New Study Reveals Molecular Signs of Parkinson's Disease

Parkinson’s Disease is a widespread chronic health issue that causes the degeneration of the central nervous system, which severely affects motor functions over time in addition to causing a number of other symptoms, including cognitive impairment, depression, fatigue, and sleeping problems. This disease is unfortunately fatal and causes a gradual degradation of the body and mind, though most of the symptoms can be managed and staved off by taking the right combination of medicine and possibly surgery.

While there is much information available about the treatments and symptoms of this disease in both its early stages and more advanced stages, the cause of Parkinson’s and it’s molecular structure have only just begun to be understood in this recent study.

 The Development of Parkinson’s Disease

Parkinson’s Disease is identified by the gradual degeneration of the central nervous system causing muscle rigidity, slow movements, and imbalance. The development of this disease is closely related to the production of neurons, neurotransmitters, and hormones that play a major role in motor functions.

The main chemical produced by the brain that contributes to motor function is dopamine, so when the nerve endings that produce dopamine become impaired or die, the motor system suffers and steadily degrades. Another set of neurotransmitters that become impaired in a person suffering from Parkinson’s disease are the nerve-endings that produce norepinephrine.

This particular chemical is one of the main messengers of the nervous system, controlling automatic bodily functions like blood pressure, heart rate, and digestion. It is largely the death and impairment of these neurotransmitters that lead to various progressive symptoms of Parkinson’s. However, the exact cause of neuronal failure remains unknown.

Parkinson’s disease affects nearly 500,000 people, and those numbers are, sadly, on the rise. While 90% of patients diagnosed are above the age of 60, the remaining 10% are within the 21-50 age bracket. It is these early cases that create the most worry, and at the same time, they show the most potential for identifying the molecular changes to the body that occur at the earliest stages of Parkinson’s disease.

What the Study Revealed

The study, published on 27th January 2020 in the journal Nature Medicine, was focused on the symptoms and development of the disease in young patients between the ages of 21 and 50. The study was conducted by a team of researchers from Cedars-Sinai and UCLA, and it first began by harvesting and generating special stem cells from young patients suffering from Parkinson’s. These stem cells are called induced pluripotent stem cells (iPSCs for short), and they are created by turning back the clock on adult cells by turning them into primitive embryonic cells.

These embryonic cells, iPSCs, can then produce genetically identical cells, replicating any type of cell in the human body. Using the iPSCs, the dopamine neurons of early-onset Parkinson’s patients were replicated, cultured in a dish, and analyzed. The goal, according to the senior author of the study Dr. Clive Svendsen, was to take the cells back to the earliest stages of their development and observe these dopamine neurons in the earliest stages of the disease, prior to major impairments.

Two major observations were detected. The first was a build-up of a protein commonly found in forms of Parkinson’s disease called alpha-synuclein in the neurons. The second observation was the malfunctioning of a number of lysosomes. Lysosomes are tiny sacs of enzymes in the cell that aid in digestion by acting as waste disposal systems, or “trash can” organelles that break down and dispose of proteins.

It could, therefore, be reasonably assumed that when the malfunctioning of these lysosomes occurs, it results in the accumulation of the alpha-synuclein protein in neuronal cells.

This technique and these observations show the first signs of early-onset Parkinson’s, which would likely imply that the build-up of alpha-synuclein over 2 or 3 decades could cause the progression of the symptoms of the disease. The greater the accumulation, the more severe the symptoms.
 
A Great Sign of Progress
These abnormalities are now being studied to determine their presence in other forms of Parkinson’s disease. The technique described in this study not only provided the team of researchers a method that helps us understand the progression of the disease on a molecular level, but also a means of drug testing.

The iPSCs were used to test a variety of drugs, one of which was found to reduce the high levels of alpha-synuclein. This drug, PEP005, was tested in both the dopamine neurons in the dish, as well as in lab mice, and was found to reduce alpha-synuclein levels. The benefit of this drug is that it has already been approved by the FDA (United States Food and Drug Administration) as a treatment for precancerous tumors of the skin.  

An additional surprising result of using the drug, PEP005, is an abnormal increase in the levels of an active protein called kinase C. However, the relation of this protein to Parkinson’s disease is still undiscovered. Experiments are being conducted to determine how the drug PEP005 might be used to treat or even prevent early-onset symptoms of Parkinson’s.

What Makes This Research So Important
Recent Study Uses Special type of stem cells to discover early signs of Parkinson's disease at younger ages


Dr. Michele Tagliati, professor and vice-chair of the Department of Neurology at Cedars-Sinai, director of the Movement Disorders Program and a co-author of the study stated that “Young-onset Parkinson's is especially heartbreaking because it strikes people at the prime of life… This exciting new research provides hope that one day, we may be able to detect and take early action to prevent this disease in at-risk individuals."

This study shows great potential for the future of Parkinson’s disease and in the discovery of possible preventive measures, treatments, and cures. This joint effort between Cedars-Sinai and UCLA also marks an important milestone in collective medical advancement.

As Dr. Shlomo Melmed of Cedars-Sinai said, “This research is an outstanding example of how physicians and investigators from different disciplines join forces to produce translational science with the potential to help patients.” This study marks one of many incredible collaborative programs from the past and hopefully for the future on Parkinson’s Disease. 

This is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.     
https://gscrochetdesigns.blogspot.com. one can see my crochet creations  
https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes    
https://kneereplacement-stickclub.blogspot.com. for info on knee replacement 

Hina by: Hina Zahid Exercise decreases inflammation and prevents cartilage damage in osteoarthritis

The researchers have shown for the first time how mechanical forces experienced by cells in joints during exercise prevent cartilage degradation by suppressing the action of inflammatory molecules which cause osteoarthritis.

The study has demonstrated the benefits of exercise on the tissues that form our joints and how this is down to tiny hair-like structures, called primary cilia, found on living cells. 

Osteoarthritis (OA) is a degenerative joint disease and a leading cause of adult disability. The etiology of OA is not clear, but common risk factors for developing OA include age, joint injury, mechanical and obesity.

Exercise is the most common non-pharmacologic therapy prescribed to patients with osteoarthritis. It can help improve health and fitness without hurting the joints.

During exercise the cartilage in joints such as the hip and knee is squashed. This mechanical distortion is detected by the living cells in the cartilage which then block the action of inflammatory molecules associated with conditions such as arthritis.

The researchers show that this anti-inflammatory effect of physical activity is caused by the activation of a particular protein, called HDAC6, which triggers changes in the proteins that form primary cilia.

Pharmaceutical drugs that blocked HDAC6 activation prevented the anti-inflammatory effects of physical activity, whilst other drug treatments were able to mimic the benefits of exercise.

Changes in length of the primary cilia, which are only a few 1000th of  millimetre, provided a biomarker of the level of inflammation. Cilia got longer during inflammation, but treatments that prevented this elongation successfully prevented inflammation.

One of the researcher said, " We have known for some time that healthy exercises is good for you-- now we know the process through which exercises prevents cartilage degradation."

Prof. and a lead researcher of the study added, " These findings may also explain the anti-inflammatory effects of normal blood flow in arteries which is important for preventing arterial disease such as atherosclerosis and aneurysm".

The researchers hope that these findings will help in the search for treatments for arthritis which affects over 3 million people in the U.K causing stiff and painful joints.

The researchers suggest the results may lead to a whole new therapeutic approach known as mechano-medicine in which drugs simulate the effect of mechanical forces to prevent the damaging effects of inflammation and treat conditions such as arthritis.

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.                                    PS- THOSE INTERESTED IN RECIPES ARE FREE TO  VIEW MY BLOG-                                                                                           https://gseasyrecipes.blogspot.com/                                                                                                                                                         FOR INFO ABOUT KNEE REPLACEMENT, YOU CAN VIEW MY BLOG-                                                  https:// kneereplacement-stickclub.blogspot.com/           

                   FOR CROCHET DESIGNS                                                                                                                                                                                                  https://gscrochetdesigns.blogspot.com

Read more at Speciality Medical Dialogues: Exercise decreases inflammation and prevents cartilage damage in osteoarthritis https://speciality.medicaldialogues.in/exercise-decreases-inflammation-and-prevents-cartilage-damage-in-osteoarthritis/

Read more at Speciality Medical Dialogues: Exercise decreases inflammation and prevents cartilage damage in osteoarthritis https://speciality.medicaldialogues.in/exercise-decreases-inflammation-and-prevents-cartilage-damage-in-osteoarthritis/

Pomegranates May Help Fight Ageing

Researchers have found that a molecule in pomegranates, transformed by microbes in the gut, may enable muscle cells to protect themselves against one of the major causes of ageing.

As we age, our cells increasingly struggle to recycle their powerhouses.

Called mitochondria, these inner compartments are no longer able to carry out their vital function, and thus accumulate in the cell, researchers said.

This degradation affects the health of many tissues, including muscles, which gradually weaken over the years.

A buildup of dysfunctional mitochondria is also suspected of playing a role in other diseases of ageing, such as Parkinson's disease, they said.

Scientists from Ecole Polytechnique Federale de Lausanne (EPFL) and Amazentis company in Switzerland identified a molecule that, all by itself, managed to re-establish the cell's ability to recycle the components of the defective mitochondria: urolithin A.

"It is the only known molecule that can relaunch the mitochondrial clean-up process, otherwise known as mitophagy. It is a completely natural substance, and its effect is powerful and measurable," said Patrick Aebischer from EPFL.

Researchers started out by testing their hypothesis on the usual suspect: the nematode C elegans.

It is a favourite test subject among ageing experts, because after just 8-10 days it is already considered elderly, they said.

The lifespan of worms exposed to urolithin A increased by more than 45 per cent compared with the control group, they said.

The results led researchers to test the molecule on animals that have more in common with humans.

In the rodent studies, like with C elegans, a significant reduction in the number of mitochondria was observed, indicating that a robust cellular recycling process was taking place.

Older mice, around two years of age, showed 42 per cent better endurance while running than equally old mice in the control group.

The fruit does not itself contain the 'miracle molecule', but rather its precursor.

That molecule is converted into urolithin A by the microbes that inhabit the intestine, researchers said.

Because of this, the amount of urolithin A produced can vary widely, depending on the species of animal and the flora present in the gut microbiome.

Some individuals do not produce any at all, they said.

Researchers are currently conducting first clinical trials to test the molecule in humans.

The findings were published in the journal Nature Medicine.

 this is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.
https://gscrochetdesigns.blogspot.com. one can see my crochet creations
https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes

https://kneereplacement-stickclub.blogspot.com. for info on knee replacement

Common mental health drug may treat arthritis

By testing the effects of lithium chloride on cartilages or connecting tissues, a team of scientists has found that it slowed the degradation associated with osteoarthritis. Osteoarthritis results in degradation of cartilages in joints leading to pain and immobility.

The study used bovine cartilage samples exposed to inflammatory molecules to follow the effects of arthritis and then treated the tissue with lithium chloride. "Osteoarthritis has a devastating impact on the lives of many people in the UK and it is vital that we look for novel ways to prevent it," said co-author Martin Knight, a professor from Queen Mary University of London (QMUL).

This commonly-used drug could be used to prevent the degradation and loss of mechanical integrity of cartilages in patients with arthritis. The researchers also found that long-term dietary use of lithium did not cause arthritis. "While we're still at an early stage in researching lithium's effects on cartilage and its suitability as a treatment, the possibility that an already widely available pharmaceutical could slow its progress is a significant step forward," Knight said.

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.






PS- THOSE INTERESTED IN RECIPES ARE FREE TO VIEW MY BLOG-
HTTP:GSEASYRECIPES.BLOGSPOT.COM      

FOR INFO ABOUT KNEE REPLACEMENT, YOU CAN VIEW MY BLOG

HTTP://KNEE REPLACEMENT-STICK CLUB.BLOGSPOT.COM/

FOR CROCHET DESIGNS- http://My Crochet Creations.blogspot.com/

Now, `oil for the joints` to help soothe joint pain

A new joint lubricant could bring longer lasting relief to millions of osteoarthritis sufferers, say researchers who developed it.

The new synthetic polymer supplements synovial fluid, the natural lubricant in joints, and works better than comparable treatments currently available.

According to the team, the best fluid supplement now available offers temporary symptom relief but provides inadequate lubrication to prevent further degradation of the cartilage surfaces that cushion the joint.

To achieve both objectives, an orthopedic surgeon  and a team of  chemistry and engineering students, fellows and clinicians have advanced the first synthetic synovial fluid.

The most common form of joint disease and a leading cause of disability in the elderly, osteoarthritis (OA) affects about 200 million people worldwide.

Characterized by pain and swelling, the disease emerges in hand, hip, knee and other commonly used joints where degradation of cartilage and synovial fluid results in bone-on-bone abrasion. Treatments range from anti-inflammatory drugs to total joint replacement.

While there`s no cure for OA, one treatment-injection of a polymer to supplement synovial fluid in the joint-promises to relieve symptoms and slow the disease`s progression by reducing wear on cartilage surfaces.

From our studies, we know our biopolymer is a superior lubricant in the joint, much better than the leading synovial fluid supplement, and similar to healthy synovial fluid.

When we used this new polymer, the friction between the two cartilage surfaces was lower, resulting in less wear and surface-to-surface interaction. It`s like oil for the joints.

Originally produced last year for another study, the new polymer mimics some of the properties of natural polysaccharides, large compounds that link repetitive sequences of sugar molecules in a chainlike pattern.


Another advantage of the biopolymer is its large molecular weight or size, which prevents it from seeping out of the joint, enabling longer lasting cartilage protection. Unlike the leading synovial fluid supplement, which lasts one or two days, the new polymer remains in the joint for more than two weeks.

Seven genetic risk factors found to be associated with common eye disorder

An international group of researchers has discovered seven new regions of the human genome — called loci — that are associated with increased risk of age-related macular degeneration (AMD), a leading cause of blindness. The AMD Gene Consortium, a network of international investigators representing 18 research groups, also confirmed 12 loci identified in previous studies. 

Combining data from multiple studies, this international effort provides insight into the molecular basis of AMD, which will help researchers search for causes of the disease and will inform future development of new diagnostic and treatment strategies.

AMD affects the macula, a region of the retina responsible for central vision. The retina is the layer of light-sensitive tissue in the back of the eye that houses rod and cone photoreceptor cells. Compared with the rest of the retina, the macula is especially dense with cone 

photo-receptors and is what humans rely on for tasks that require sharp vision, such as reading, driving, and recognizing faces. As AMD progresses, such tasks become more difficult and eventually impossible. Some kinds of AMD are treatable if detected early, but no cure exists. An estimated 2 million Americans have AMD.

Scientists have shown that age, diet, and smoking influence a person’s risk of developing AMD. Genetics also plays a strong role. AMD often runs in families and is more common among certain ethnicities, such as people of Asian or European descent.

Since the discovery that certain variations in the gene for complement factor H — a component of the immune system — are associated with major risk for AMD, research groups around the world have conducted genome-wide association studies to identify other loci that affect AMD risk. 

The AMD Gene Consortium combined data from 18 research groups to increase the power of prior analyses. The current analysis identified seven new loci near genes. As with the previously discovered 12 loci, these seven loci are scattered throughout the genome on many different chromosomes.

A large number of samples was needed to detect additional genetic variants that have small but significant influences on a person’s disease risk.  By cataloguing genetic variations associated with AMD, scientists are better equipped to target corresponding biological pathways and study how they might interact and change with age or other factors, such as smoking.

The 19 loci that were found to be associated with AMD implicate a variety of biological functions, including regulation of the immune system, maintenance of cellular structure, growth and permeability of blood vessels, lipid metabolism, and atherosclerosis.

As with other common diseases, such as type 2 diabetes, an individual person’s risk for getting AMD is likely determined not by one but many genes. Further comprehensive DNA analysis of the areas around the 19 loci identified by the AMD Gene Consortium could turn up undiscovered rare genetic variants with a disproportionately large effect on AMD risk. Discovery of such genes could greatly advance scientists’ understanding of AMD pathogenesis and their quest for more effective treatments.