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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 have Parkinson's
diseases as well and thought it would be nice to have a place where
updated news is in one place. That is why I began this blog.
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. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. This is a free site for all.
Thank you.


Saturday, May 20, 2017

Tau Prevents Synaptic Transmission at Early Stage of Neurodegeneration

NEUROSCIENCE NEWS

Summary: Study reveals Tau proteins disrupt synaptic transmission in early stages of neurodegenerative diseases.

Source: VIB Flanders.

Tau proteins are best known as the proteins that are stacked to form neuronal “tangles” in Alzheimer’s patients’ brains, but they also play a role in many other brain disorders such as Parkinson’s and Huntington’s disease. NeuroscienceNews.com image is for illustrative purposes only.


Tau proteins are involved in more than twenty neurodegenerative diseases, including various forms of dementia. These proteins clump together in patients’ brains to form neuronal tangles: protein aggregation that eventually coincides with the death of brain cells. Prof. Patrik Verstreken’s research team (VIB-KU Leuven) has now discovered how tau disrupts the functioning of nerve cells, even before it starts forming tangles. They immediately suggest a way to intervene in this process.

Tau proteins are best known as the proteins that are stacked to form neuronal “tangles” in Alzheimer’s patients’ brains, but they also play a role in many other brain disorders such as Parkinson’s and Huntington’s disease. In healthy circumstances, tau proteins are connected to the cytoskeleton of nerve cells, where they support the cells’ structural stability. In the nerve cells of patients, however, tau is dislodged from the cytoskeleton and ultimately tangles together to form protein accumulations that disrupt the nerve cell’s functioning.

Early spoilsport
But even before these protein accumulations are formed, the dislodged tau impedes the communication between nerve cells. VIB’s research team has described a new mechanism for this in the journal Nature Communications.

Professor Patrik Verstreken (VIB-KU Leuven) explains: “We have demonstrated that when mutant tau dislodges from the cytoskeleton, it mainly settles at the synapses of the nerve cells. This was not only the case in fruit flies and rats but also in the brain cells of human patients. Vesicles containing chemicals are released at these synapses, which serve as the means of communication between two different nerve cells. When tau settles at the synapse, it locks onto the vesicles, inhibiting synaptic transmission.”

Fundamental research with prospects for therapeutic applications
These new insights are the result of a close collaboration between different laboratories at VIB, the universities of Leuven, Louvain-la-Neuve (both in Belgium), and Edinburgh (UK), and with researchers from Janssen Pharmaceutica. They pave the way for a possible treatment.

“Now that we know how tau inhibits synaptic transmission, we can look for ways to prevent it.” Patrik Verstreken already provided proof of principle: “If we stop tau from locking onto the vesicles in the nerve cells of rats and fruit flies, we can prevent the inhibition of synaptic transmission and also the death of nerve cells.” Further research should reveal whether this strategy will also be useful for patients.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: Sooike Stoops – VIB Flanders 
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Tau association with synaptic vesicles causes presynaptic dysfunction” by Lujia Zhou, Joseph McInnes, Keimpe Wierda, Matthew Holt, Abigail G. Herrmann, Rosemary J. Jackson, Yu-Chun Wang, Jef Swerts, Jelle Beyens, Katarzyna Miskiewicz, Sven Vilain, Ilse Dewachter, Diederik Moechars, Bart De Strooper, Tara L. Spires-Jones, Joris De Wit & Patrik Verstreken in Nature Communications. Published online May 11 2017 doi:10.1038/ncomms15295


Abstract

Tau association with synaptic vesicles causes presynaptic dysfunction
Tau is implicated in more than 20 neurodegenerative diseases, including Alzheimer’s disease. Under pathological conditions, Tau dissociates from axonal microtubules and missorts to pre- and postsynaptic terminals. Patients suffer from early synaptic dysfunction prior to Tau aggregate formation, but the underlying mechanism is unclear. Here we show that pathogenic Tau binds to synaptic vesicles via its N-terminal domain and interferes with presynaptic functions, including synaptic vesicle mobility and release rate, lowering neurotransmission in fly and rat neurons. Pathological Tau mutants lacking the vesicle binding domain still localize to the presynaptic compartment but do not impair synaptic function in fly neurons. Moreover, an exogenously applied membrane-permeable peptide that competes for Tau-vesicle binding suppresses Tau-induced synaptic toxicity in rat neurons. Our work uncovers a presynaptic role of Tau that may be part of the early pathology in various Tauopathies and could be exploited therapeutically.
“Tau association with synaptic vesicles causes presynaptic dysfunction” by Lujia Zhou, Joseph McInnes, Keimpe Wierda, Matthew Holt, Abigail G. Herrmann, Rosemary J. Jackson, Yu-Chun Wang, Jef Swerts, Jelle Beyens, Katarzyna Miskiewicz, Sven Vilain, Ilse Dewachter, Diederik Moechars, Bart De Strooper, Tara L. Spires-Jones, Joris De Wit & Patrik Verstreken in Nature Communications. Published online May 11 2017 doi:10.1038/ncomms15295

http://neurosciencenews.com/tau-neurodegeneration-synaptic-transmission-6727/

Offshore hospitals begin dispensing cannabis oil to patients, while failed drug policies in the USA prohibit compassionate medicine

Friday, May 19, 2017 by: 





(Natural NewsMedical cannabis may be effective in managing chronic pain and inflammation and in treating neurodegenerative disorders such as Parkinson’s disease and Alzheimer’s. It is also said to be a viable treatment for epilepsy, multiple sclerosis, for sleep disorders, and chronic cancer pain, among other maladies.

Although research is ongoing, marijuana reportedly works with the endocannabinoid system in the body to modulate levels of pain and anxiety, which gives it the ability to alleviate symptoms of a wide range of disorders. (RELATED: Read more about medical marijuana at CannibasCures.news.)
In fact, just last month, Natural Blaze identified 100 studies that purport to show that cannabis can cure a variety of different cancers.

The use of medical cannabis is currently legal in 28 U.S. states, although cannabis is illegal under federal law. There is an increasing momentum behind legalizing recreational marijuana at the state level beyond those states where it has already been authorized, which is a separate matter with broad societal ramifications upon which reasonable people can reach different conclusions.

President Trump supports medical marijuana and during the campaign indicated that issue of legalizing the use of marijuana should be left up to the states on an individual basis. Attorney General Jeff Sessions, however, is viewed as more of a hardliner on recreational and medicinal weed.

Hospitals outside of the US are starting to take note of the medicinal benefits of cannabis

After purchasing about 13 quarts of the substance from a firm in Canada, a hospital in the Grand Cayman Islands is now dispensing cannabis oil, which contains a combination of active cannabis ingredients such as THC and CBD, to a select group of eligible and closely monitored patients who live in the Caymans, which are situated in the western Caribbean, south of Cuba.

Grand Cayman’s CTMH Doctors Hospital and Cayman Pharmacy Group explained its decision as follows, CNS Business reported.

“These advancements in medicinal cannabis have been proven successful in multiple case studies around the world,” the hospital officials said. “These case studies reveal life changing results for patients suffering with many conditions such as chronic pain, neuropathic pain and seizures. As with all medications, care and caution must be exercised to minimise risks and maximise health benefits.”

It is an understatement to note that Big Pharma is hardly a fan of medical cannabis or other natural remedies in general.

The Waking Times website claims, however, that physicians are waking up to the benefits of cannabis oil as they gradually accept its therapeutic benefits. “Success stories about using cannabis oil to treat illness continue to surface, and the medical establishment is listening.” The website goes on to note that “In addition to the Cayman Islands, doctors in other parts of the world are giving medicinal cannabis the attention it deserves.”

The website adds that even with the ongoing opposition from the feds, which includes the DEA, more American hospitals will “start dispensing cannabis oil and other cannabis-based medications in the near future.”

Sources:

http://www.naturalnews.com/2017-05-19-offshore-hospitals-begin-dispensing-cannabis-oil-to-patients-while-failed-drug-policies-in-the-usa-prohibit-compassionate-medicine.html

Human Intelligence Is Limited. That’s Why We Need Synthetic Intelligence.

Ben Stecher takes a look at why artificial intelligence will be a good thing for the future of humans.




Three times a day I take a drug called levodopa. I take it because my brain does not produce enough dopamine; without it, my hands and feet shake and I have difficulty getting my body to do what I want it to do. These are symptoms of Parkinson’s disease and mean that many of my dopamine producing neurons have died. But, thanks to levodopa, I can feed my brain synthetic dopamine.

It is an incredible little drug that we discovered to be naturally produced in the broad bean plant, pictured here. (The fact that nature makes in this plant the exact molecule that is missing in my brain leaves me dumb-founded.) In the first half of the 20th century we figured out how to chemically produce the compound, allowing us to manufacture it in mass quantities and distribute it to Parkinson’s disease patients world-wide. That we figured all that out is a testament to our ingenuity and our intelligence. If someone was diagnosed with Parkinson’s just 60 years ago, there would be nothing that any doctor could do for them. I owe my ability to function today to this plant and to human intellect.
But it is not good enough. Every time I take this drug, it floods my entire brain with dopamine; while this does produce a cool high and also makes me more alert and focused, it has some negative effects. In any drug that you might take, from the THC in marijuana to the caffeine in coffee, there are chemicals in them that bind to receptors in your brain. This either stimulates or inhibits neurons, which has a cascade of other effects. One of them is that when taken regularly, the brain produces extra receptors in anticipation of the drug; that is why tolerance goes up. This might not sound like such a bad thing, but it does alter the chemistry and structure of your brain.

While the altered structure that results from too much caffeine may not be that harmful, other drugs, like synthetic dopamine, can be. Most people who take levodopa for many years start to experience a side-effect of the drug called dyskinesia that makes it very difficult to control one’s body. To combat this side effect, we have other drugs that further alter your brain, which eventually leads to more drugs to combat the harmful effects of the previous drug. Before long, patients end up spending most of their day shoving pills into their mouth and the disease becomes incredibly difficult to manage.
Also, every person’s brain is wired differently, and as a result the effects of drugs produce a slightly different response in each one of us. For now, the pharmaceutical industry is built around a one-drug-fits-all motto, and until we get to the point where we can have a personalized approach to treating diseases, this will continue to be the case.
But the biggest impediment to figuring out diseases such as Parkinson’s or Alzheimer’s is the astounding complexity of the brain itself. As James Watson put it, “The brain is the last and grandest biological frontier, the most complex thing we have yet discovered in our universe. It contains hundreds of billions of cells interlinked through trillions of connections. The brain boggles the mind.”
So what to do? Well, it is very likely that the mechanisms underlying neurodegeneration, which everyone will suffer from to some degree, are just too complex for us to figure out. The number of factors that one needs to consider to make sense of such diseases is incredibly long, most likely too long for any human, or even any group of humans, to make sense of. While we have come pretty far in our treatment of such diseases and have some exciting new therapies in the pipeline, there is no cure on the horizon and the reality is that we might just not be smart enough to figure these things out.
The same can be said for a number of riddles that we are still faced with. In the end, the reason why we can’t figure out how to deal with climate change, or what the origins of the universe are, or even how to settle the Israeli-Palestinian conflict is that there are limits to what we are capable of and for some issues, like the latter, there is the added difficulty of having too much human stupidity in the way.
Which is why the creation of artificial intelligence might ultimately be a good thing. Just like every parent hopes that their child will be smarter than they are, the hope is that if we give birth to an artificial form of intelligence it will be wiser than we are and may be able to figure out many of the problems in the world that we can not.
And we might be a lot closer to bringing about AI than most people think…

https://futurism.com/human-intelligence-limited-why-need-synthetic-intelligence/

Disease threatens to ravage their minds, bodies and voices. They’re fighting back.

May 19, 2017

Tina MacDonald of Oakdale challenges her body, mind and voice in a multitasking exercise during a PWR!Moves class taught by Lori Dodd on Wednesday (05-17-17) at Core Fitness in the Roseburg Square shopping center in Modesto, Calif. Deke Farrow jfarrow@modbee.com


Feet planted behind her, Tina MacDonald leaned over an inverted balance-training dome and gripped the edge of the base with her hands. She pulled one leg up past her elbow, slapping her foot on the ground with purpose. Then it was back with that leg, forward with the other.
She quickly and repeatedly alternated between legs, each time calling out a word, letter or number – or the color it was written in – on papers taped to the floor on each side of the dome. “Black! Green! Red! X! 4! Red! ...”
I BELIEVE THAT I HAVE POWER OVER PARKINSON’S.
The affirmation the women say at the close of their PWR Moves class
The multitasking exercise worked her body, but also her mind and her voice. She, like two other women working out with her Thursday afternoon, is trying to protect those things – her very essence – against the disease trying to steal them.
Oakdale resident MacDonald, 62, and Stockton residents Leslie Sherman, 72, and Maureen Conway, 69, have Parkinson’s, a disorder of the central nervous system that affects movement, often including tremors.
In their fight against it, they’re employing nutrition, medication and – perhaps most important, they believe – exercise. Between them, the women walk, do stationary cycling, dance, do yoga and more. Together, they take the PWR!Moves classes taught by physical therapist Lori Dodd at Core Fitness in Modesto’s Roseburg Square shopping center.
AN ESTIMATED 10 MILLION PEOPLE WORLDWIDE LIVE WITH PARKINSON’S DISEASE. IN THE UNITED STATES, AS MANY AS ONE MILLION INDIVIDUALS LIVE WITH PARKINSON’S, WHICH IS MORE THAN THE COMBINED NUMBER OF PEOPLE DIAGNOSED WITH MULTIPLE SCLEROSIS, MUSCULAR DYSTROPHY AND LOU GEHRIG’S DISEASE.
PWR stands for Parkinson Wellness Recovery, the Arizona-based nonprofit whose founder and CEO Becky Farley created the PWR!Moves program.
Dodd, a licensed physical therapist with 30 years’ experience, got PWR!Moves-certified in the fall and began teaching classes in January. She’d never known the best way to work with Parkinson’s sufferers, she said, until attending the World Parkinson’s Congress in Portland, Ore., in September. She had planned to become certified in another Parkinson’s-fighting program, Rock Steady Boxing, until MacDonald contacted her and asked her to pursue PWR!Moves instead.
So far, MacDonald, Sherman and Conway are Dodd’s only PWR!Moves students, and she loves working with them. “They’re driven ... taking charge of their lives and doing everything they can to slow the progression of their disease, which is really inspiring,” Dodd said. “They want to maintain a normal life as long as possible, and if they’re willing to fight, I have to help them.”
THE DAYS THAT WE DON’T EXERCISE, IT’S NOT A GOOD DAY. OUR BODIES START TIGHTENING UP, WE DON’T MOVE AS EASILY.
Maureen Conway
Sherman, diagnosed 10 years ago, always has exercised and been fitness-minded, she said. The extra advantage of PWR!Moves, she said, is that the exercises have practical applications. They help with getting in and out of a car or a restaurant booth, stepping over obstacles, reaching for items on a shelf. Even everyday activities like walking and talking. “That’s why we yell out the numbers (while exercising), because your voice gets softer and softer as you progress in your disease sometimes. But every person has different symptoms, we don’t all do the exact same thing.”
The exercises help with strength, coordination and balance, while the cardio “keeps your brain alive,” Conway said.
Mild cognitive impairment is a common symptom of Parkinson’s. Many sufferers feel distracted or disorganized, according to the Parkinson’s Disease Foundation, or have difficulty planning and carrying through tasks. They may have trouble remembering information, or finding the right words when speaking. 
AS IS THE CASE WITH MANY NEUROLOGICAL DISORDERS, THE CAUSE OF PARKINSON’S DISEASE IS NOT KNOWN.
“Speaking is one of the problems we often have,” Conway said. “Talking slowly and getting the words out. If it seems like we can’t think of it –”
“– that’s because we really can’t,” Sherman interjected.
Conway, who learned a little more than a year ago that she had Parkinson’s, said the first thing she was told was she likely had symptoms for a while, without realizing what they meant. “By the time you’re diagnosed, you’re already in pretty bad shape,” she said. “They say you’ve already lost 75 percent of your dopamine by the time they diagnose you. ... It takes a lot of time to undo the damage that’s been done.”
The exercises she, Sherman and MacDonald do – combined with their positive, “kick-butt” attitude – help with that and then help stave off the disease’s ravages. 
WHAT’S NICE ABOUT THIS CLASS IS WHEN YOU TAKE IT AND YOU LEARN THE EXERCISES, IT REMINDS YOUR BRAIN NOT TO SLUMP OVER, IT REMINDS YOU TO STAND UP STRAIGHT AND SWING YOUR ARMS WHEN YOU’RE WALKING.
Tina MacDonald, noting that a slumped walk is common among Parkinson’s patients
They’d love to have more company in their class – men and women alike, and sufferers of not just Parkinson’s but other ailments. The exercises can benefit someone rebuilding strength after a stroke, for example, MacDonald said.
“A lot of people who are more advanced in the disease are a little afraid to do the exercises,” Sherman said. And Dodd agreed that while watching her three strong students is inspiring, it also can be a bit intimidating. But, she said, a lot of the exercises can be done in sitting or standing positions for those not up to the full range of movement.
To learn more about the local PWR!Moves classes, contact Dodd at 209-606-6410 or lori@loridoddpt.com.
http://www.modbee.com/news/article151669212.html#storylink=cpy
Read more here: http://www.modbee.com/news/article151669212.html#storylink=cpy

Friday, May 19, 2017

Acorda Therapeutics to Present Update on Phase 3 Study of Inbrija In Parkinson’s Patients

MAY 19, 2017  BY JOANA FERNANDES, PHD




Acorda Therapeutics will soon release novel data on its Phase 3 SPAN-PD trial (Study 004, NCT02240030) investigating the experimental drug Inbrija (CVT-301) as a potential therapy for patients with Parkinson’s disease.
Acorda presents its poster, “Inhaled levodopa (CVT-301, 84-mg dose) significantly improves motor function during OFF periods in Parkinson’s disease subjects: A Phase 3 Study (SPAN-PD),” June 5 at the International Congress of Parkinson’s Disease and Movement Disorders in Vancouver.
Inbrija is an inhaled formulation of levodopa (L-dopa) under development to treat “off” episodes, or re-emergence of Parkinson’s motor symptoms, in patients taking oral carbidopa/levodopa. It delivers a precise amount of the medication into the lungs and reaches the brain shortly after.
The SPAN-PD trial enrolled 351 Parkinson’s patients experiencing “off” episodes to evaluate the safety and effectiveness of inhaled Inbrija compared to a placebo. Researchers assessed the drug’s effectiveness by changes in the Unified Parkinson’s Disease Rating Scale (UPDRS) Part III motor score, a measure of motor impairment, at 30 minutes following treatment with 84 mg of Inbrija at 12 weeks.
Results showed that patients on Inbrija reported a change of -9.83 compared to -5.91 for placebo, which indicated improvement of motor function.
Two other Phase 3 studies investigated the long-term safety of Inbrija: CVT-301-005 (NCT02352363) and CVT-301-004E (NCT02242487). The CVT-301-005 study enrolled 271 Parkinson’s patients with no history of asthma or other chronic lung disease, to assess pulmonary function after one year of treatment.
The CVT-301-004E study included 149 patients who were given 84 mg of CVT-301 and 146 patients who were treated with 60 mg. Safety findings were similar to those reported in the CVT-301-005 study. These patients were given Inbrija (84 mg) up to five times a day and standard of care. Results were compared to those of 127 patients who received only standard of care (control group). No difference has been found between the two groups, showing that treatment with Inbrija does not change pulmonary function in Parkinson’s patients.
Common side effects included mild to non-severe cough, nasopharyngitis (cold), dyskinesia (involuntary movements) and falls.
Acorda, based in Ardsley, New York, plans to ask the U.S. Food and Drug Administration for a New Drug Application. It’ll also file a Marketing Authorization Application (MAA) to the European Medicines Agency this year to treat Parkinson’s patients with Inbrija, and plans to support its applications by the positive results obtained in the Phase 3 studies.
“We are excited to be preparing an NDA in the U.S. and an MAA in the EU, which we plan to submit by the end of the second quarter and end of the year, respectively,” Dr. Burkhard Blank, Acorda’s chief medical officer, said in a press release. “Data from our clinical program have shown that Inbrija has the potential to be an important new treatment option for people with Parkinson’s who experience off periods, which can be extremely disruptive in their lives.”
https://parkinsonsnewstoday.com/2017/05/19/parkinsons-therapy-inbrija-focus-phase-3-update-vancouver-conference-ac/

Team discovers neural stem cells can become blood vessels

May 19, 2017

Professor Ricardo Pardal and his team. Credit: University of Seville


Mother cells from the adult carotid body can transform into blood vessels as well as neurons. This discovery could have important repercussions on the treatment of such diseases as pediatric tumors and Parkinson's.

Researchers from the University of Seville and the Seville Institute of Biomedicine (IBiS) have just published a scientific article in the journal Cell Reports, in which they show that mother cells from the adult carotid body can transform into blood vessels, as well as into neurons. The work was led by the post-doctoral researcher Valentina Annese.
"We believe that the ability to produce blood vessels from neural stems cells could directly affect the growth of certain types of tumours on the infant population," said the project's main researcher, Ricardo Pardal.

The carotid body is a small structure of nerve tissue situated at the fork of the carotid artery. Its function is to act as a chemoreceptor in the blood. It monitors oxygen pressure in the blood and plays a role in the regulation of breathing.

The plasticity of adult mother cells, or the somatic mother cells, to cross boundaries and to differ in unrelated cell types has been a subject of debate over the last decade. Neural crest stem cells (NCSCs) show notable plasticity during their development, but it is not known if adult NCSCs maintain this plasticity.

"We find that the adult stem cells from the carotid body taken from the neural crest (CBSCs) are capable of experiencing endothelial differentiation, as well as their already described role in neurogenesis, contributing to both neurogenic and angiogenic processes that take place during acclimation to hypoxia. In addition, the conversion of CBSCs into blood vessels is dependent on the hypoxia-inducible factor (HIF) and is sensitive to vascular cytokines released in hypoxia, such as erythropoietin. Our data highlights a notable physiological plasticity in an adult population of stem cells specifically from tissue, and they could have an impact on the use of those cells for cellular therapy," Pardal said.


More information: Valentina Annese et al, Physiological Plasticity of Neural-Crest-Derived Stem Cells in the Adult Mammalian Carotid Body, Cell Reports (2017). DOI: 10.1016/j.celrep.2017.03.065

Journal reference: Cell Reports

Provided by: University of Seville

https://medicalxpress.com/news/2017-05-team-neural-stem-cells-blood.html

What it's really like to live with dementia

May 19, 2017 by Catherine Bailey, Katie Brittain And Sue Tiplady, The Conversation

Dementia doesn’t have to mean the end of hobbies and interests. Credit: Pexels


More than 225,000 people develop dementia every year – that's roughly one person every three minute. At the moment, 850,000 people in the UK are living with dementia. This figure is set to rise to two million by 2051.

Dementia is a progressive disease of the brain that mainly affects older people – although is not a "normal" part of ageing. Of the 850 000 known cases of dementia in the UK, some 40,000 are aged under 65.

It is a collection of brain diseases – with Alzheimer's the most common – and is not just about memory loss. Everyone experiences it differently, from behaviour change, to difficulty processing conversations, to confusion over everyday tasks – such as working out how to make a cup of tea.

As academics researching in this area with other organisations, we work directly alongside people living with dementia, as well as their carers, families and communities. And while we understand a lot about the disease – including how it affects a person's health and the impact it can have on their personal lives – we do not know what it's really like to live with dementia, day in, day out.

Gym and swim
This is why it's critical to listen to those who can tell it as it is – which is what a large part of our research is about. Susan Small who was a dementia support worker and a carer says:

People should not be defined by their dementia, but given opportunities and experiences to enjoy life and relationships – and indeed take a few risks now again. We need to learn to listen more to what the person with dementia is telling us.
It is important for people to get a correct, early diagnosis, as long as it is followed up with timely information and support. Too little information can leave the person with dementia and those close to them, feeling ill prepared – yet too much information can leave people fearful of their future.

Barbara Dow who cared for her husband Al and is now a dementia campaigner agrees, stressing that a timely diagnosis enabled them to plan for the future together. This meant they could move house to be nearer to family and facilities where they could both continue much loved hobbies such as dancing. She said: Al continued to lead a full life to the best of his abilities. If he could not dance, then he could go to the gym and swim.

She also speaks of humour lessening frustration and maintaining self-esteem: Al might forget who had just spoken on the phone. We used to say it was Mr or Mrs Whatsit, have a bit of a laugh together about it and then I would dial 1471.

My life, my terms
People living with dementia – and their carers – also speak of the need to emphasise what is achieved, rather than what isn't.
Ken Clasper, a university college engineer, was diagnosed with Lewy Body dementia at the age of 56. This is the same type of dementia that actor Robin Williams had and can cause depression, paranoia, Parkinson's disease and confusion.

Clasper told us that although he may need more time to process information, "please don't answer for me, just give me time". He suggests that it's also important for others to know the person with dementia, and for example, their life-long interests and passions. He is a keen nature lover and photographer and bought equipment that helps him to continue to take photographs.

Other people with dementia have spoken of enjoying being outdoors on their own, and while this may cause some understandable anxiety to friends and family, they stress the importance of being able to "get on with life in their own way" – with family and community support.

Learning to adapt
These experiences show that much of living with dementia is about cycles of loss and adjustment, of change and adaptation – and of partial resolution. Partial, because life does not stay the same – we shift and change with circumstance as a progressive disease is experienced and lived through.
As the Alzheimer's Society's campaign to unite against dementia succinctly portrays, how this indiscriminate disease can affect anyone.

How a person might live with dementia depends on who they are, their own individual diagnosis as well as their support network and connections. But it is important to remember that people can and do live well with dementia.
Of course, there will be peaks and troughs, good days and bad, but rather than just seeing everyone with dementia as "sufferers", or as "brave battlers" of a debilitating disease, it is important to remember that dementia can be lived with as well. To do this, we need to listen to and learn from, those who know what it's really like – those people who have the actual lived experience.

Provided by: The Conversation


https://medicalxpress.com/news/2017-05-dementia_1.html