I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.
I COPY NEWS ARTICLES PERTAINING TO RESEARCH, NEWS AND INFORMATION FOR PARKINSON'S DISEASE, DEMENTIA, THE BRAIN, DEPRESSION AND PARKINSON'S WITH DYSTONIA. I ALSO POST ABOUT FUNDRAISING FOR PARKINSON'S DISEASE AND EVENTS. I TRY TO BE UP-TO-DATE AS POSSIBLE.
I AM NOT RESPONSIBLE FOR IT'S CONTENTS. I AM JUST A COPIER OF INFORMATION SEARCHED ON THE COMPUTER. PLEASE UNDERSTAND THE COPIES ARE JUST THAT, COPIES AND AT TIMES, I AM UNABLE TO ENLARGE THE WORDING OR KEEP IT UNIFORMED AS I WISH.IT IS IMPORTANT TO UNDERSTAND I AM A PERSON WITH PARKINSON'S DISEASE. I HAVE NO MEDICAL EDUCATION,
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THIS IS FOR YOU TO READ AND TO ALWAYS KEEP AN OPEN MIND.
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THANK YOU FOR VISITING! TOGETHER WE CAN MAKE A DIFFERENCE!
WHERE:The Plantation Golf and Country Club 10500 Dartington Drive
Ft. Myers, Florida33913
United States
Team Fox Swing for the Cure is pleased to announce our Fifth Annual Charity Golf Tournament—Swing for the Cure—supporting Parkinson’s Research. Our event will be held at The Plantation Golf and Country Club (10500 Dartington Drive, Fort Myers, FL 33913), on January 26, 2017, registration starting at 7:30 am.
The Team’s mission is to continue to bring Parkinson’s awareness to Southwest Florida and to help find a cure by donating the much needed private funding. As such, all net proceeds will be donated to Team Fox – the grassroots fundraising program at The Michael J. Fox Foundation for Parkinson’s research (MJFF). To date we have donated over $92,000 to the MJFF, and our goal this year is to raise $30,000.
Finding a cure drives our mission. Your help is needed! Please commit to sponsoring this event. You can also help by making a financial donation directly to http://www2.michaeljfox.org/goto/swingforthecure.
All net proceeds are donated to The Michael J. Fox Foundation; and in 2017; 100% all donations made by Team Fox members will go directly to research. Checks and credit cards will receive a 501 (c) 3 receipt directly from the MJFF.
No one is immune to PD! One person in every 500 suffers from Parkinson’s, with patients being diagnosed at the early age of 13. In Southwest Florida alone there are over 10,000 people diagnosed with PD. Parkinson’s is a chronic degenerative neurological disorder with no known cure. Patients have different symptoms; however, sadly in the end, they all reach the same point of total incapacitation, until death.
The MJFF is on the fast track to finding a cure and is making strides to improve the therapies for people not only living with PD but other neurological disorders.
Parkinson’s disease is a disorder in which the nervous system gradually deteriorates. Movement is reduced. The disease most commonly starts with a small tremor in a person’s hand. Early symptoms also include slow movements, stiffness, lack of facial expression and slurred speech.
While there is no cure for Parkinson’s disease, there are medications to treat symptoms.
Symptoms of Parkinson’s Disease
The symptoms for Parkinson’s disease are different for each person. They usually include:
Tremors or shaking. This usually starts in the hands or fingers, especially the thumb and forefinger, even at rest.
Slowed movements (bradykinesia). As Parkinson’s progresses, the ability to move decreases and movements become slower. Walking and getting out of your seat becomes difficult.
Muscle stiffness. You may find that you have decreased range of motion, and pain caused by stiff muscles.
Poor posture and balance. You may have a stooped posture and/or problems balancing.
Reduction in automatic movements. You may find that you are unable to perform some unconscious actions like smiling and blinking.
Changes in speech. You may have problems with your speech, and/or find that your speech is soft, quick, or slurred. You may also start speaking with a monotone.
Changes with writing. You may no longer be able to write well, or you may only be able to write in small letters.
See a doctor right away if you notice that you have any of the above symptoms. This will help to diagnose the disease early and allow you to begin symptom-relieving treatments early.
Causes of Parkinson’s Disease
Parkinson’s disease is called by the gradual death of nerve cells in the brain called neurons. The loss of neurons results in a decrease in a chemical messenger called dopamine that is produced by certain neurons. Due to the reduction in dopamine levels, the brain has abnormal activity that causes the symptoms observed in Parkinson’s.
The specific cause of Parkinson’s disease is not known. Factors known to contribute include:
Specific genetic mutations can cause Parkinson’s disease. These are uncommon. Some gene variations may also increase the risk of Parkinson’s disease, each by a small amount.
Having been exposed to some toxins can increase the risk of Parkinson’s disease later in life, but this has a small contribution.
Lewy bodies in the brain. Clumps of protein called Lewy bodies are found in brain cells of Parkinson’s patients. They are a hallmark of the disease, although it is unclear how they may cause Parkinson’s disease.
Alpha-synuclein in Lewy bodies. Many substances make up Lewy bodies, and one of them is called alpha-synuclein. It is usually found in clumps that cannot be broken down by the brain cells, and is a focus of Parkinson’s disease research.
Risk factors of Parkinson’s Disease
Risk factors for Parkinson’s include:
The risk of Parkinson’s increases with age. Parkinson’s normally develops around ages 60 and up.
Men have a greater risk of developing Parkinson’s than women.
Family history. If a close relative has or has had Parkinson’s, your risk is increased. This increase in risk is small unless many family members have had Parkinson’s.
Toxin exposure. There is an increased risk of Parkinson’s due to exposure to pesticides and herbicides.
Complications of Parkinson’s Disease
Additional problems arise in Parkinson’s disease, including:
Difficulties with thinking. In later stages of the disease, dementia and other thinking difficulties arise.
Emotional changes. Depression, anxiety, fear, and lack of motivation can be treated with medications.
Problems with swallowing. Due to a slowed or lost ability to swallow, drooling may occur.
Sleep problems. Parkinson’s results in frequent waking at night, waking up early, and sleeping during the day. Medications are available to relieve these problems.
Urination problems. There may be difficulty urinating, or an inability to control urination.
Constipation can be caused by the reduced functioning of the digestive tract.
Low blood pressure. Low blood pressure results in light-headedness and dizziness when quickly standing.
Problems with smelling. Odors may not be easily identified or distinguished.
Pain can occur in specific locations, or throughout the body.
Lack of energy and tiredness is found to occur in Parkinson’s.
Sexual dysfunction. Sexual performance and desire is reduced.
Tests and diagnosis of Parkinson’s Disease
There are no tests available to diagnose Parkinson’s. A neurologist, who is a doctor that specializes in the nervous system, uses a combination of symptoms, medical history and physical and neurological examinations to diagnose Parkinson’s. Blood tests and imaging tests (e.g., MRI, ultrasound and PET scans) may be used to rule out other causes of your symptoms.
A medication for Parkinson’s called carbidopa-levodopa may be given to you. A Parkinson’s diagnosis is confirmed if symptoms are significantly reduced by the drug.
A diagnosis sometimes requires multiple appointments with neurologists to track symptoms over time.
Medications
Although there isn’t a cure for Parkinson’s, there are medications that can help to relieve symptoms, sometimes significantly. For later stage Parkinson’s, surgery is an option.
Medications prescribed for Parkinson’s include:
Carbidopa-levodopa. Levodopa, a chemical that can enter the brain and is converted to dopamine, is the most effective treatment for Parkinson’s. It is combined with carbidopa, a chemical that prevents the conversion of levodopa to dopamine before it enters the brain. This medication can sometimes cause light-headedness or nausea. Higher levodopa doses may cause involuntary movements (dyskinesia).
The benefits from carbidopa-levodopa reduce and become less predictable (wax and wane) as the disease progresses.
As of 2015, carbidopa-levodopa is available in a gel form called Duopa. It is delivered straight to the small intestine through a feeding tube. This form of the medication helps to lessen the fluctuations in the benefits of the drug experienced by people with advanced Parkinson’s by making the drug levels more constant in the blood. A small surgery is required to place the feeding tube. The risks associated with having a tube include that it may fall out, or the placement site may become infected.
Dopamine agonists. These drugs are not converted into dopamine, but act like dopamine in the brain. They do not treat Parkinson’s symptoms as well as levodopa, but last longer and also help to relieve the waxing and waning of levodopa effects. Examples of dopamine agonists include ropinirole (Requip), and pramipexole (Mirapex), as well as rotigotine in patch form (Neupro), and apomorphine in injectable form (Apokyn).
Dopamine agonists can also cause light-headedness and nausea, as well as sleepiness, hallucinations and compulsive behaviours (e.g., gambling, heightened sex drive, and overeating).
MAO-B inhibitors. These medications helps to stop an enzyme called monoamine oxidase B (MAO-B) in the brain from breaking down dopamine. MAO-B inhibitors include rasagiline (Azilect) and selegiline (Zelapar, Eldepryl). They may cause sleeplessness, nausea, and, when combined with carbidopa-levodopa, hallucinations.
COMT inhibitors. This type of medication stops an enzyme called catechol-O-methyltransferase from breaking down dopamine in the brain. It is used as a supplement to levodopa. The most commonly used COMT inhibitor is entacapone (Comtan). There is also tolcapone (Tasmar), but because of the high risk of liver damage and liver failure associated with it, it is not usually prescribed. Side effects of COMT inhibitors are diarrhea and dyskinesias.
These drugs block the action of a chemical messenger in the brain called acetycholine that helps control muscle movement. They improve tremors, but do not help to relieve muscle stiffness and slowness as much. They were the first drugs to be widely used for the treatment of Parkinson’s, but are now less commonly used due to their many side effects, including constipation, confusion, memory impairment, hallucinations, dry mouth, and problems urinating.
Amantadine works by increasing dopamine release and blocking dopamine reuptake in the brain. It can be used alone for short-term relief of mild Parkinson’s disease, or combined with carbidopa-levodopa in advanced Parkinson’s to help control dyskinesias. Side effects include hallucinations, swelling of the ankles, and skin mottling.
Deep brain stimulation (DBS). DBS is a surgical procedure used to treat Parkinson’s, in which electrodes are implanted into a certain part of the brain. A generator to which the electrodes are attached is implanted near the collarbone. The generator sends electrical pulses through the electrodes to the brain to improve Parkinson’s symptoms.
The risks associated with DBS include stroke, hemorrhage and infections at implantation sites. Adjustments and replacements of different parts of the system are further complications.
DBS is usually prescribed for advanced Parkinson’s in which the benefits from levodopa have become unstable, and can also help with dyskinesias, tremors, and movement stiffness and slowness. Symptoms that do not respond to levodopa will not be helped by DBS, except for tremor.
Lifestyle
Lifestyle changes can play a big part in relieving the symptoms of Parkinson’s. Some lifestyle changes include:
Food choices. Eating food with lots of fiber and staying hydrated can relieve the constipation associated with Parkinson’s.
Routine exercise improves balance, flexibility and strength, and also reduces the cognitive symptoms of Parkinson’s including anxiety and depression.
Physical therapy. A physical therapist may be needed to design and facilitate an individualized exercise program. Programs can include exercises like dancing, swimming, stretching, walking, and water aerobics. There are also exercises specifically targeted to improving your balance, flexibility and walking ability.
Speech therapy. Speech problems can be improved with a speech-language pathologist.
Occupational therapy. An occupational therapist can help make daily activities easier including writing, eating, bathing and dressing.
Alternative medicine
Alternative medicine that can help with the symptoms of Parkinson’s include:
Massage helps to relieve stiff muscles and induce overall relaxation.
Tai chi. Tai chi is an ancient Chinese exercise appropriate for any age and ability that incorporates controlled, slow, and flowing movements. Tai chi can improve balance, flexibility and strength, reducing the risk of falls for advanced Parkinson’s patients.
This treatment involves the insertion of very thin needles into certain points of the body in order to relieve pain.
Stationary poses and gentle stretches help to improve balance, flexibility and muscle strength. Yoga can be adapted to all ages and abilities.
Quiet reflection and focusing the mind on the present moment can relieve stress and reduce pain.
Music, art, and pet therapy. These therapies are used to induce relaxation, and improve mood, speech and walking ability.
Alexander technique. This technique involves thinking about the use of muscles during posturing and balancing, and helps to relieve pain and stiffness in muscles.
Coenzyme Q10. Taking high doses of this supplement may help in early Parkinson’s disease if taken for 16 months and longer.
In Parkinson's Disease there is a decreased risk of cancer, except for melanoma. This study
specifically evaluated the risk of brain tumor in Parkinson's Disease. A brain tumour is a
growth of cells that multiplies in an uncontrollable way. It can be cancerous (malignant) or
non-cancerous (benign). The symptoms can include : severe headaches, seizures, nausea,
vomiting and drowsiness, mental or behavioural changes, progressive weakness on one side
of the body, vision problems, or speech problems.
For more information go to :
http://www.nhs.uk/Conditions/brain-tumours/Pages/Introduction.aspx
This extensive study involved nearly 3000 people with Parkinson's
Disease. The risk of developing a brain tumor was found to be
significantly higher in people with Parkinson's Disease. The risk of
developing a brain tumor was more than doubled. Benign brain
tumor exhibited a slightly higher risk. The risk developing a benign
brain tumor was even higher in females. An analysis of the age
groups found that mostly only those between 50 and 64 years old
had a higher risk of developing a brain tumor.
The researchers concluded that people with Parkinson's Disease are at a higher risk of
developing a brain tumor but that the exact underlying causes require further investigation.
Summary: A new study raises the question of whether a genetic mutation associated with neurodegeneration in one environment could act in a positive way in a different setting.
Source: Arizona State University.
These researchers examined how the apolipoprotein E (ApoE) gene might function differently in an infectious environment than in the urban industrialized settings where ApoE has mostly been examined. NeuroscienceNews.com image is for illustrative purposes only.
A new study shows cognitive decline may be influenced by the interaction of genetics and … worms?.
You’ve likely heard about being in the right place at the wrong time, but what about having the right genes in the wrong environment? In other words, could a genetic mutation (or allele) that puts populations at risk for illnesses in one environmental setting manifest itself in positive ways in a different setting?
That’s the question behind a recent paper published in FASEB Journal by several researchers including lead author Ben Trumble, an assistant professor at Arizona State University’s School of Human Evolution and Social Change and ASU’s Center for Evolution and Medicine.
These researchers examined how the apolipoprotein E (ApoE) gene might function differently in an infectious environment than in the urban industrialized settings where ApoE has mostly been examined. All ApoE proteins help mediate cholesterol metabolism, and assist in the crucial activity of transporting fatty acids to the brain. But in industrialized societies, ApoE4 variant carriers also face up to a four-fold higher risk for Alzheimer’s disease and other age-related cognitive declines, as well as a higher risk for cardiovascular disease.
The goal of this study, Trumble explains, was to reexamine the potentially detrimental effects of the globally-present ApoE4 allele in environmental conditions more typical of those experienced throughout our species’ existence — in this case, a community of Amazonian forager-horticulturalists called the Tsimane.
“For 99% of human evolution, we lived as hunter gatherers in small bands and the last 5,000-10,000 years — with plant and animal domestication and sedentary urban industrial life — is completely novel,” Trumble says. “I can drive to a fast-food restaurant to ‘hunt and gather’ 20,000 calories in a few minutes or go to the hospital if I’m sick, but this was not the case throughout most of human evolution.”
Due to the tropical environment and a lack of sanitation, running water, or electricity, remote populations like the Tsimane face high exposure to parasites and pathogens, which cause their own damage to cognitive abilities when untreated.
As a result, one might expect Tsimane ApoE4 carriers who also have a high parasite burden to experience faster and more severe mental decline in the presence of both these genetic and environmental risk factors.
But when the Tsimane Health and Life History Project tested these individuals using a seven-part cognitive assessment and a medical exam, they discovered the exact opposite.
In fact, Tsimane who both carried ApoE4 and had a high parasitic burden displayed steadier or even improved cognitive function in the assessment versus non-carriers with a similar level of parasitic exposure. The researchers controlled for other potential confounders like age and schooling, but the effect still remained strong. This indicated that the allele potentially played a role in maintaining cognitive function even when exposed to environmental-based health threats.
For Tsimane ApoE4 carriers without high parasite burdens, the rates of cognitive decline were more similar to those seen in industrialized societies, where ApoE4 reduces cognitive performance.
“It seems that some of the very genetic mutations that help us succeed in more hazardous time periods and environments may actually become mismatched in our relatively safe and sterile post-industrial lifestyles,” Trumble explains.
Still, the ApoE4 variant appears to be much more than an evolutionary leftover gone bad, he adds. For example, several studies have shown potential benefits of ApoE4 in early childhood development, and ApoE4 has also been shown to eliminate some infections like giardia and hepatitis.
“Alleles with harmful effects may remain in a population if such harm occurs late in life, and more so if those same alleles have other positive effects,” adds co-author Michael Gurven, professor of anthropology at University of California, Santa Barbara. “Exploring the effects of genes associated with chronic disease, such as ApoE4, in a broader range of environments under more infectious conditions is likely to provide much-needed insight into why such ‘bad genes’ persist.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Aaron Pugh –Arizona State University Image Source: NeuroscienceNews image is in the public domain.
Original Research:Abstract for “Apolipoprotein E4 is associated with improved cognitive function in Amazonian forager-horticulturalists with a high parasite burden” by Benjamin C. Trumble, Jonathan Stieglitz, Aaron D. Blackwell, Hooman Allayee, Bret Beheim, Caleb E. Finch, Michael Gurven and Hillard Kaplan in FASEB Journal. Published online December 28 2016 doi:10.1096/fj.201601084R
Abstract
Apolipoprotein E4 is associated with improved cognitive function in Amazonian forager-horticulturalists with a high parasite burden
The apolipoprotein E4 (E4) allele is present worldwide, despite its associations with higher risk of cardiovascular morbidity, accelerated cognitive decline during aging, and Alzheimer’s disease (AD). The E4 allele is especially prevalent in some tropical regions with a high parasite burden. Equatorial populations also face a potential dual burden of high E4 prevalence combined with parasitic infections that can also reduce cognitive performance. We examined the interactions of E4, parasite burden, and cognitive performance in a traditional, nonindustrialized population of Amazonian forager-horticulturalists (N = 372) to test whether E4 protects against cognitive decline in environments with a heavy pathogen burden. Contrary to observations in industrial populations, older adult E4 carriers with high parasite burdens either maintained or showed slight improvements in cognitive performance, whereas non-E4 carriers with a high parasite burden showed reduced cognitive performance. Being an E4 carrier is the strongest risk factor to date of AD and cognitive decline in industrial populations, it is associated with greater cognitive performance in individuals facing a high parasite and pathogen load, suggesting advantages to the E4 allele under certain environmental conditions. The current mismatch between postindustrial hygienic lifestyles and active parasite-rich environs may be critical for understanding genetic risk for cognitive aging.
“Apolipoprotein E4 is associated with improved cognitive function in Amazonian forager-horticulturalists with a high parasite burden” by Benjamin C. Trumble, Jonathan Stieglitz, Aaron D. Blackwell, Hooman Allayee, Bret Beheim, Caleb E. Finch, Michael Gurven and Hillard Kaplan in FASEB Journal. Published online December 28 2016 doi:10.1096/fj.201601084R
Diseased brain tissue from an Alzheimer's patient
showing amyloid plaques (in blue) located in the gray matter of the brain. Dr Cecil H
Fox/Science Source/Getty Images
In a disappointment to
Alzheimer's patients and researchers, drugmaker Eli Lilly said in late November
that a clinical trial of solanezumab, an experimental medication to treat the
degenerative neurological condition, had failed.
The company has pressed
on with tests of solanezumab, despite mixed results in
earlier studies. The latest test, involving more than 2,000 patients, found the
drug didn't significantly slow cognitive decline in patients with mild dementia
from Alzheimer's.
The sad refrain is a
familiar one, unfortunately.
Solanezumab is just the
latest casualty in a decades-long parade of
disappointing dementia drug trials. But the frustration brought by this
particular failure could signal a shift in Alzheimer's research — a shift away
from targeting accumulations of so-called amyloid protein in the brain, long
considered by many in the field to be the crux of Alzheimer's pathology.
Ever since Dr. George G.
Glenner's 1984 discovery that
amyloid is the main component of the plaques that riddle the
Alzheimer's-afflicted brain, it has been assumed that the protein somehow
contributes to the disorder — that it jams up cellular machinery, rendering
neurons unable to effectively communicate, to form new memories, to remember
where the keys are.
Like many other failed
medications for symptomatic Alzheimer's, solanezumab works by attacking amyloid
in the brain.
So in light of the new
findings, is it finally time to let the amyloid theory go? The answer isn't
clear.
"The low magnitude
of effects would lend support to the idea that it might be time to move on from
amyloid," says Weill Cornell Medical College neurologist Dr. Richard
Isaacson, who wasn't involved in the solanezumab study. "Yet though the
study failed overall, there were improvements in cognition and function in
treated patients."
He points out that
perhaps the tested dose wasn't high enough or that the patients' disease was
too advanced to respond. By the time symptoms of Alzheimer's arise, the brain
is already speckled with amyloid. Two other ongoing trials should confirm
whether solanezumab is more effective in patients at risk for Alzheimer's, but
who have not yet developed symptoms, he says.
Solanezumab, an antibody,
works by attacking amyloid floating in cerebrospinal fluid. A different type of
investigational medication, so-called BACE inhibitors, prevent amyloid
formation in the first place, by neutralizing an enzyme that cuts away amyloid
from a larger protein. Biogen's aducanumab, another experimental drug
that's far along in clinical testing,
binds to and clears amyloid that is already ensnared in plaques.
Earlier this year the FDA
granted aducanumab fast-track status after
results from a small, early-stage study suggested that it reduces amyloid
plaques and slows cognitive decline in people with very early stage disease.
Those people did have amyloid deposits visible with positron emission
tomography imaging. At the Clinical Trials on Alzheimer's Disease and Dementia
meeting in San Diego in early December, follow-up data were presented that
confirmed cognitive improvement out to two years of treatment.
"The good news is
that there are a number of trials in progress with different anti-amyloid drugs
in asymptomatic subjects; and that one failed drug doesn't mean that another
won't have an effect," says Dr. James Burke, professor of medicine and
psychiatry at Duke University's Alzheimer's Disease Research Center.
"These trials also suggest that the best chance for a significant effect
on cognition is likely to be treating asymptomatic people with amyloid deposits
on imaging."
Yet, Burke adds, if these
trials don't show a significant clinical benefit, the focus on amyloid will
likely end.
In any event, Weill's
Isaacson feels that researchers should be looking to other options. "I've
never been a firm believer in the amyloid hypothesis being the be-all and
end-all as to the cause of Alzheimer's," says Isaacson. "I think it's
much more complicated and there are probably many roads leading to the
disease."
Fluorescent
deconvolution micrograph of cultured glial cells expressing tau protein (in
red). Glial cells are nervous system cells that provide structural support
and protection for neurons(nerve cells). Accumulation of tau in brain tissue is
linked with a number of neurodegenerative diseases, including Parkinson's
disease and Alzheimer's disease Roger J. Bick, Kha Dinh/Mya
C. Schiess / UT-Houston Medical/Science Source
One such road might be to target the tau protein,
which also accumulates in tangles inside the Alzheimer's-hindered brain.
Another involves treating the inflammation that occurs with dementia, as the
immune system attempts to clear clustered amyloid. Even simpler are dietary
interventions. Mediterranean-like diets high in omega-3 fatty acids show
particular promise in slowing cognitive decline.
Whether it's antibiotics, probiotics or vaccines, the
list of potential Alzheimer's treatments being considered goes on.
"The bottom line is we need to take more shots on
goal," says Isaacson. "The next frontier is recognizing that there
probably isn't a one-size-fits-all approach, and that using targeted therapies
based on a person's own biology and genetics will bring the most benefit. The
future of Alzheimer's therapeutics is in precision medicine."
As in so many other disorders, fully understanding
Alzheimer's disease might ultimately entail figuring out how our bodies
interact with the trillions of microbes living in our guts, or our
"microbiota." Research in animals and humans suggest that certain
combinations of these organisms may rev up the immune system in ways that
contribute to dementia. A study
published in July in Scientific Reports found that a
long course of antibiotic treatment to alter gut flora in dementia-prone mice
reduced the number and size of amyloid plaques in the brain.
Bret Stetka is a writer based in New York and an
editorial director at Medscape. His work has appeared
in Wired, Scientific American and on The Atlantic.com. He
graduated from University of Virginia School of Medicine in 2005. He's also on
Twitter: @BretStetka.
