Significance: A healthy nutritional status is essential for proper brain development and for the maintenance of optimal cognitive function during adulthood and aging. The effects of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) and vitamin supplementation or deficiency on neurodevelopment have been extensively studied in healthy infants and postweaning laboratory animals, but little is known about the influence of these micronutrients on the cognitive and neurochemical consequences of chronic stress during adolescence. We provide evidence that a diet supplemented with ω-3 PUFAs and vitamin A prevents deleterious cognitive impairment and shift of microbiota composition induced by social instability stress during adolescence, and that amelioration is maintained through adulthood, suggesting that a healthy diet may have long-lasting beneficial effects and help fight off neurodegenerative diseases.

Histamine axons originate from a single source, the tuberomamillary nucleus of the posterior hypothalamus, to innervate almost all CNS regions. This feature, a compact cell group with widely distributed fibers, resembles that of other amines systems, such as noradrenaline or serotonin, and is consistent with a function for histamine over a host of physiological processes, including the regulation of the sleep-wake cycle, appetite, endocrine homeostasis, body temperature, pain perception, learning, memory and emotion. An important question is whether these diverse physiological roles are served by different histamine neuronal subpopulation. While the histamine system is generally regarded as one single functional unit that provides histamine throughout the brain, evidence is beginning to accumulate in favour of heterogeneity of the histamine neurons. The aim of this review is to summarize experimental evidence demonstrating that histamine neurons are heterogeneous, organized into functionally distinct circuits, impinging on different brain regions, and displaying selective control mechanisms. This could imply independent functions of subsets of histamine neurons according to their respective origin and terminal projections.

The increase in the incidence of neurodegenerative diseases, in particular Alzheimer’s Disease (AD), is a consequence of the world′s population aging but unfortunately, existing treatments are only effective at delaying some of the symptoms and for a limited time. Despite huge efforts by both academic researchers and pharmaceutical companies, no disease-modifying drugs have been brought to the market in the last decades. Recently, several studies shed light on Carbonic Anhydrases (CAs, EC 4.2.1.1) as possible new targets for AD treatment. In the present review we summarized preclinical and clinical findings regarding the role of CAs and their inhibitors/activators on cognition, aging and neurodegeneration and we discuss future challenges and opportunities in the field.