HomeFeatured Unique Visual Stimulation May Be New Treatment For Alzheimer’s

NEUROSCIENCE NEWSDECEMBER 10, 2016

Summary: Inducing gamma oscillations appears to suppress amyloid production and could prove an effective treatment potential for Alzheimer’s.

Source: MIT.

After an hour of stimulation at 40 hertz, the researchers found a 40 to 50 percent reduction in the levels of beta amyloid proteins in the hippocampus. Stimulation at other frequencies, ranging from 20 to 80 hertz, did not produce this decline. NeuroscienceNews.com image is adapted from the Picower Institute for Learning and Memory video.

Noninvasive technique reduces beta amyloid plaques in mouse models of Alzheimer’s disease.

Using LED lights flickering at a specific frequency, MIT researchers have shown that they can substantially reduce the beta amyloid plaques seen in Alzheimer’s disease, in the visual cortex of mice.

This treatment appears to work by inducing brain waves known as gamma oscillations, which the researchers discovered help the brain suppress beta amyloid production and invigorate cells responsible for destroying the plaques.

Further research will be needed to determine if a similar approach could help Alzheimer’s patients, says Li-Huei Tsai, the Picower Professor of Neuroscience, director of MIT’s Picower Institute for Learning and Memory, and senior author of the study, which appears in the Dec. 7 online edition of Nature.

“It’s a big ‘if,’ because so many things have been shown to work in mice, only to fail in humans,” Tsai says. “But if humans behave similarly to mice in response to this treatment, I would say the potential is just enormous, because it’s so noninvasive, and it’s so accessible.”

Tsai and Ed Boyden, an associate professor of biological engineering and brain and cognitive sciences at the MIT Media Lab and the McGovern Institute for Brain Research, who is also an author of the Nature paper, have started a company called Cognito Therapeutics to pursue tests in humans. The paper’s lead authors are graduate student Hannah Iaccarino and Media Lab research affiliate Annabelle Singer.

“This important announcement may herald a breakthrough in the understanding and treatment of Alzheimer’s disease, a terrible affliction affecting millions of people and their families around the world,” says Michael Sipser, dean of MIT’s School of Science. “Our MIT scientists have opened the door to an entirely new direction of research on this brain disorder and the mechanisms that may cause or prevent it. I find it extremely exciting.”

Brain wave stimulation

Alzheimer’s disease, which affects more than 5 million people in the United States, is characterized by beta amyloid plaques that are suspected to be harmful to brain cells and to interfere with normal brain function. Previous studies have hinted that Alzheimer’s patients also have impaired gamma oscillations. These brain waves, which range from 25 to 80 hertz (cycles per second), are believed to contribute to normal brain functions such as attention, perception, and memory.

In a study of mice that were genetically programmed to develop Alzheimer’s but did not yet show any plaque accumulation or behavioral symptoms, Tsai and her colleagues found impaired gamma oscillations during patterns of activity that are essential for learning and memory while running a maze.

Next, the researchers stimulated gamma oscillations at 40 hertz in a brain region called the hippocampus, which is critical in memory formation and retrieval. These initial studies relied on a technique known as optogenetics, co-pioneered by Boyden, which allows scientists to control the activity of genetically modified neurons by shining light on them. Using this approach, the researchers stimulated certain brain cells known as interneurons, which then synchronize the gamma activity of excitatory neurons.

After an hour of stimulation at 40 hertz, the researchers found a 40 to 50 percent reduction in the levels of beta amyloid proteins in the hippocampus. Stimulation at other frequencies, ranging from 20 to 80 hertz, did not produce this decline.

Tsai and colleagues then began to wonder if less-invasive techniques might achieve the same effect. Tsai and Emery Brown, the Edward Hood Taplin Professor of Medical Engineering and Computational Neuroscience, a member of the Picower Institute, and an author of the paper, came up with the idea of using an external stimulus — in this case, light — to drive gamma oscillations in the brain. The researchers built a simple device consisting of a strip of LEDs that can be programmed to flicker at different frequencies.

Using this device, the researchers found that an hour of exposure to light flickering at 40 hertz enhanced gamma oscillations and reduced beta amyloid levels by half in the visual cortex of mice in the very early stages of Alzheimer’s. However, the proteins returned to their original levels within 24 hours.

The researchers then investigated whether a longer course of treatment could reduce amyloid plaques in mice with more advanced accumulation of amyloid plaques. After treating the mice for an hour a day for seven days, both plaques and free-floating amyloid were markedly reduced. The researchers are now trying to determine how long these effects last.

Furthermore, the researchers found that gamma rhythms also reduced another hallmark of Alzheimer’s disease: the abnormally modified Tau protein, which can form tangles in the brain.

“What this study does, in a very carefully designed and well-executed way, is show that gamma oscillations, which we have known for a long time are linked to cognitive function, play a critical role in the capacity of the brain to clean up deposits,” says Alvaro Pascual-Leone, a professor of neurology at Harvard Medical School who was not involved in the research. “That’s remarkable and surprising, and it opens up the exciting prospect of possible translation to application in humans.”

Tsai’s lab is now studying whether light can drive gamma oscillations in brain regions beyond the visual cortex, and preliminary data suggest that this is possible. They are also investigating whether the reduction in amyloid plaques has any effects on the behavioral symptoms of their Alzheimer’s mouse models, and whether this technique could affect other neurological disorders that involve impaired gamma oscillations.

Two modes of action

The researchers also performed studies to try to figure out how gamma oscillations exert their effects. They found that after gamma stimulation, the process for beta amyloid generation is less active. Gamma oscillations also improved the brain’s ability to clear out beta amyloid proteins, which is normally the job of immune cells known as microglia.

“They take up toxic materials and cell debris, clean up the environment, and keep neurons healthy,” Tsai says.

In Alzheimer’s patients, microglia cells become very inflammatory and secrete toxic chemicals that make other brain cells more sick. 

However, when gamma oscillations were boosted in mice, their microglia underwent morphological changes and became more active in clearing away the beta amyloid proteins.

Researchers in Li-Huei Tsai’s laboratory at the Picower Institute for Learning and Memory have shown that disrupted gamma waves in the brains of mice with Alzheimer’s disease can be corrected by a unique non-invasive technique using flickering light.

“The bottom line is, enhancing gamma oscillations in the brain can do at least two things to reduced amyloid load. One is to reduce beta amyloid production from neurons. And second is to enhance the clearance of amyloids by microglia,” Tsai says.

The researchers also sequenced messenger RNA from the brains of the treated mice and found that hundreds of genes were over- or underexpressed, and they are now investigating the possible impact of those variations on Alzheimer’s disease.

ABOUT THIS GENETICS RESEARCH ARTICLE

Funding: The research was funded by the JPB Foundation, the Cameron Hayden Lord Foundation, a Barbara J. Weedon Fellowship, the New York Stem Cell Foundation Robertson Award, the National Institutes of Health, the Belfer Neurodegeneration Consortium, and the Halis Family Foundation.

Source: Anne Trafton – MIT

Image Source: NeuroscienceNews.com image is adapted from the Picower Institute for Learning and Memory video.

Video Source: The video is credited to the Picower Institute for Learning and Memory.

Original Research: Abstract for “Gamma frequency entrainment attenuates amyloid load and modifies microglia” by Hannah F. Iaccarino, Annabelle C. Singer, Anthony J. Martorell, Andrii Rudenko, Fan Gao, Tyler Z. Gillingham, Hansruedi Mathys, Jinsoo Seo, Oleg Kritskiy, Fatema Abdurrob, Chinnakkaruppan Adaikkan, Rebecca G. Canter, Richard Rueda, Emery N. Brown, Edward S. Boyden & Li-Huei Tsai in . Published online December 7 2016 doi:10.1038/nature20587

Abstract

Gamma frequency entrainment attenuates amyloid load and modifies microglia

Changes in gamma oscillations (20–50 Hz) have been observed in several neurological disorders. However, the relationship between gamma oscillations and cellular pathologies is unclear. Here we show reduced, behaviourally driven gamma oscillations before the onset of plaque formation or cognitive decline in a mouse model of Alzheimer’s disease. Optogenetically driving fast-spiking parvalbumin-positive (FS-PV)-interneurons at gamma (40 Hz), but not other frequencies, reduces levels of amyloid-β (Aβ)1–40 and Aβ 1–42 isoforms. Gene expression profiling revealed induction of genes associated with morphological transformation of microglia, and histological analysis confirmed increased microglia co-localization with Aβ. Subsequently, we designed a non-invasive 40 Hz light-flickering regime that reduced Aβ1–40 and Aβ1–42 levels in the visual cortex of pre-depositing mice and mitigated plaque load in aged, depositing mice. Our findings uncover a previously unappreciated function of gamma rhythms in recruiting both neuronal and glial responses to attenuate Alzheimer’s-disease-associated pathology.

“Gamma frequency entrainment attenuates amyloid load and modifies microglia” by Hannah F. Iaccarino, Annabelle C. Singer, Anthony J. Martorell, Andrii Rudenko, Fan Gao, Tyler Z. Gillingham, Hansruedi Mathys, Jinsoo Seo, Oleg Kritskiy, Fatema Abdurrob, Chinnakkaruppan Adaikkan, Rebecca G. Canter, Richard Rueda, Emery N. Brown, Edward S. Boyden & Li-Huei Tsai in . Published online December 7 2016 doi:10.1038/nature20587

http://neurosciencenews.com/alzheimers-visual-stimulation-5721/

I hope my Parkinson’s play changes the way doctors deal with diagnosis

Author: Almaz OhenePublished: 8 December 2016

Sue Wylie is an actor and drama teacher with young-onset Parkinson’s disease, who wrote a hard-hitting play about the remarkable friendship between a middle-aged woman with Parkinson’s and a teenage boy who loves free running. Here, she opens up about her traumatic diagnosis, how it inspired ‘Kinetics’ and why she’d like the medical profession to listen to their patients

Hi Sue, thanks for taking the time to speak to us. Tell us about the inspiration behind your play ‘Kinetics’.

The doctor who delivered my diagnosis five years ago was quite cold and lacked empathy – it felt like a slap in the face. I have since switched consultants. Initially, I was in a period of shock and denial. But then I thought that I should write about my experience. I was aware that quite a lot of my friends were curious and would have liked to ask about it, but somehow didn’t know how.

So ‘Kinetics’ is based on a true story. There is a real Lukas who goes by the name of Laszlo, and I am the real-life version of Rose. Laszlo came to my attention when he has getting into trouble for free running on the school roof. It became clear that he was in danger of getting kicked out of school before he completed his GCSEs. I suggested we write a short monologue for him to perform, in which he could express the frustrations that made him go free running. But then inspiration hit – I got a tingle on my neck and realised it would be a far more interesting story to contrast his world of movement to my ever decreasing one.

There’s an early scene in the play where Rose’s GP tells her she has Parkinson’s in a very callous manner. What has your personal experience been with doctors and neurologists throughout your Parkinson’s journey?

I hope that some of the medical professionals who came to see the show have realised that delivering a diagnosis with a prognosis such as that of Parkinson’s disease with ‘objectivity’, can often come across as detachment. Speaking to other people with Parkinson’s, the experience I had wasn’t just unique to me.“It was like I was undressing in front of people and peeling back layers of emotion”

What did it feel like to be performing, what is essentially your personal Parkinson’s story, in front of a group of strangers?

It was like I was undressing in front of people and peeling back layers of emotion. Lots of people came up to me afterwards to say how they recognised their own Parkinson’s story in the play. It feels good to be a spokesperson, but there is also lot of humour in the play, which is also really liberating. I was quite nervous during the first few runs, but then as it got such a great reaction, it gave me some validation. I got used to the fact that people were enjoying the performance and that was a great feeling!

Why did you choose to host Q&A sessions with the audience after the show?

That question and answer segment was there from the first live production of the show and it became clear that it was an integral part of what we were aiming to do with the play. We had a medical professional sitting on the panel, which meant that technical questions could be asked and answered with integrity. Dr Ralph Gregory, a neurologist based in Dorset, was really instrumental in finding the doctors for the panel in virtually every town we performed in. I’ve had people email me after the show, saying that they felt inspired to go back to their doctors and ask the questions that they hadn’t been comfortable talking about before.

How did you manage your symptoms while acting on stage?

Rehearsal days were the trickiest because they were the longest days. I doubled up on medication, because when they start to wear off you get slow, and vocally quite weak – obviously on stage this isn’t what you want. The drawback, however, was that I experienced a lot of dyskinesia as a side effect of the extra medication. Ironically, I had to use my good right hand to portray Rose’s tremor as the extra meds decreased the usual tremor in my left.

How did you prepare for show nights?

We did really good physical and vocal warm ups – to be honest they would probably help on me on day-to-day basis too – and on performance days I’d make sure I wasn’t getting too tired. I’d just potter around during the day and have a nap, before heading out for the performance in the early evening.

What challenges did you face putting on the tour?

Although we were technically ‘on tour’ for six weeks, I got lifts from my husband or took the train to each of the theatres, as don’t sleep well and prefer to spend nights at home – so that I can prowl around in familiar surroundings!

What kind of messages or feedback have you received from audience members?

It’s been fantastic! I have received a lot of emails from people with Parkinson’s, saying things like: “Your words could have been my words.” I’ve actually made friends with a fair few.

How was the play received from region to region?

In Devon, we were in quite a rural place with an older audience. They listened very intently, but didn’t laugh, whereas the younger audiences laughed in all the right places.

What attributes were you looking for when casting the actors?

The character of Lukas was first played by Laszlo – as the original piece was a monologue – so we knew we needed someone who was physically capable. The actor that we cast, Roly Botha, came from a physical theatre background. He began training with Jackson Turner, a specialist Parkour trainer, and within a couple of days, Roly had mastered a lot of the skills. “Delivering a diagnosis with ‘objectivity’ can often come across as detachment”

The part of Lucas required quite an emotional range and a sense of humour. Kate McGregor, the director, was happy to cast Roly as he takes direction well. All directors look for that quality in an actor. Since we were going to be on the road for a few weeks, we had to make sure we all gelled, which we really did.

How much did you know about Parkour before you began work on the play?

Watching the youngsters in workshops with Jackson Turner really helped me understand the thrill that Lazslo got from free running. In actual fact, Sébastien Foucan, who is widely accepted as the founder of Parkour and free running, was going be involved with the play, but unfortunately another filming project cropped up, which meant that he wasn’t free.

How important is it that people remember that Parkinson’s doesn’t discriminate and anyone can develop it?

It’s very important! Audience members who had no direct experience of Parkinson’s understood this, so we were pleased. Adding issues such as the other, lesser-known non-motor symptoms, such as vocal power weakening, and some loss of facial expressions, was a way to try to educate the audience. The mantra that we have at the very end, “accept, adapt, adjust”, actually came from an email from a lady I was in contact with at the writing stage, and it just felt right, so I asked for her permission to include it.

What next for Kinetics?

Because of my background in radio, I’d like to turn it into a radio play and we have plans to team up with film director Ceri Higgins – who was behind the ‘Dance for Parkinson’s’ project – to produce a short film version.

We’re also in talks with the theatre in Bristol to go back in early 2018. But what is most exciting is that we have partnered with Patricia Miller, CEO of Dorset County Trust Hospital, to launch a campaign to change the ways in which patient letters are written. They’re currently written in third person, about the patient, not for the patient and we’d like to see some improvements made.

 An inspiring play about Parkinson’s and Parkour is coming to a theatre near you

http://parkinsonslife.eu/sue-wylie-kinetics-parkinsons-play-doctors-diagnosis/

Shedding Light on a Cell That May Contribute to Alzheimer’s and ALS

NEUROSCIENCE NEWSDECEMBER 9, 2016

Summary: New research could help scientist better understand the role of astrocytes in neurodegenerative diseases.

Source: UCLA.

The hippocampus of a mouse with the artificial Cre/ERT2 gene, showing astrocytes glowing green. Neurosciencenews image is credited to Baljit Khakh lab/David Geffen School of Medicine at UCLA.

An achievement by UCLA neuroscientists could lead to a better understanding of astrocytes, a type of cell in the brain that is thought to play a role in Lou Gehrig’s disease, also called amyotrophic lateral sclerosis, or ALS; Alzheimer’s disease; Huntington’s disease; and other neurological disorders.

The researchers are the first to have bred mice in which an artificial gene called Cre/ERT2, a basic tool for studying the functions of cells, can be activated exclusively in astrocytes. A paper describing their work was published online today in the journal Neuron.

Neuroscientists have been trying for years to engineer mice in which Cre/ERT2 or other artificial genes can be activated just in astrocytes without significant “leakage” into other cell types.

“We’ll now be able to delete or mutate astrocyte genes that are suspected of contributing to diseases such as ALS to see whether they really do contribute,” said Baljit Khakh, professor of physiology and neurobiology at the David Geffen School of Medicine at UCLA. “That, in turn, could open up many new strategies for treating those diseases.”

To give the mice the Cre/ERT2 gene, Khakh and colleagues inserted it into another gene, Aldh1-l1. Aldh1-I1 had been found in a previous study to only be active in adult astrocytes. 

Cre/ERT2 normally can be activated in mice by giving them a drug called tamoxifen, which is best known as a breast cancer treatment. The UCLA researchers, however, built the combination gene so that tamoxifen could only “turn on” the Cre/ERT2’s when it was in astrocytes. The researchers also verified that the gene becomes active in virtually all astrocytes in the adult mouse brain but in virtually no other cells.

Scientists have known that astrocytes perform a variety of routine functions throughout the brain, and it is believed that they have a major influence on how the brain works and how humans and other animals behave. But what scientists haven’t been able to explain very well is how, at the molecular level, astrocytes accomplish all of these functions.

The UCLA advance should provide a powerful tool that scientists can use to solve that puzzle.

“The availability of these mice makes possible experiments that I think will keep researchers busy for many years to come,” Khakh said.

In initial demonstrations, Khakh and his team used the mice to learn more about a phenomenon called “calcium signaling,” through which astrocytes influence the functions of neurons, and also to identify for the first time the genes that are normally active in adult mouse astrocytes.

Astrocytes have also been linked to several neurological diseases, including ALS, a usually fatal disease in which neurons that control muscles face progressive destruction. Several recent studies on ALS have identified astrocytes as a significant cause of the deaths of these neurons. How astrocytes end up harming neurons in ALS remains a mystery, but the mice with Cre/ERT2 should enable researchers to tackle that question more effectively than they could have before, Khakh said.

ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE

The study’s lead authors are Rahul Srinivasan, Tsai-Yi Lu and Hua Chai, of Khakh’s laboratory. Other co-authors are Ji Xu, Ben Huang, Peyman Golshani and Giovanni Coppola, all of UCLA. 

Funding: The study was supported by a grant from the National Institutes of Health.

Source: David Olmos – UCLA

Image Source: This NeuroscienceNews.com image is credited to Baljit Khakh lab/David Geffen School of Medicine at UCLA.

Original Research: Abstract for “New Transgenic Mouse Lines for Selectively Targeting Astrocytes and Studying Calcium Signals in Astrocyte Processes In Situ and In Vivo” by Rahul Srinivasan, Tsai-Yi Lu, Hua Chai, Ji Xu, Ben S. Huang, Peyman Golshani, Giovanni Coppola, Baljit S. Khakh in Neuron. Published online December 8 2016 doi:10.1016/j.neuron.2016.11.030

Abstract

New Transgenic Mouse Lines for Selectively Targeting Astrocytes and Studying Calcium Signals in Astrocyte Processes In Situ and In Vivo

Highlights

•Cre/ERT2 mice were made to achieve astrocyte-specific genetic manipulations in vivo

•Knockin Lck-GCaMP6f mice were made to study astrocyte calcium signals in vivo

•Mice were used to determine the adult cortical astrocyte transcriptome

•New, well-characterized, and much needed in vivo genetic resources are provided

Summary

Astrocytes exist throughout the nervous system and are proposed to affect neural circuits and behavior. However, studying astrocytes has proven difficult because of the lack of tools permitting astrocyte-selective genetic manipulations. Here, we report the generation of Aldh1l1-Cre/ERT2 transgenic mice to selectively target astrocytes in vivo. We characterized Aldh1l1-Cre/ERT2 mice using imaging, immunohistochemistry, AAV-FLEX-GFP microinjections, and crosses to RiboTag, Ai95, and new Cre-dependent membrane-tethered Lck-GCaMP6f knockin mice that we also generated. Two to three weeks after tamoxifen induction, Aldh1l1-Cre/ERT2 selectively targeted essentially all adult (P80) brain astrocytes with no detectable neuronal contamination, resulting in expression of cytosolic and Lck-GCaMP6f, and permitting subcellular astrocyte calcium imaging during startle responses in vivo. Crosses with RiboTag mice allowed sequencing of actively translated mRNAs and determination of the adult cortical astrocyte transcriptome. Thus, we provide well-characterized, easy-to-use resources with which to selectively study astrocytes in situ and in vivo in multiple experimental scenarios.

“New Transgenic Mouse Lines for Selectively Targeting Astrocytes and Studying Calcium Signals in Astrocyte Processes In Situ and In Vivo” by Rahul Srinivasan, Tsai-Yi Lu, Hua Chai, Ji Xu, Ben S. Huang, Peyman Golshani, Giovanni Coppola, Baljit S. Khakh in Neuron. Published online December 8 2016 doi:10.1016/j.neuron.2016.11.030

http://neurosciencenews.com/cre-ert2-alzheimers-als-5717/

Honeybee Memories Could Unlock Another Piece of Alzheimer’s Puzzle

NEUROSCIENCE NEWSDECEMBER 8, 2016

Summary: Blocking DNA methylation affects memory formation in honeybees, a new study reports.

Source: Frontiers.

“Honeybees have an amazing capacity to learn and remember,” says the researcher. “They can count up to four, and orientate themselves by learning patterns and landmarks. They are also social insects that interact, teach and learn, making them successful foragers. Bees remember how to find a food source, how good the source was, and how to return to the hive.” Neurosciencenews image is for illustrative purposes only.

Researchers show a molecular mechanism that regulates memory specificity over time, and point to how understanding memory in honeybees could help us combat degenerative brain diseases.

A breakdown of memory processes in humans can lead to conditions such as Alzheimer’s and dementia. By looking at the simpler brain of a honeybee, new research published in Frontiers in Molecular Neuroscience, moves us a step towards understanding the different processes behind long-term memory formation.

“We show that DNA methylation is one molecular mechanism that regulates memory specificity and re-learning, and through which experiences of the organism could be accumulated and integrated over their lifetime,” says Dr Stephanie Biergans, first author of the study and researcher at the University of Queensland, Australia.

“Honeybees have an amazing capacity to learn and remember,” says the researcher. “They can count up to four, and orientate themselves by learning patterns and landmarks. They are also social insects that interact, teach and learn, making them successful foragers. Bees remember how to find a food source, how good the source was, and how to return to the hive.”

As such, the honeybee can form complex memories through processes much like those happening in human brains. But, the honeybee brain is simpler and they have a smaller genome. This makes them an ideal model for investigating how the different processes needed for long-term memories happen.

Scientists know that when a memory is formed, molecular changes can trigger physical changes to the brain, including new or altered neural connections and activity. These build up over a lifetime to create our long-term memory.

One series of molecular changes that can occur due to experience or environmental changes and that affect memory formation is the differential expression of certain genes, mediated, among others, through processes collectively called epigenetic mechanisms. They regulate gene expression through modifications of the DNA or its associated proteins, without changing the genes themselves.

“We knew that DNA methylation is an epigenetic process that occurs in the brain and is related to memory formation,” Biergans explains. “When we block this process in honeybees it affects how they remember.”

Biergans taught two groups of honeybees to expect sugar in the presence of a particular smell. One group learned over an extended period, being exposed to the sugar and smell together many times. The other was given the combination only once. Using an inhibitor compound, Biergans halted DNA methylation in some bees in each group. The bees’ memory formation in the two groups were tested and compared, with and without, DNA methylation occurring. By changing the smell that accompanied the food, Biergans and colleagues also found that DNA methylation affects how a bee can re-learn.

“When the bees were presented with sugar and a smell many times together, the presence of DNA methylation increased memory specificity – they were less responsive to a novel odour. On the other hand, when only introduced to the combination once, DNA methylation decreased specificity,” she summarises.

For a foraging honeybee, this makes total sense. When a bee gets food from a single flower, it’s not worthwhile remembering how it smells. That bee will have a general memory of the site, but will shop around and try other flowers – there is no specificity to its foraging. But, when each flower with that smell proves over and over to be a good source of nourishment, the bee will stick to those flowers and seek them out.

DNA methylation also occurs in the human brain and the team’s findings are key to understanding how we remember. And, how we forget.

“By understanding how changes to the epi-genome accumulate, manifest and influence brain function, we may, in the future, be able to develop treatments for brain diseases that also develop over a lifetime. There is thought to be a genetic predisposition for some conditions, such as Alzheimer’s and dementia, but in many cases environmental factors determine whether the disease will manifest,” Biergans concludes.

ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE

Funding: The study was funded by the Australian Research Council and National Health and Medical Research Council of Australia, the Deutsche Forschungsgemeinschaft DFG, the Australian Research Council Future Fellowship, and the University of Queensland Postgraduate Research Scholarship and Travel Award.

Source: Monica Favre – Frontiers

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

Original Research: Full open access research for “DNA Methylation Adjusts the Specificity of Memories Depending on the Learning Context and Promotes Relearning in Honeybees” by Stephanie D. Biergans, Charles Claudianos, Judith Reinhard and C. G. Galizia in Frontiers in Molecular Neuroscience. Published online September 12 2016 doi:10.3389/fnmol.2016.00082

Abstract

DNA Methylation Adjusts the Specificity of Memories Depending on the Learning Context and Promotes Relearning in Honeybees

The activity of the epigenetic writers DNA methyltransferases (Dnmts) after olfactory reward conditioning is important for both stimulus-specific long-term memory (LTM) formation and extinction. It, however, remains unknown which components of memory formation Dnmts regulate (e.g., associative vs. non-associative) and in what context (e.g., varying training conditions). Here, we address these aspects in order to clarify the role of Dnmt-mediated DNA methylation in memory formation. We used a pharmacological Dnmt inhibitor and classical appetitive conditioning in the honeybee Apis mellifera, a well characterized model for classical conditioning. We quantified the effect of DNA methylation on naïve odor and sugar responses, and on responses following olfactory reward conditioning. We show that (1) Dnmts do not influence naïve odor or sugar responses, (2) Dnmts do not affect the learning of new stimuli, but (3) Dnmts influence odor-coding, i.e., ‘correct’ (stimulus-specific) LTM formation. Particularly, Dnmts reduce memory specificity when experience is low (one-trial training), and increase memory specificity when experience is high (multiple-trial training), generating an ecologically more useful response to learning. (4) In reversal learning conditions, Dnmts are involved in regulating both excitatory (re-acquisition) and inhibitory (forgetting) processes.

“DNA Methylation Adjusts the Specificity of Memories Depending on the Learning Context and Promotes Relearning in Honeybees” by Stephanie D. Biergans, Charles Claudianos, Judith Reinhard and C. G. Galizia in Frontiers in Molecular Neuroscience. Published online September 12 2016 doi:10.3389/fnmol.2016.00082

http://neurosciencenews.com/alzheimers-honeybee-memories-5709/

People loved Shay Healy's brave account of battling with Parkinson's disease on the Late Late Show

December 10, 2016

One of the most inspirational performances that the show has had.

Renowned Irish songwriter, broadcaster and journalist Shay Healy was a guest on this week's Late Late Show and aside from performing an extremely moving version of Stardust, his account of dealing with Parkinson's disease has won plenty of plaudits.

The former host of Nighthawks and Where Are They Now? was diagnosed with Parkinson's disease in 2004 and he was extremely open about discussing the devastating impact that the long-term degenerative disorder continues to have on his ability to perform routine tasks.

"The tips of my fingers have gone numb, so I can't pick up peas if they fall on the floor. I can't do simple things like tie my laces anymore" he said.

Healy also recalled a galling story which involved four people in Nassau Street, Dublin actually walking over him after he fell to the floor.

The composer of What's Another Year, Ireland's winning entry in the 1980 Eurovision Song Contest, wasn't solely focused on the negatives though because he selflessly shifted the attention towards the magnificent work that the organisation MOVE 4 PARKINSON'S do to help those that have been diagnosed with the disease.

The majority of viewers were then absolutely blown away with his rousing and inspirational version of the famous track, Stardust.

Take a look.

Here's the interview along with some of the words of admiration for Healy's appearance on the show..

https://www.joe.ie/fitness-health/watch-people-loved-shay-healys-honest-and-brave-account-of-battling-with-parkinsons-on-the-late-late/570268

Last resort treatment for Parkinson’s disease: Former cop finds astounding relief from medical marijuana

 December 10, 2016 by: Daniel Barker

NaturalNews) Although there has been little scientific research conducted so far regarding the use of cannabis to treat Parkinson’s disease, the anecdotal evidence provided by an ex-cop named Larry Smith makes a very strong case for its efficacy.

Smith, who served 26 years in law enforcement before retiring in 1999, has been battling Parkinson’s for 20 years. His story is the subject of an upcoming documentary, Ride With Larry, which chronicles his fight against the disease.

Larry has been successful in controlling some of his symptoms through exercise, with particular emphasis on the use of a recumbent bicycle. In fact, the documentary follows Larry as he embarks on a 300-mile bike journey across South Dakota.

Larry Smith tries medicinal marijuana to combat worsening Parkinson’s symptoms

As Larry Smith’s disease progressed, he explored every treatment available to ease the symptoms. Recently, he turned to medical marijuana and found it to be amazingly effective in alleviating his dyskinesia (uncontrollable movements) and other symptoms.

On the Ride With Larry Facebook page, a three-part video series follows Larry and his wife, Elizabeth, as they travel to San Diego to try medical marijuana for the first time – medical marijuana is not legal in their home state, South Dakota.

In Part One of the series, Larry and Elizabeth arrive in San Diego and visit a doctor who gives him a prescription for medical marijuana. At this point, Larry’s symptoms are pronounced – he has trouble walking and is in pain, despite the 20 pills he takes each day.

In Part Two, the pair visit a marijuana dispensary and obtain $40 worth of cannabis buds. Elizabeth mentions the fact that one of Larry’s prescriptions costs $3,000 each time to fill.

In Part Three, a fellow Parkinson’s sufferer visits Larry and gives him some cannabis oil. At this point, Larry’s symptoms are pronounced, he has difficulty speaking and is in obvious pain as he tries to control his movements.

An astounding transformation using one drop of cannabis oil

Within just a few minutes of placing one drop of cannabis oil under his tongue, Larry’s body completely relaxes – his tremors are gone, he can speak normally and his hands are steady.

It’s an astounding transformation. The video has now been viewed by nearly 40 million people, a testament to the dramatic nature of its content, and to the fact that many people are interested in the benefits of cannabis for treating Parkinson’s and other debilitating and difficult-to-treat conditions.

Yet medicinal marijuana remains illegal in many states, and is still prohibited by federal law.

“A person like me could really use marijuana,” said Larry in Part Three of the series. “And it makes me pretty angry that I can’t get it in my home state.”

Part Three also includes an interview with Dr. Daniele Piomelli, pharmacology professor at UC Irvine medical school, who said:

“The number one frustration that I have is knowing that there is this untapped potential — that comes from what marijuana is teaching us — to generate new medicines, and being stuck because of financial issues or political issues. That is extremely frustrating.”

Dr. Piomelli refers to animal experiments that have shown how marijuana alleviates Parkinson’s symptoms, and to anecdotal evidence such as Larry Smith’s experience, but acknowledges that there is little incentive to carry out further research, since there is no money to be made by Big Pharma on a plant that is so cheap and easy to grow.

“Pharmaceutical companies have no interest in marijuana because they cannot sell it,” said Dr. Piomelli.

It will be interesting to see how the new administration approaches the issue. If President Trump truly wants to serve the interests of the American people, he must see to it that medical marijuana is made available to every single person who can benefit from its use.

Sources:

TheAntiMedia.com

RideWithLarryMovie.com

http://www.naturalnews.com/2016-12-10-as-last-resort-to-cure-his-parkinsons-disease-former-cop-finds-astounding-relief-from-medical-marijuana.html

Stars back Witney man who has raised more than £3,000 for Parkinson's charity

December 9, 2016

John Foster (right) showing his book to Ian Hislop

A POET living with Parkinson’s has raised more than £3,000 for research into the disease after releasing a book of Christmas jokes, riddles and rhymes.

John Foster who lives at Standlake, near Witney, was diagnosed with Parkinson’s in 2005 and developed a severe tremor.

He had Deep Brain Stimulation to help control his tremor which enabled him to continue writing and performing his poetry in schools, libraries and at festivals.

He released his book Christmas Crackers in October and has so far sold more than 700 copies, with proceeds going to Oxford Parkinson’s Disease CentreMr Foster performed a reading at the concert held at Christ Church (pictured) at the weekend and met with comedians Ian Hislop and Rory Bremner at the event. 

He said: “It was great to have the support of Ian and Rory at the concert and to be able to discuss Christmas Crackers with them.

“I also took the opportunity to show them the brilliant illustrations by Oxford artist Korky Paul and cartoonist Gerald Scarfe which have really helped to bring the book to life.”

“I’ve been overwhelmed by the response to the book from people all over the UK.

“It’s wonderful to have raised such an amount for Parkinson’s research.”

Director of fundraising at Parkinson’s UK Paul Jackson-Clark said: “I’d like to say thank you to John for donating the proceeds of his popular book to research into Parkinson’s.

“There are a lot of exciting studies happening in Oxford which we are pleased to fund, but this wouldn’t be possible without the determination of fundraisers like John.

“I hope even more people decide to add this book to a Christmas stocking this year.”

http://health.einnews.com/article/357366554/cIRbySle251kuhYp?lcf=Hzf-KE6h-Xmcpvzwcdl3CuzbRmZ8XaTUdg3y3lN96pg%3D

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