572, the M1 positive allosteric modulator BQCA or the M4 positive allosteric modulator VU0152100 before performing an object recognition memory task. VU0364572 at 0.1 mg/kg, BQCA at 1.0 mg/kg and VU0152100 at 3.0 and 30.0 mg/kg improved the memory performance of rats that performed poorly at baseline, yet the improvements in memory performance were the most statistically robust for VU0152100 at 3.0 mg/kg. The results suggested that selective M1 and M4 receptor activation each improved memory but that the likelihood of obtaining behavioral efficacy at a given dose might vary between subjects even in healthy groups depending on baseline performance. These results also highlighted the potential of drug therapies that selectively target M1 or M4 receptors to improve memory performance in individuals with impaired memory.

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