Progress in Parkinson's disease research is at a glance.

October 24, 2020 // -- This issue brings you the latest research advances in Parkinson's and I hope readers and friends will enjoy it.
1. PNAS: Break the traditional cognition! Lipids or play a key role in the on-the-go development of Parkinson's disease! DOI:10.1073/pnas.2003021117 In a recent study published in the international 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 results 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 use of lipids in cells and their effects on other organs, such as many people know that lipids play a key role in increasing the risk of cardiovascular disease, and like the cardiovascular disease model, the researchers based on animal models of Parkinson's disease and lipid-induced Parkinson's disease also revealed pathological processes of lipid dependence in the brain, which means that researchers can clearly observe abnormal lipid function and increased levels of neurologic inflammation in the body. In the
study, researchers observed congenital lipid changes in dopamine-energy neurons and other nearby brain glial cells, such as small glial cells and astrological glial cells in the brains of patients with Parkinson's disease, especially small glial cells and astrological glial cells, which exhibit abnormal patterns of intracellular paper storage, which are directly related to the significant accumulation of lipids in dopamine-energy neurons, the most susceptible brain cells in the course of the disease.
researchers said there was a statistical correlation between overall lipid triglyceride levels and levels of lipid-induced inflammatory stress markers in brain tissue in patients with Parkinson's disease, and in an experimental animal model that simulated Parkinson's disease, the researchers observed a very similar image of brain cells and pathology, which is directly related to the loss of enzyme function in the glucosin glycosidease gene, which may lead to the accumulation of glycolipids.
the researchers point out that small glial cells, which largely control the function of macrophages and immune cells in the brain, may load more lipids during the progression of Parkinson's disease, while star-shaped glial cells that normally support lipid maintenance lose some of their lipids, while neurons are in a reverse linear manner compared to surrounding astrological glial cells. Accumulation of lipids, the study suggests, may have a statistically significant correlation with a molecule called GPNMB, a stress-immune response molecule associated with astrological glial cells, which usually suppress certain inflammatory signals that are directly related to lipid accumulation and total triglyceride levels in the black body region of the brain. 'It's worth noting that we were able to simulate these findings in parkinson's disease and healthy aging individuals, and that the interaction between small glial cells and astrocytes in susceptible brain regions (or blocking lipid breakdown path paths in cellular lysosomes) may be a strong risk factor for Parkinson's disease in the population,' said
researcher Ole Isacson.
The findings in this paper support scientists' hypothesis about lipid inflammation during the on occurrence and progression of Parkinson's disease, which may help researchers develop new targeted therapies by revealing the pathological manifestations of Parkinson's disease, which may partly move away from traditional cognitions that are limited to neurons and protein accumulation.
Next, the researchers will continue to delve deeper into how the interactions between lipid cells in the brain become adaptive and pathological over time, and how this cellular mechanism induces Parkinson's disease and Louisian dementia.
2. Brain: Scientists reveal the molecular link between inflammation in the body and Parkinson's disease DOI:10.1093/brain/awaa246 In a study published in the international journal Brain, scientists from the University of Luxembourg and others revealed inflammation and Parkin. In the paper, researchers found two biomarkers that could be used to assess the status and progression of Parkinson's disease, and the results suggest that anti-inflammatory drugs are used to target the processes that affect the body's immune system or potentially affect the disease (at least some patients).
About 15% of Parkinson's disease cases are related to known genetic backgrounds, with mutations in the Parkin and PINK1 genes being the most common causes, so revealing the cellular mechanisms altered by genetic mutations may be important for developing new therapeutic tools, researchers said in the study. Analysis of the serums of 245 participants in two separate studies found increased levels of mitochondrial DNA (mtDNA) and interlebinin 6 (IL-6) circulating in the body of patients with mutations in the Parkin or PINK1 gene.
researchers point out that the absence of Parkin or PINK1 proteins may lead to impaired mitochondrial autophagy, and that abnormal mitochondrial levels induce the release of mitochondrial DNA, which induces inflammation and increases levels of IL-6 in the body's blood, which is thought to play a key role in the development of neurodegenerative diseases, and the results suggest that anti-inflammatory drugs are used to treat or hopefully slow the progression of disease in patients with Parkinson's disease.
By studying the differences between patients carrying Parkin or PINK1 gene mutations on one chromosome (hybrid) or two chromosomes, the researchers found that detecting levels of systemic inflammation in the patient's blood or as a special biomarker indicating the genetic form of these Parkinson's diseases showed higher levels of IL-6 in both chromosomes than in patients with mutations on both chromosomes, but higher levels in patients with hybrids compared to healthy control populations. Levels of IL-6 in the body have also increased significantly, which may indicate that hemp mutations may form a strong risk factor for early Parkinson's disease, and even before these hybrid carrier diseases occur, researchers can detect disease at an early stage by monitoring levels of IL-6 in their body serum, similarly, circulating gland DNA levels or as an effective indicator of the progression of disease in hybrid Parkin/PINK1 mutants.
The study has potential clinical application value and significance by detecting biomarkers present in the patient's body serum or helping to indicate the progression of the disease, and the findings are expected to help researchers develop new therapies that target patients with Parkin/PINK1-related congenital immunological responses, said Grünewald, a researcher.
3. Nat Commun: Micro-brain "tweezers" help treat Parkinson's DOI: 10.1038/s41467-020-18689-x A cooperative study led by Dr Nora Bengoa-Vergniory of The Parkinson's Disease Centre in Oxford suggests that a compound called "molecular tweezers" could be a promising disease-improved treatment for Parkinson's disease.
group of researchers suggests that tiny compounds known as molecular tweezers could be a promising treatment for Parkinson's disease.
the new drug works by pulling apart toxic protein lumps formed in the brain during Parkinson's disease.
, the therapy has shown potential to target toxic protein lumps formed in neurodegenerative diseases such as Alzheimer's disease.
, the team investigated whether a specific molecular tweezer, CLR01, could reduce the formation of protein clumps in Parkinson's cells and mouse models.
studies have shown that CLR01 reduces clusters of Parkinson's α-synactical nucleoprotein formation and prevents the death of human neurons made from stem cells.
researchers tested CLR01 in a mouse model of Parkinson's disease that stimulates the formation of protein clusters and mimics the motor symptoms experienced by people with the disease, including tremors and slow movement.
as mice age, CLR01 therapy reduces the appearance of exercise problems and the formation of toxic protein clusters in the brain.
, the team showed that CLR01 was less effective in older animals with faster progressive Parkinson's disease.
this work shows that the use of protective therapies early in Parkinson's disease is essential for effective treatment.
results highlight that CLR01 represents a candidate for the treatment of Parkinson's disease and highlights the need for further research in this area.
lead researcher Dr Nora Bengoa-Vergniory said: "Future investments in identifying the right treatment window for these and other treatments are critical to the success of these and other treatment strategies.
" results were published recently in the journal Nature Communications.
4. Move Disorders: Parkinson's patients have a higher risk of dying from COVID19 DOI: 10.1002/mds.28325 A new study of about 80,000 patients shows that people with Parkinson's disease are 30 percent more likely to die from COVID-19 than those without neurodegenerative diseases.
new analysis by researchers at the University of Iowa Health Care based on patient data from the TriNetX COVID-19 research network suggests that Parkinson's disease is a separate risk factor for dying from COVID-19.
team, led by neurologist Nandakumar Narayanan, collected the relevant COVID-19 patient cohorts on July 15 and analyzed their mortality data eight weeks later.
they found that the mortality rate for COVID19 patients without Parkinson's disease was 5.5% (4,290 out of 78,355), while the mortality rate for COVID19 patients with Parkinson's disease rose to 21.3% (148 out of 694).
, people with Parkinson's disease are usually older than control patients, with a higher proportion of men.
all these factors also increased the risk of COVID-19 death.
In turn, the researchers used two methods to address these differences: logical regression based on age, gender, and race, matching each Parkinson's patient to five non-Parkinson's patients of age, gender, and race, and performing conditional logical regression.
both cases, the researchers found that PD patients had a 30 percent higher risk of dying from COVID-19.
study was published in the journal Moving Disorder.
"We are aware of the limitations of this study; it is retrospective data from a single database, but we are confident that these data show that Parkinson's disease is a separate risk factor for death in COVID-19," said Naayanan, an associate professor of neurology at the University of California, Los Angeles.
we believe this observation will provide guidance to clinicians and public health leaders who treat people with Parkinson's disease.
findings could also help provide information to Parkinson's patients and their doctors about the growing importance of preventing COVID-19 infections, the researchers said.
5. Neurology: Coffee Helps Prevent Parkinson's DOI: According to a new study published In the journal Neurology on September 30, 2020, drinking coffee may reduce the risk of parkinson's disease even in people with genetic mutations associated with Parkinson's disease.
"These results could help future research to explore caffeine-related therapies to reduce the risk of Parkinson's disease in people carrying associated genetic mutations," said study author Grace Crotty, M.D., of Massachusetts General Hospital in Boston and a member of the American Academy of Sciences.
, caffeine levels in the blood may also be used as biomarkers to help identify risk.
earlier studies have shown that coffee intake can prevent the development of Parkinson's disease in people who do not have a genetic risk.
study looked at people with genetic mutations that increase the risk of Parkinson's disease.
the mutation is located in a gene rich in LRRK2 kinases rich in leucine, and the presence of abnormal gene mutations does not necessarily mean that people will necessarily develop the disease, so the researchers hope to identify other genetic or environmental factors that affect whether people develop the disease.
study compared 188 people with Parkinson's disease with 180 without Parkinson's.
two groups included people with LRRK2 gene mutations and those without LRRK2 gene mutations.
researchers looked at the amount of caffeine in the blood, the amount of other chemicals that caffeine produces when it is metabolized in the body, and the differences between groups.
people with the LRRK2 gene mutation had 76 percent lower levels of caffeine in their blood than those without Parkinson's.
people with Parkinson's disease with a normal copy of the gene had a 31 percent lower concentration of caffeine in their blood than non-carriers without Parkinson's.
caffeine intake was also lower in the diet of people with genetic mutations with Parkinson's disease.
people with Parkinson's disease consume 41 percent less caffeine per day than those without Parkinson's disease, regardless of whether they have a genetic mutation or not.
we don't know if people who are prone to Parkinson's tend not to drink coffee, or if some people with mutations drink a lot of coffee and benefit from it," he said. "6. Cell Stem Cell: Dopamine produced by transplanting human stem cells.