Numerous degenerative neurological conditions, most notably Parkinson's disease, have been linked to an excessive buildup of alpha synuclein (a-syn) in the brain. Intraneuronal inclusions, often known as Lewy bodies, are neuropathological characteristics seen in Parkinson's disease, Lewy body dementia, and other synucleopathies. The aggregation of a-syn is their main structural component. A-syn accumulation, aggregation, and ensuing Lewy body formation can be attributed to a variety of biological processes. These include genetic changes in parkin, synuclein, or the deubiquitinating enzyme ubiquitin C-terminal hydrolase (UCH-L1), which results in less efficient removal of a-syn via the ubiquitin proteasomal pathway (UPP). Additionally, environmental variables and an age-related decline in antioxidant defense mechanisms that heighten oxidative stress and can have an impact on the formation or clearance of a-syn are intracellular insults.
We focused on changes in the aggregation and clearance of a-syn as impacted by the UPP and the oxidative stress pathways in our dynamic models of a-syn processing in both normal and various disease states. A free radical profile similar to that observed in vivo after exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is produced during simulation of enhanced oxidative stress (MPTP). To replicate the kinetics of a-syn that correlates to the neuropathology reported for the sporadic and hereditary types of Parkinson's disease, different model parameters of oxidative stress, UPP failure, or both routes are used. With the use of this in silico model, it is possible to evaluate the kinetics of pathway elements and more accurately identify and validate key pharmaceutical targets.
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When it comes to population evolution and genetics, we cannot fail to cite the Hardy-Weinberg principle which emphasizes that if evolutionary factors such as natural selection, mutation, migration and genetic oscillation do not act on a particular population, the frequencies genotypic proportions will remain constant.
The five requirements for a population to be in Hardy-Weinberg equilibrium are:
- Large-scale breeding population: For a population to be in Hardy-Weinberg equilibrium, it is important that this population is large, as small populations favor genetic drift (unanticipated fluctuations in allele frequencies from one generation to another).
- Random mating: In order for the Hardy-Weinberg equilibrium to occur, it is necessary that the mating occur at random, with no preference for certain groups within the population. In this case, we say that the population is in panmixia, that is, they all mate at random.
- No mutations: Mutations alter the total alleles present in a population (gene pool). Therefore, in a Hardy-Weinberg equilibrium population, no mutations should occur.
- No gene flow: When there is gene flow due to migration or immigration of individuals, some genes may be included or excluded from the population. Thus, in an equilibrium situation, no gene flow occurs.
- Lack of natural selection: For a population to be in Hardy-Weinberg equilibrium, natural selection must not be acting on it. If natural selection acts, some genotypes will be selected, modifying the allelic frequencies of the population.
So it will float on top of the water
Water, which is a chemical compound of hydrogen and oxygen in the ratio two hydrogen atoms for every oxygen atom, contains H2O molecules.