Stress and misfolded proteins result to dysfunction in the cell, often leading to neurodegenerative diseases and aging. Misfolded proteins form toxic aggregates that threaten cell's stability and normal functions. In order to restore its homeostasis, the cell activates the UPR system. Leading role in the restoration play the molecular chaperones which target the misfolded proteins with the purpose of either helping them to unfold and refold to their natural state or lead them degradation. This paper aims to present some of the most known molecular chaperones and their relation with diseases associated to protein misfolding and neurodegeneration, as well as the role of chaperones in proteostasis.

Programmed death-ligand 1 (PD-L1) has been speculated to play a critical role in suppression of the immune system and it can be upregulated in cancer cells, which may allow cancers to evade the host immune system. MicroRNAs (miRNAs) are small non-coding RNA molecules (containing about 22 nucleotides), that function in RNA silencing and post-transcriptional regulation of gene expression. MiRNAs were found deregulated (upregulated or downregulated) and implicated in cancer development with various roles which depend on their gene target. Using targetscan web server prediction algorithm, we concluded that miR-140-3p is a targeting mirRNA with conserved consequential pairing of target region for PD-L1. Moreover, by reviewing all the available cancer studies in Pub/Medline about miR-140-3p, was found permanently down regulated. Furthermore, in recent immunotherapy related clinical trials in most cancers, evaluated PD-L1, it is found overexpressed. In the near future, in vitro or in vivo studies need to validate whether there is direct correlation between PD-L1 overexpression and miR-140-3p downregulation as targetscan performed algorithm predicted.

Recent biomedical research studies are focused in the mechanisms by which misfolded proteins lead to the generation of oxidative stress in the form of reactive oxygen species (ROS), often implicated in neurodegenerative diseases and aging. Moreover, biological experiments are designed to investigate how proteostasis depends on the balance between the folding capacity of chaperone networks and the continuous flux of potentially nonnative proteins. Nevertheless, biological experimental methods can examine the protein folding quality control mechanisms only in individual cells, but not in a multicellular level. Formal models offer a dynamic form of modelling, which allows to explore various parameter values in an integrated time-dependent system. This paper aims to present a formal approach of a mathematical descriptive model using as example a representation of a known molecular chaperone system and its relation to diseases associated to protein misfolding and neurodegeneration.

Huntington's disease is a neurodegenerative disorder of the brain that is caused by the mutation of the gene which produces a protein called huntingtin (htt). The mutation is based on the continuous repetition of the trinucleotide CAG which in turn makes the protein toxic for the brain cells. As a result neurons which contain the mutant protein begun to atrophy. The loss of those brain cells can cause many problems to the patients, even death. The aim of this paper is to report the problems caused to the brain by the mutant protein, specifically in the area of basal ganglia, the area that is the most affected by the disease, as well as the symptoms and metabolic changes to which the patient is subjected. Finally, the summary of the methods for a more timely and accurate diagnosis of the disease is based on these changes in order to simplify and facilitate the lives of inflicted people by means of the administration of the appropriate treatment.

Huntington's disease as a neurodegenerative disease is characterized by motor and cognitive impairment. The disease is caused by the mutation of the gene that produces the huntingtin protein causing the repetition of trinucleotide CAG. The mutant protein reacts with other proteins inside and out of the cell causing problems to its normal function and cell death. Recent advances in the signal analysis have engendered EEG with the status of a true brain mapping and brain imaging method able of providing spatio-temporal information regarding brain (dys)function. Authors aim to review objectively and quantitatively the neurophysiological basis of the disease in HD patients as compared to normal controls, with the use of brain imaging in general and EEG brain imaging methods.