Brain Rewiring in Parkinson’s Disease May Contribute to Abnormal Movement

NEUROSCIENCE NEWS  SEPTEMBER 16, 2017

Summary: Abnormal activity involving the globus pallidus may be responsible for movement dysfunction in Parkinson’s disease, a new study reports.

Source: Northwestern University.

The prevailing consensus was that excessive patterning of the subthalamic nucleus (STN), a component of the basal ganglia, by the cerebral cortex was linked to the symptomatic expression of Parkinson’s disease, including muscle rigidity and slowness of movement. NeuroscienceNews.com image is in the public domain.

The brain’s own mechanisms for dealing with the loss of dopamine neurons in Parkinson’s disease may be a source of the disorder’s abnormal movement, according to a Northwestern Medicine study published in Neuron.

The study suggests the loss of dopamine may cause the brain to rewire in a maladaptive manner, contributing to impaired movement in Parkinson’s disease. These findings also suggest that there are fundamental problems with scientists’ traditional model of Parkinson’s disease, said senior author Mark Bevan, PhD, professor of Physiology at Northwestern University Feinberg School of Medicine.

The prevailing consensus was that excessive patterning of the subthalamic nucleus (STN), a component of the basal ganglia, by the cerebral cortex was linked to the symptomatic expression of Parkinson’s disease, including muscle rigidity and slowness of movement, according to Bevan.

“When one saw a burst of activity in the cortex that was consistently followed by an abnormal burst of activity in the STN, scientists assumed that the direct connection between the two was responsible,” Bevan said.

Thus, Bevan and his colleagues, including lead author Hong-Yuan Chu, PhD, a post-doctoral fellow in the Bevan Lab, expected to see transmission in the cortex-to-STN pathway increase as dopamine levels dropped. Instead, they found the opposite: the strength of the pathway decreased massively.

“Like most scientists who come across something unexpected, we thought we’d done something wrong,” Bevan said. “So, we used multiple, complementary approaches but everything pointed to the same conclusion.”

Further investigation suggested abnormal activity in a more indirect pathway from the cortex to the STN, involving the globus pallidus, was responsible. Abnormal activity in the indirect pathway leaves the STN vulnerable to excessive excitation, triggering compensatory plasticity that ultimately proved to be harmful, according to the study.

When the scientists prevented this maladaptive plasticity in late-stage Parkinson’s models, they found the symptoms improved, pointing to a link between compensation and motor dysfunction.

“According to the classic model, these adaptations should be homeostatic and preserve STN function,” Bevan said. “Preventing them should make the symptoms much worse — but it made them better instead.”

While the compensatory mechanisms may initially keep the brain operating normally under conditions of moderate dopamine neuron loss, as the disease progresses and more dopamine neurons die, the adaptations may become so extreme that they impair movement, according to the study.

These results suggest that there are fundamental flaws in our traditional understanding of brain dysfunction in Parkinson’s disease, Bevan said.

For Bevan, the unexpected results in this study served as a reminder that scientists must remain open-minded.

“It’s easy to be emotional and cling to your hypothesis,” Bevan said. “You have to be dispassionate, open-minded, and look at the data — if the data is not consistent with the hypothesis then you have to reject it and come up with a new one.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: This study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke grants 2R37 NS041280, P50 NS047085, 5T32 NS041234, and F31 NS090845. Confocal imaging work was performed at the Northwestern University Center for Advanced Microscopy, which was supported by National Cancer Institute Cancer Center Support grant P30 CA060553.

Source: Marla Paul – Northwestern University

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Abstract for “Loss of Hyperdirect Pathway Cortico-Subthalamic Inputs Following Degeneration of Midbrain Dopamine Neurons” by Hong-Yuan Chu, Eileen L. McIver, Ryan F. Kovaleski, Jeremy F. Atherton, and Mark D. Bevan in Neuron. Published online September 13 2017 doi:10.1016/j.neuron.2017.08.038

Abstract

Loss of Hyperdirect Pathway Cortico-Subthalamic Inputs Following Degeneration of Midbrain Dopamine Neurons

Highlights

•Cortico-STN synaptic transmission is reduced by 50%–75% in PD mice

•Increased striato-pallidal transmission triggers cortico-STN input loss

•Cortico-STN input loss in PD mice is NMDAR dependent

•Reduction of STN plasticity is therapeutic in PD mice

Summary

The motor symptoms of Parkinson’s disease (PD) are linked to abnormally correlated and coherent activity in the cortex and subthalamic nucleus (STN). However, in parkinsonian mice we found that cortico-STN transmission strength had diminished by 50%–75% through loss of axo-dendritic and axo-spinous synapses, was incapable of long-term potentiation, and less effectively patterned STN activity. Optogenetic, chemogenetic, genetic, and pharmacological interrogation suggested that downregulation of cortico-STN transmission in PD mice was triggered by increased striato-pallidal transmission, leading to disinhibition of the STN and increased activation of STN NMDA receptors. Knockdown of STN NMDA receptors, which also suppresses proliferation of GABAergic pallido-STN inputs in PD mice, reduced loss of cortico-STN transmission and patterning and improved motor function. Together, the data suggest that loss of dopamine triggers a maladaptive shift in the balance of synaptic excitation and inhibition in the STN, which contributes to parkinsonian activity and motor dysfunction.

“Loss of Hyperdirect Pathway Cortico-Subthalamic Inputs Following Degeneration of Midbrain Dopamine Neurons” by Hong-Yuan Chu, Eileen L. McIver, Ryan F. Kovaleski, Jeremy F. Atherton, and Mark D. Bevan in Neuron. Published online September 13 2017 doi:10.1016/j.neuron.2017.08.038

http://neurosciencenews.com/parkinsons-movement-brain-7503/

Spasmodic Dysphonia Diagnosis & Treatments : By Dr. De Leon by defeatparkinsons

September 13, 2017

 Dr. De Leon by defeatparkinsons

"The most precious things in speech are the pauses.." Ralph Waldo Emerson

Since September is National Dystonia Awareness Month, I thought I would talk about a symptom that affects many in our population known as spasmodic dysphonia (SD) This is a rare disorder of unknown etiology; it is a type of dystonia that affects the laryngeal muscles causing involuntary sustained muscle contraction of the vocal cords. There is a co –morbidity between SD and ET of 25% more than seen in normal population. People may have both essential tremors (ET) affecting vocal cords as well as dysphonia of laryngeal muscles. Furthermore, patients who exhibit this type of dystonia have a 7% risk of developing dystonia in another part of the body.

In order to obtain proper treatment one must first get correct diagnosis.

The person that diagnosis this condition can be an ENT physician as well as a neurologists. However, because there is a higher incidence of having other dystonia’s and /or tremors one usually also requires follow up and treatment by an MDS. It is important to note that SD, a type of focal dystonia, can be its own disease or be a symptom of another neurological disorders like generalized dystonia, ET, Parkinson’s and Maggie's syndrome.

Since this s a voice disorder it causes impediments in speech and communication which can be both embarrassing and also socially devastating as when the dysphonia is so severe there is no perceptible voice. This lack or inability for one person to communicate with another verbally can lead to depression and social isolation. Hence, it is imperative to get diagnosed properly and seek right treatment as to not experience social stigma.

Spasmodic dysphonia is a lifelong condition commonly affecting women especially between the ages of 30-50. This disorder can lead to voice breaking, being tight or strained. This type of dystonia can interfere with word elocution to complete detriment and speech impediment if no audible sounds are made.

Researchers believe it may be due to problems in the basal ganglia hence associated with other movement disorders. However, it can start after a cold, flu, injury to voice box, trauma/surgery, and even stress.

There are two common types:

Adductor spasmodic dysphonia- this is the MOST COMMON type causing sudden involuntary spasms triggering the vocal cords to stiffen and slam shut. The spasms interfere with the vocal cord vibration hence diminishing the quality of sound. Speech sounds are strained and effortful. Of note; these do not occur when singing, laughing, speaking at high pitch, or speaking with breathing in.

Abductor spasmodic dysphonia-this type causes sudden spasm causing vocal cords to open and since vibrations cannot take place when vocal cords are apart sound is difficult. Speech is very weak, breathy, whispery, and quiet. Of Note: these do not occur with laughing or singing.

So how do you treat-

Botox is the mainstay of treatment although it is not a cure and works best for adductor dysphonia. Having a team of specialist as I mentioned above as well as a speech pathologists is of great benefit. However, voice therapy per say has limited use unless the dysphonia is due to a hyperfunctional behavior. There are also a couple of surgeries that have been investigated and still being evaluated for their efficacy. These are called thyroplasty (which essentially require remodeling of the thyroid cartilage shape to relax and move the vocal cords somewhat laterally (to the side).

However, if you are experiencing spasms and pain or difficulty singing, or at high pitch need to be evaluated by ENT and make sure there are no masses or inflammation caused by reflux. Sometimes asthma can cause whispery speech because of inability to take in air. May also require visit to pulmonologist.

As with everything else make note of when symptoms occur, what triggers it, what makes it better, how long they last, relation to food intake (some people are extremely sensitive to pumpkin, and pumpkin seeds, as well as peanuts), symptom relation to dopamine intake, if have PD.

Sometimes drinking warm teas (ginger with honey and lemon) helps ease and improve symptoms particularly if inflammation caused by irritation of vocal cords or virus. [This is my favorite remedy! works great plus ginger is good for digestive system.]

Recommendations to make speech better:

• Avoid noisy environments- damages vocal cords – (also means talk only within your capabilities)- I have to remember this one because I always lose my voice in a crowded room.
• Stay hydrated- especially if doing public speaking- I have to drink twice as much water when I speak!
• Avoid irritants like alcohol, tobacco, substances that dry the throat.
• Avoid screaming
• Avoid clearing throat forcibly
• Sleep well.
• Treat TMJ

For more information: https://www.dysphonia.org – National Spasmodic Dysphonia Association

Sources:  http://www.hopkinsmedicine.org/healthlibrary/conditions/otolaryngology/spasmodic_dysphonia_85,P00468

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146022/

http://emedicine.medscape.com/article/864079-treatment

A Big thank you to Dr. De Leon!

Copied without permission:

https://defeatparkinsons.com/2017/09/13/spasmodic-dysphonia-diagnosis-treatments-by-dr-de-leon/

Posture and Safety

https://youtu.be/6nZU-acHQQ4

https://youtu.be/omHFY2jMGpU

https://youtu.be/x6unDVh4U4Y

My thanks to Sherry Klingelhofer for giving us these wonderful video's!

,         

Unveiling the Mystery of Why We Age

NEUROSCIENCE NEWS   SEPTEMBER 16, 2017

Summary: Researchers have identified genes that contribute to autophagy. The findings shed light on the origins of the aging process and provide evidence that aging arises as a quirk of evolution.

Source: Johannes Gutenberg University Mainz.

Getting old, it’s something that happens to everyone and nearly every species on this planet, but the question is, should it? NeuroscienceNews.com image is in the public domain.

Breakthrough in understanding the origin of the ageing process.

Researchers at the Institute of Molecular Biology (IMB) in Mainz have made a breakthrough in understanding the origin of the ageing process. They have identified that genes belonging to a process called autophagy – one of the cells most critical survival processes – promote health and fitness in young worms but drive the process of ageing later in life. This research published in the journal Genes & Development gives some of the first clear evidence for how the ageing process arises as a quirk of evolution. These findings may also have broader implications for the treatment of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s disease where autophagy is implicated. The researchers show that by promoting longevity through shutting down autophagy in old worms there is a strong improvement in neuronal and subsequent whole body health.

Getting old, it’s something that happens to everyone and nearly every species on this planet, but the question is, should it? In a recent publication in the journal Genes & Development titled “Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans,” the laboratory of Dr. Holger Richly at IMB, has found some of the first genetic evidence that may put this question to rest.

As Charles Darwin explained, natural selection results in the fittest individuals for a given environment surviving to breed and pass on their genes to the next generation. The more fruitful a trait is at promoting reproductive success, the stronger the selection for that trait will be. In theory, this should give rise to individuals with traits which prevent ageing as their genes could be passed on nearly continuously. Thus, despite the obvious facts to the contrary, from the point of evolution ageing should never have happened. This evolutionary contradiction has been debated and theorised on since the 1800s. It was only in 1953 with his hypothesis of antagonistic pleiotropy (AP) that George C. Williams gave us a rational explanation for how ageing can arise in a population through evolution. 

Williams proposed that natural selection enriches genes promoting reproductive success but consequently ignores their negative effects on longevity. Importantly, this is only true when those negative effects occur after the onset of reproduction. Essentially, if a gene mutation results in more offspring but shortens life that’s fine. This is because there can be more descendants carrying on the parent’s genes in a shorter time to compensate. Accordingly, over time, these pro-fitness, pro-ageing mutations are actively selected for and the ageing process becomes hard-wired into our DNA. While this theory has been proven mathematically and its implications demonstrated in the real world, actual evidence for genes behaving in such as fashion has been lacking.

This evidence has now arrived according to the co-lead author of the paper Jonathan Byrne, “The evolutionary theory of ageing just explains everything so nicely but it lacked real evidence that it was happening in nature. Evolution becomes blind to the effects of mutations that promote ageing as long as those effects only kick in after reproduction has started. Really, ageing is an evolutionary oversight.” Jonathan continues “These AP genes haven’t been found before because it’s incredibly difficult to work with already old animals, we were the first to figure out how to do this on a large scale.” He explains further “From a relatively small screen, we found a surprisingly large number of genes [30] that seem to operate in an antagonistic fashion.” Previous studies had found genes that encourage ageing while still being essential for development, but these 30 genes represent some of the first found promoting ageing specifically only in old worms. “Considering we tested only 0.05% of all the genes in a worm this suggests there could be many more of these genes out there to find,” says Byrne.

The evidence for ageing driven by evolution was not the only surprise the paper had in store, according to Thomas Wilhelm, the other co-lead author on the paper. “What was most surprising was what processes those genes were involved in.” Not content to provide just the missing evidence for a 60-year-old puzzle, Wilhelm and his colleagues went on to describe what a subset of these genes do in C. elegans and how they might be driving the ageing process. “This is where the results really get fascinating,” says Dr. Holger Richly, the principal investigator of the study. “We found a series of genes involved in regulating autophagy, which accelerate the ageing process.” These results are surprising indeed, the process of autophagy is a critical recycling process in the cell, and is usually required to live a normal full lifetime. 

Autophagy is known to become slower with age and the authors of this paper show that it appears to completely deteriorate in older worms. They demonstrate that shutting down key genes in the initiation of the process allows the worms to live longer compared with leaving it running crippled. “This could force us to rethink our ideas about one of the most fundamental processes that exist in a cell,” Richly explains. “Autophagy is nearly always thought of as beneficial even if it’s barely working. We instead show that there are severe negative consequences when it breaks down and then you are better off bypassing it all together. It’s classic AP. In young worms, autophagy is working properly and is essential to reach maturity but after reproduction, it starts to malfunction causing the worms to age,” he continues.

In a final revelation, Richly and his team were able to track the source of the pro longevity signals to a specific tissue, namely the neurons. By inactivating autophagy in the neurons of old worms they were not only able to prolong the worms life but they increased the total health of the worms dramatically. “Imagine reaching the halfway point in your life and getting a drug that leaves you as fit and mobile as someone half your age who you then live longer than, that’s what it’s like for the worms,” says Thomas Wilhelm. “We turn autophagy off only in one tissue and the whole animal gets a boost. The neurons are much healthier in the treated worms and we think this is what keeps the muscles and the rest of the body in good shape. 

The net result is a 50% extension of life.”

While the authors do not yet know the exact mechanism causing the neurons to stay healthier for longer, this finding could have real world implications. “There are many neuronal diseases associated with dysfunctional autophagy such as Alzheimer’s, Parkinson’s, and Huntington’s disease, it is possible that these autophagy genes could represent a good way to help preserve neuronal integrity in these cases,” elaborates Thomas Wilhelm. While any such a treatment would be a long way off, assuming such findings could be recapitulated in humans, it does offer a tantalising hope; prevent disease and get younger and healthier while doing it.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Ralf Dahm – Johannes Gutenberg University Mainz

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Abstract for “Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans” by Thomas Wilhelm, Jonathan Byrne, Rebeca Medina, Ena Kolundžić, Johannes Geisinger, Martina Hajduskova, Baris Tursun, and Holger Richly in Genes and Development. Published online September 7 2017 doi:10.1101/gad.301648.117

Abstract

Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans

Autophagy is a ubiquitous catabolic process that causes cellular bulk degradation of cytoplasmic components and is generally associated with positive effects on health and longevity. Inactivation of autophagy has been linked with detrimental effects on cells and organisms. The antagonistic pleiotropy theory postulates that some fitness-promoting genes during youth are harmful during aging. On this basis, we examined genes mediating post-reproductive longevity using an RNAi screen. From this screen, we identified 30 novel regulators of post-reproductive longevity, including pha-4. Through downstream analysis of pha-4, we identified that the inactivation of genes governing the early stages of autophagy up until the stage of vesicle nucleation, such as bec-1, strongly extend both life span and health span. Furthermore, our data demonstrate that the improvements in health and longevity are mediated through the neurons, resulting in reduced neurodegeneration and sarcopenia. We propose that autophagy switches from advantageous to harmful in the context of an age-associated dysfunction.

“Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans” by Thomas Wilhelm, Jonathan Byrne, Rebeca Medina, Ena Kolundžić, Johannes Geisinger, Martina Hajduskova, Baris Tursun, and Holger Richly in Genes and Development. Published online September 7 2017 doi:10.1101/gad.301648.117

http://neurosciencenews.com/aging-process-evolution-7501/

Big Data Algorithm Diagnoses Majority of Parkinson’s Cases

Fri, 09/15/201

by  Seth Augenstein

Parkinson’s Disease shows a predictable degenerative process of tremors, falls and trouble sleeping. But that’s all in hindsight. By the time it is actually diagnosed, it’s already progressed to a point where it can’t be slowed or mitigated.

Big data algorithms scanning population-level health data may hold a clue in diagnosing the disease early, predicting what profile of patient is likely to develop the disease, according to a new study in the journal Neurology.

“Using only demographic data and selected diagnosis and procedure codes readily available in administrative claims data, it is possible to identify individuals with a high probability of eventually being diagnosed with (Parkinson’s),” write the scientists from Washington University of St. Louis, University of Pennsylvania and University of the Witwatersand in South Africa.

About 200,000 patients who were on Medicare in 2009 were incorporated in the data set. The 89,790 who were diagnosed with Parkinson’s were mixed in with more than 118,000 control patients who did not have the disease.

By further incorporating the health records of the patients from 2004 through 2009, the scientists developed an “elastic net algorithm” that scored key hallmarks in the medical histories.

The Parkinson’s factors included the trademark tremors, but also weight loss, various chronic kidney diseases, posture abnormalities, psychiatric and cognitive problems, gastrointestinal aberrations, sleep disturbances, fatigue, and injuries (especially from falls).

The factors that appeared to weigh against a Parkinson’s diagnosis included obesity conditions like gout, smoking, cancer, cardiovascular disease, allergies, and injuries that were related to wear-and-tear of activity (like hip replacements).

Overall, the algorithm successfully predicted a majority of Parkinson’s cases.

About 73 percent of the diagnosed in 2009 were picked out by the computer model. At the same time, the machine selected 83 percent of the people who would not be diagnosed.

Brad Racette, the senior author from Washington University, said the algorithm could be used to identify Parkinson’s patients and their unique medical records trail long before the disease has gotten too far.

“Using this algorithm, electronic medical records could be scanned and physicians could be alerted to the potential that they patients may need to be evaluated for Parkinson’s disease,” he said, in a school statement. 

https://www.laboratoryequipment.com/news/2017/09/big-data-algorithm-diagnoses-majority-parkinsons-cases

Drugs in disguise heal the brain

September 12, 2017

Credit: Aalborg University

The treatment of brain diseases is on the verge of a breakthrough. Researchers from Aalborg University are developing a new method that 'smuggles' medicine past the brain's defense systems, giving hope that diseases such as Alzheimer's can one day be cured.

Today, diseases such as Alzheimer's, Huntington's, epilepsy and Parkinson's are not curable; we can only treat the symptoms. This is due to the fact that brain cells – unlike all the body's other organs – are enclosed in an advanced defense system that keeps medicine out.

By using a new method to 'sneak' biological medicine into brain cells, AAU researchers hope that within a few years they will be able to cure a wide range of neurological diseases that we cannot treat today because medicine cannot penetrate the blood-brain barrier.

There is still some way to go before the method can be used in humans, but there are already positive results, and when it succeeds it will be a major breakthrough for medical science.

Ferry to the brain

In order to be able to penetrate the blood-brain barrier and enter the brain cells, brain researcher Torben Moos, along with a team of researchers at AAU, has developed a method he calls the 'ferry to brain'.

Simply put, the method involves making a transport system that can carry drugs through the barrier by packaging them into things that normally slip through. If the drug is stored under a shell that resembles an amino acid or protein, it is closed in. When the shell passes through the barrier, the drug will be released so that it can work directly on the brain cells.

"We're attempting to develop systems that make the brain unable to tell the difference between what we send in and what it otherwise would have gotten," says brain researcher Torben Moos, Professor in the Department of Health Science and Technology at Aalborg University.

"The goal is to make a kind of universal transport system that can always penetrate the barrier and that can be used to send different types of drugs into the brain."

The brain has its own defenses

"In order to maintain the special environment around the brain cells, there is an additional barrier between the brain and the rest of the body. This protects the brain and lets only those things penetrate that it needs," explains brain researcher Torben Moos, Professor in the Department of Health Science and Technology at Aalborg University.

"You can compare it to sitting in closed room while things float by outside. If something passes by that the brain would like to have, it can open the door and stick out a hand to grab it, but otherwise it doesn't open the door. That is how the brain communicates with its surroundings in the bloodstream," says Torben Moos.

The blood-brain barrier is vital for the brain to function properly, but if we are to treat diseased areas of the brain with medicine, it is a serious obstacle that many types of drugs cannot get past.

Results give hope

Drug treatment can broadly be divided into two different groups: Synthetic molecules that you ingest in pill form – or biological drugs which can be proteins or nucleic acids that affect the genetic development of the body's cells.

A biological drug could get a cell to stop producing a disease-causing protein or shut down a cell that produces mutated proteins that can, for example, cause hereditary diseases.

Until now we have not been able to use biological drugs to treat neurological diseases – because they cannot get past the blood-brain barrier. But the method from AAU is showing positive results and creates hope for the future.

"We have become very adept at getting through the barrier and entering the brain's blood vessels, but we still need to refine the way medicine progresses further into the brain cells. You could say that we are halfway to the goal," says Professor Torben Moos.

Provided by: Aalborg University

https://medicalxpress.com/news/2017-09-drugs-disguise-brain.html

Cat faeces may cause cancer, Parkinson's disease, says study

THE ASIAN AGE    Sept.16, 2017

A new study now suggests that a parasite commonly found in cat faeces may cause Alzheimer’s, Parkinson’s and even cancer.

The parasite, toxoplasma gondii, which is carried by around 30 percent of cats at any one time and shed in their stools, may alter over 1,000 genes associated with cancer.

Once the human is infected, proteins from the parasite can alter communication between brain cells, which may increase a person’s risk of developing Alzheimer’s, Parkinson’s and epilepsy.

Pregnant women have always been advised to avoid cat faeces as the parasite is known to cause miscarriages, still births and often damage the foetus’ development, but new research shows that its effects are more widespread.

Speaking about the discovery, study author Dr Dennis Steindler from Tufts University in Massachusetts said that the study is a paradigm shifter.

The study found that the parasite is also liked to increased risk of Alzheimer's, Parkinson's and epilepsy.

The parasite is thought to increase the risk of these conditions by releasing proteins that alter communication between brain cells.

The findings were published in the journal Nature. 

http://www.asianage.com/life/health/160917/cat-faeces-may-cause-cancer-parkinsons-disease-says-study.html

Painting for Parkinson’s - 77 paintings of 77 counties in 77 days

Sept. 15, 2017  By Melinda Stotts

Norman artist Tim Kenney was in Miami last week working on the sixth of 77 paintings he has planned with a portion of proceeds from each going to the Nicole Jarvis Parkinson’s Research Foundation.

MIAMI – His personality is as big, bold and bright as his paintings, and Norman artist Tim Kenney’s heart is wonderfully big too.

Kenney was in Miami last week painting the sixth of 77 paintings he is creating in 77 days of scenes from each of the 77 counties in Oklahoma.

He is donating a portion of the proceeds from the sales of each painting to the Nicole Jarvis Parkinson’s Research Foundation, an Oklahoma organization dedicated toward efforts to find a cure for the chronic illness.

Jarvis, a 44-year-old, OB/GYN Physician, and mother of twins, was diagnosed with Young Onset Parkinson’s Disease, and she’s a friend of Kenney’s.

Kenney is an abstract impressionist and colorist who paints with bold colors and strokes to create paintings with feeling and excitement. His work sells for hundreds to thousands of dollars and is growing in popularity with collectors across the country.

He started the 77 county endeavor on Sept. 4 in Jefferson County, and he has braved Oklahoma weather, hail, heat, sun and rain as he makes his way to each county to paint. His 77th and final painting in the series will be painted in Norman on Nov. 19.

“They’re all 16 by 20 inches, they’re $680 each, and 20 percent will go to fund Parkinson’s research,” Kenney said. “Nicole was diagnosed six years ago, and we’re great friends. I give my paintings to a lot of good charities in Norman; the American Heart Association, Chamber of Commerce, the United Way and those type of things.”

A retired contractor in sales and marketing, Kenney took up painting while caring for his ailing mother, and he hasn’t stopped since. Kenney is a prolific artist and paints every day creating and capturing fantastic images.

“I’m a full-time artist now. I started eight years ago,” he said. “I started painting at 52 years-old, and I’m 61 now. It’s been crazy. I had never done a painting before that age.”

He paints with oil on stretched canvas with palette knives and brushes painting in plain air, outdoors on location.

“These are oil paintings, and I use a very thick paint and pallet knife, so it takes about a month to six weeks to dry,” Kenney said. “It takes about four hours to paint each one probably. I will start them on location and finish them in the evening.”

In Ottawa County, he set up at the gateway arch on Main Street in Miami and drew onlookers who watched him paint.

“This one has already been pre-sold, but I ’m not going to say who bought it. He’s a great guy, but I don’t know if he wants me to name him,” he said.

The artist has painted in Jefferson County, Stephens County, Washita County, Greer County, Mayes County, Ottawa County, Craig County and Osage County so far, and was heading to the next county after a side trip.

Kenney has already pre-sold 34 of the 77 county paintings to collectors and locals interested in obtaining their county’s piece.

The subject or view depicted in each of the paintings is sometimes requested by the buyer, and other pieces are depictions of places he is directed to by locals.

“The day before yesterday I was in Santa Fe to drop off paintings for a show, and so I painted on the way in and out of state. When I came back in the state I stopped at Greer County,” Kenney said. “I pulled into Mangum in Greer, and I asked them, ‘Where should I paint?’ and they all told me this spot called Jay Buckle Springs. Everybody knew about it, and I mean everybody. Of course, I never heard of it, and I drove towards it and ran into another small town, Willow. A lady drove me up there. It’s a natural spring where they all swim.”

He posted a photo of the completed Greer painting on his Facebook page, and almost immediately one of Kenney’s Norman friends bought it because he lived near the spring growing up as a child.

In Mayes County Kenney was inspired by natural beauty.

“We stopped real early at sun up, and there was a beautiful sunrise coming, so I stopped right there and painted,” he said. “It was great.”

In another county, he painted a lake by request where the art buyer had fished in his youth with his grandparents.

“He was really emotional about it. It was pretty cool,” Kenney said.

Kenney took a short break after painting in Miami to travel to Ohio and cheer on Oklahoma University’s Sooners against Ohio State in their last football game with his friends Dale Baker, and David Thompson.

The artist has an overall plan for the 77 county journey but has been flexible with his course as he travels around the state.

“It changes daily,” Kenney said of his route. “I just had a grandson Friday, and I had to make sure Duke was okay. He’s my fifth grandson.”

Once all 77 Oklahoma county paintings are completed Kenney intends to show the collection in Norman. He may also offer prints of the Oklahoma paintings due to the large interest shown in the pieces.

“The bad ones too, there’s always one person who likes the bad ones. My wife likes them all,” Kenney said with a laugh. “At least that’s what she tells me, who knows what she really thinks.”

Kenney posts daily on Facebook throughout the journey and posts photos of the pieces once they are completed.

This isn’t the first time Kenney has set off on such an artistic journey. In May of 2014, he made a 50-day tour with the goal of painting 50 paintings in 50 states in 50 days donating a portion of the proceeds to Parkinson’s research. He accomplished that goal, painting the final art piece on the 50th day in Santa Fe, New Mexico of his grandmother’s house, which is now the Georgia O’Keeffe Museum Research Center.

“I flew to Hawaii and Alaska, and I drove 12,800 miles. It was a great, great trip and I had a ball,” Kenney said.

Kenney’s artwork can now be found in galleries in Santa Fe, New Mexico, Breckenridge and Vail, Colorado, Gulf Shores, Alabama, Oklahoma City and Norman with up and coming shows scheduled as well.

Asked what his next painting project would be, Kenney said, “I did the 50 states, and now Oklahoma. This is pretty big, and this is a real challenge, so we’ll see.”

To follow Kenney’s journey and see his artwork visit his Facebook page at ‘Tim Kenney Art’ or his website www.timkenneyfineart.com.

http://www.miamiok.com/news/20170915/painting-for-parkinsons---77-paintings-of-77-counties-in-77-days