ABSTRACT
The sustainable development goal #2 aims at ending hunger and malnutrition by 2030. Given the numbers of food insecure and malnourished people on the rise, the heterogeneity of nutritional statuses and needs, and the even worse context of COVID-19 pandemic, this has become an urgent challenge for food-related policies. This paper provides a comprehensive microsimulation approach to evaluate economic policies on food access, sufficiency (energy) and adequacy (protein, fat, carbohydrate) at household level. The improvement in market access conditions in Kenya is simulated as an application case of this method, using original insights from households' surveys and biochemical and nutritional information by food item. Simulation's results suggest that improving market access increases food purchasing power overall the country, with a pro-poor impact in rural areas. The daily energy consumption per capita and macronutrients intakes per capita increase at the national level, being the households with at least one stunted child under 5 years old, and poor households living areas outside Mombasa and Nairobi, those which benefit the most. The developed method and its Kenya's application contribute to the discussion on how to evaluate nutrition-sensitive policies, and how to cover most households suffering food insecurity and nutrition deficiencies in any given country. Supplementary Information: The online version contains supplementary material available at 10.1007/s12571-021-01215-2.
ABSTRACT
The molecular mechanisms causing the loss of dopaminergic neurons containing neuromelanin in the substantia nigra and responsible for motor symptoms of Parkinson's disease are still unknown. The discovery of genes associated with Parkinson's disease (such as alpha synuclein (SNCA), E3 ubiquitin protein ligase (parkin), DJ-1 (PARK7), ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL-1), serine/threonine-protein kinase (PINK-1), leucine-rich repeat kinase 2 (LRRK2), cation-transporting ATPase 13A1 (ATP13A), etc.) contributed enormously to basic research towards understanding the role of these proteins in the sporadic form of the disease. However, it is generally accepted by the scientific community that mitochondria dysfunction, alpha synuclein aggregation, dysfunction of protein degradation, oxidative stress and neuroinflammation are involved in neurodegeneration. Dopamine oxidation seems to be a complex pathway in which dopamine o-quinone, aminochrome and 5,6-indolequinone are formed. However, both dopamine o-quinone and 5,6-indolequinone are so unstable that is difficult to study and separate their roles in the degenerative process occurring in Parkinson's disease. Dopamine oxidation to dopamine o-quinone, aminochrome and 5,6-indolequinone seems to play an important role in the neurodegenerative processes of Parkinson's disease as aminochrome induces: (i) mitochondria dysfunction, (ii) formation and stabilization of neurotoxic protofibrils of alpha synuclein, (iii) protein degradation dysfunction of both proteasomal and lysosomal systems and (iv) oxidative stress. The neurotoxic effects of aminochrome in dopaminergic neurons can be inhibited by: (i) preventing dopamine oxidation of the transporter that takes up dopamine into monoaminergic vesicles with low pH and dopamine oxidative deamination catalyzed by monoamino oxidase (ii) dopamine o-quinone, aminochrome and 5,6-indolequinone polymerization to neuromelanin and (iii) two-electron reduction of aminochrome catalyzed by DT-diaphorase. Furthermore, dopamine conversion to NM seems to have a dual role, protective and toxic, depending mostly on the cellular context. Dopamine oxidation to dopamine o-quinone, aminochrome and 5,6-indolequinone plays an important role in neurodegeneration in Parkinson's disease since they induce mitochondria and protein degradation dysfunction; formation of neurotoxic alpha synuclein protofibrils and oxidative stress. However, the cells have a protective system against dopamine oxidation composed by dopamine uptake mediated by Vesicular monoaminergic transporter-2 (VMAT-2), neuromelanin formation, two-electron reduction and GSH-conjugation mediated by Glutathione S-transferase M2-2 (GSTM2).