Researcher Professor Per Andren says the findings of this paper are expected to help develop new treatments for the ongoing Parkinson's disease, a key neurotransmitter The slow death of nerve cells with dopamine can lead to typical symptoms of the disease, such as stiffness and tremors, and treatment with the drug L-doba (a prelude to dopamine) initially works well, but after a few years, the effects of each dose become more short-lived.
patients also experience adverse side effects, such as the body's rapid alternating stiffness and uncontrolled movements, and these symptoms become more severe over time.
In the end, the therapeutic benefits of L-Doba are clearly affected, and patients' symptoms become weaker, and researchers do not yet know which neurochemical mechanisms cause these side effects, an involuntary movement collectively known as L-Dopa-induced dyskinesia.
: New Discovery! Diabetes drugs may slow the progression of Parkinson's disease! Doi:10.1523/ENEURO.0330-20.2020 In a recent study published in the international journal eneuro, scientists from the University of Warwick and others in the United Kingdom said that a drug to treat diabetes may help slow the progression of Parkinson's disease.
Parkinson's disease is marked by the degeneration of dopamine neurons in the brain, which play a key role in the movement and coordination of the body, and when these dopamine neurons deteriorate, they induce symptoms such as motor inability, slow movement, stiffness and numbness.
The affected dopamine-energy neurons accumulate a special protein called α synactin, which forms the structure of the Louis small body, where levels are directly related to the severity of the disease, and α synactal nucleoproteins in the early stages of aggregation produce a series of toxic effects that many event researchers do not know about.
in this study, entitled "Alpha-synuclein aggregates increased conductance of substantia nigra dopamine neurons, an effect partly reversed by the KATP channel resedor glibenclamide", the researchers found that by introducing a low-concentration structure-determined α synaptic nucleoprotein aggregate into a single dopamine-energy neuron, the cell membrane's channel is turned on, greatly reducing the neurotic membrane.
image Source: Wikipedia:6 Nature: Revealing the mechanism by which Hsp70 companion protein dissolves α-synaptic nuclear protein aggregates, promising to develop a new treatment for Parkinson's disease doi:10.1038/s41586-020-2904-6do i:10.1038/s41586-020-2906-4 In many neurodegenerative diseases such as Parkinson's disease, protein aggregates called amyloid fibril form in the brain and are thought to cause neuron cell death.
, neurons also have a cell defense mechanism that fights amyloid fibers and can even dissolve formed amyloid fibers.
this defense mechanism is based on the activity --- partner protein, the hot shock protein 70 family (Hsp70--- protein folding.
in two new studies, researchers from the German Cancer Research Centre and the University of Heidelberg studied how the Hsp70 system breaks down starchy fibers formed by Parkinson's disease-specific α-synaptic nucleoprotein (α-synuclein) in test tubes.
led by Dr. Bernd Bukau, they expect their findings to provide new insights into how Parkinson's disease is developed and the measures that may be taken to influence it.
study was published online in two papers in the journal Nature.
both bacteria and human cells, proteins in cells need to be folded into their natural state.
amino acid chains that make up proteins give specific three-dimensional structures that enable the proteins to function.
this correct folding state is constantly threatened by external and internal factors, which can lead to incorrect folding and thus disrupt the function of the protein.
risk is that damaged proteins will come together, or condense into longer chains, or amyloid fibers.
, for example, this is the case with α-synactal nucleoproteins in Parkinson's disease.
these amyloid fibers are the starting point for the formation of larger deposits.
: The commonly used diabetes drug Essenathione may be expected to help prevent or treat Parkinson's disease doi:10.1093/brain/awaa262 A study published in the international journal Brain by scientists from University College London and others has found In an article in which drugs for type 2 diabetes may be expected to reduce the risk of Parkinson's disease in patients, researchers tested a drug called exenatide, which could be used as a potential treatment for Parkinson's disease in upcoming clinical trials, and the results support the redirection of diabetes drugs to treat Parkinson's disease. In the
study, researchers analyzed the medical records of 100,288 people with type 2 diabetes from the Health Improvement Network database, and said people with type 2 diabetes were often at increased risk of Parkinson's disease compared to those who did not have type 2 diabetes, but the common therapeutic drugs: GLP-1 agonists and DPP4 inhibitors, did not appear to reverse the increased risk of Parkinson's disease.
PNAS: Breaking traditional cognition! Lipids or play a key role in the on-the-go development of Parkinson's disease! doi:10.1073/pnas.20030211117 In a study published in the journal Proceedings of the National Academy of Sciences, scientists from institutions such as McLean Hospital found that lipid changes in a class of key brain cells may play a key role in inflammation and Parkinson's disease, and the findings are expected to help develop new treatments for Parkinson's disease.
researcher Oeystein R. Brekk said that in this study, we revealed the importance of co-use, storage, and transport of lipids between different types of brain cells in Parkinson's disease, and we also shed light on the molecular mechanisms that balance cell lipids, especially neutral lipids, and that scientists still have many shortcomings in understanding the key role lipids play in neurodegenerative diseases.
However, researchers are well aware of the effects of lipid use in cells and their changes on other organs, such as the key role that lipids play in increasing the risk of cardiovascular disease, as in the cardiovascular disease model, which researchers have studied based on animal models of Parkinson's disease and lipid-induced Parkinson's disease