Why ADHD Kids Say I DON’T KNOW So Often

ide his bike (Who wouldn’t?). I asked Matt why he kept cancelling and he said, “I don’t know.” That got me thinking about how, in the past, I would have been slightly irritated at him wasting my time, not accepting my help, and being generally defiant.

We often become distressed by our children’s seeming inability to do simple things, like ask for help, put away their clothes, or turn in homework. We become disappointed and ultimately angry, and we confront our child.

“Why can’t you do this? It’s so simple. Everyone else is doing it with no trouble at all. Why can’t you?”

And you know the response, right?

“I don’t know.”

Gah! Why do they DO that?

ADHD children are very sensitive and having an angry parent is overwhelming to the senses. They may yell at you or try to distract you by talking about your faults. They may hide in their rooms or they may do what you want but give you the silent treatment. ADHD children are rarely able to manage their emotions in the moment, as they’re actually happeningIn confusion, frustration, and sadness that they’ve disappointed you, “I don’t know” becomes an easy way to slow things down, to stop the barrage of parental expectations.

Here’s what “I don’t know” really means:

  • I can’t help you. I don’t seem to be able to make myself do what I want to do.
  • Please don’t be mad.
  • I can’t take more nagging.
  • Do we have to keep having the same conversation? That won’t change me.
  • You can keep asking but I don’t have a different answer.
  • I feel like a loser and I’m trying to cover it up.
  • I don’t want to say the wrong thing.
  • I’m embarrassed by being a failure.
  • If I could answer to your satisfaction, I would.
  • My mind is (actually) blank.

This is why ADHD kids say “I don’t know” so often.boy with post-its

It has little to do with defiance and a lot to do with self-esteem and/or not being able to access information in a timely manner.

The truth is that Matt wasn’t wasting my time. I still had my time.

He wasn’t refusing my help. He just couldn’t handle this particular responsibility.

He wasn’t being defiant either. In fact, his response had nothing to do with me. He was simply postponing relief and prolonging his misery because he didn’t know how to make a different decision.

Change your response

The solution is to change the way you respond. Believe me, I know this is difficult. Sometimes it’s like pulling teeth to get an answer that contains some real information!

Instead of being frustrated, put yourself in your child’s shoes.

  • Imagine what it must be like to know that you’re having a regular conversation but you can’t respond in a regular way.
  • Imagine what it’s like to disappoint your parents, yet again.
  • Imagine experiencing this for an extended period of time.

My childhood experience

I remember, very well, the absolute confusion and disappointment I felt when I vowed to be good and couldn’t manage to hold it together for even 30 minutes. I had NO IDEA how I got from Point A to Point B, from my vow to my misbehavior.

This isn’t a moral issue or a problem with your child’s integrity. This is an Executive Function challenge. The pre-frontal cortex hasn’t developed enough to handle the demands being made.

One thing you can do to help your child is to say, “I’m sorry. I didn’t give you much time to think about this. I would really appreciate it if you’d take some time to think this over and let me know your answer. I’ll check back with you tomorrow/in an hour/after I get home…”

The moral of the story is:

Don’t take it personally, Don’t assume defiance, Practice patience, Be encouraging, and Give your child or teen the grace and dignity to JUST. NOT. KNOW.

When they do know, they’ll tell you.

Do you have any thoughts on this issue that you can share with another parent? Just scroll down to the comments section. I love hearing from you.

xo, Yafa

Copyright 2018 Yafa Luria/Margit Crane All Rights Reserved


What troubles you about parenting an ADHD child or teen?

Let’s talk! No judgment, no salesy come-on. However you WILL receive a good deal of TLC and a slew of strategies. You can say anything. You can cry. You can swear. Your confidentiality is guaranteed, and I promise to listen and give you hope and relief. (You might even find yourself spontaneously doing a happy dance).

“Thank you Yafa. You’ve given me incredibly helpful tools! It was really a pleasure to speak with you. I’ll be back in touch in the coming weeks.” Stella R, Portland, OR.

“I really appreciate that I could be vulnerable and you didn’t shoot me down. I feel comfortable with you and your humor brightened the call.” Danielle A, Bellingham, WA.

“I talked with you a year ago, Yafa, and your voice is always in my head, guiding me. I just wanted to email and thank you.” April W, Queensland, Australia

“Thank you for your encouraging, enlightening suggestions.” Jill E, Seattle, WA.

Thank you for ‘being there’ to share your wealth of knowledge and personal experience with us who are ‘floundering’ and ‘lost in the forest’ when it comes to ‘dealing with special and difficult circumstances’.Gratefully yours, Rochelle H, Alberta, Canada xox ((((BIG HUGS)))

Cerebral palsy: guide for parents

About one in every 400 babies is born with cerebral palsy. How much do you know about this condition? Would you cope if this happened to your child?

Some children with cerebral palsy manage to lead near-normal lives, others need constant care. Here is what parents of cerebral palsy children can do to give their children the best chance in life.

Learn more about the condition
A child who has cerebral palsy has difficulty with posture and movement. This is because of problems in the area of the brain, which control movement. This can either be the result of brain damage or sections that have not developed properly. This damage can take place during pregnancy, childbirth or during childhood. But the end result remains the same: the brain is unable to control muscle co-ordination properly.

There are many different types of cerebral palsy – in fact no two children with cerebral palsy are precisely alike. Some are so lightly affected that they have little more than a slight weakness or a limp, while others can have difficulties crawling, walking, sitting, talking, feeding or using their hands. Some children are affected on only one side of their bodies; others are affected mainly in the legs, while others are affected all over their bodies. A worst case scenario is when a child cannot control his/her muscles at all and will need to be looked after for the rest of their lives.

But not only movement is affected by cerebral palsy. Other areas of the brain could also be influenced. That is why many children with cerebral palsy also can have mental impairment, epilepsy, have difficulty swallowing or controlling their facial expressions, have difficulty speaking and could have problems seeing and hearing properly.

But that paints a very bleak picture, which is often far from the reality for a child with cerebral palsy. About half of all children with cerebral palsy have above average, average or only slightly below average intelligence and can therefore benefit from formal education, often in mainstream schools. The rest of the children have moderate to very severe intellectual disabilities. These children benefit from admission to training schools or special care centres.

In some cases the associated difficulties may be more handicapping than the movement problems. Probably the most devastating disability is the inability to communicate. Where a child does not have the use of his/her hands nor intelligible speech, it often requires considerable time, patient observation and experience to determine the child’s true intellectual level.

How is it treated?
It may be difficult to diagnose cerebral palsy in very young infants. The condition can often not be detected until a child does not develop the movement, posture and balance necessary for sitting and standing. Some types of cerebral palsy rarely become obvious before the child reaches two years of age.

There is no cure because damaged or underdeveloped brain cells cannot be restored. But treatment early in life can greatly improve the quality of life of these children. One person alone cannot manage cerebral palsy – ideally there should be team involved in the treatment. Apart from a doctor, occupational-, speech- and physiotherapists, other important members of the team include other medical specialists, the social worker, the psychologist, teachers and other caregivers.

But it is the parent who plays the most important role. The treatment team should give parents home programmes so that treatment can continue at home.

What you can do at home
One of the many things parents can do, is to help their children to communicate as best as they can.

The Cerebral Palsy Clinic offers the following tips:

  • Speak slowly and clearly.
  • Make eye contact when you speak.
  • Discuss whatever your child is interested in.
  • Use gestures, facial expression and body language when talking.
  • Label all items. For example, during bath time, label the bath items around such as soap, tap, towel and water.
  • Stick to the same words. For example, if the family uses the word “coat”, use it until your child understands and/or can say the word, then introduce the word “jacket”.
  • Improve vocabulary. For example, if the child says “car” the adult might say “mommy’s car” or “fast car” depending on the child’s interest.
  • Model the correct words for your child. If a child says something wrong, never say that it is wrong, rather repeat the word in the correct way. For example, if your child says “tock” for “sock”, you must repeat the right word.
  • Use words that express your child’s feelings, wants and intentions. For example, if your child points to a tap, you might say: “Drink/want drink”. Or if your child falls, you could say: “Ow, that hurt”.
  • Pause often and give your child a chance to process the information.
  • Use open-ended questions to encourage responses. For example: “I wonder who’s in the box?”.
  • Use as many words in a sentence as your child can or with one or two extra words.
  • Talk to your child about what is happening at the moment.
  • Take turns when you communicate – encouraging your child to respond.
  • Read to your child.

12 Struggles Of Having An Outgoing Personality But An Anxious Mind

Outgoing people with anxious minds – or minds that overthink – tend to feel anxiety the most intensely, often because we don’t talk about it. And by “often” I mean never.

Our anxiety is a contrast to our big, bold personalities. Strangers would never guess it. We never know when to fight or flight, and our self-angst is maxed out. We are often the life of the party but can also be mind-numbingly introspective, questioning everything.

1.  Our day normally goes something like this: Anxiety: Okay but what if – Me: Homie we went over this a thousand times and we totally resolved it. Anxiety: Yeah but I’ve looked at it from a new angle and there are like 15 more reasons why you should worry about it. Me: ……go on.

2.  We’re kind of a conundrum because we love people and need to be surrounded by people to be happy, but our over-thinking and our apprehension to immediately trust someone is, in fact, what makes us very selective about who we surround ourselves with.

3.  That might mean we’ll have lots of friends or acquaintances but very few close friends who we share our world with. But when we do, they become our entire life.

4.  We still find it easy to talk and connect with people – we can be charming creatures and when we do choose to grace a party with our presence, we are the life of it.

5.  But then we wake up in the morning and of course, we are over-thinking everything – Ahhh what did I say to that one person that rather die than act like an idiot in front of? Did I talk too much? And what did they mean by “I’ll see you soon?” What does “soon” even mean? Like soon soon? Or “soon”?

6.  Although we are very bold and outgoing, sometimes even the smallest things can stress us out and override our nerves. Whether it’s picking up our dry cleaning, finishing a project for work or making a call to our doctor, just the thought of having to deal with it makes our minds race.

7.  Dating is hard, we have to explain that we’re not insecure control freaks, we just think. A lot.

8.  I mean you don’t have to call us back right away when you’re out, but just know that our mind is playing out a bunch of horrible scenarios in which you’ve cheated. Or died. That’s right, if we reach your voicemail, we can’t help but consider that you might not be alive.

9.  Even the smallest gestures make us melt. We tend to be overwhelmed very easily, so anything you do to make our life easier is greatly appreciated. Picking us up for a date, playing with our hair when we’re watching a movie, calling to see how we’re feeling or making us a cup of tea comes with the highest of thanks. We will never take your gestures for granted.

10.  We’re hardest on ourselves, we are always gripped by the feeling that there’s more that we should be, or could be, doing in our life.

11.  We try to trick our brain by doing as many things as we can during the day so we can fall asleep at night – HA HA what were we thinking? This is our brain’s prime time to annoy us; it won’t miss this opportunity.

12.  We ebb and flow between wanting to be surrounded by many people, reveling in the attention we receive, to being very selective and sort of wanting to isolate ourselves to recharge and be left alone with our thoughts. Needless to say, we’re enigmas wrapped in bacon.

6 Things People Need to Stop Getting Wrong About Social Anxiety

For people with social anxiety, it can be frustrating to have to deal with the rest of the world not understanding what they’re going through—and casually misusing the phrase to refer to everyday experiences of discomfort or shyness. Thankfully, YouTube star Jessie Paege shared a spot-on tweet to help clarify what having social anxiety really means.

“Social anxiety is not ‘omggg I love Netflix and I hate everyone,'” Paege wrote earlier this week. “It’s longing to go to social situations that are easy for other people, wanting to use your voice, but feeling stifled, feeling trapped in your thoughts, and so much more.”

In fact, social anxiety (aka social phobia), is an intense anxiety or fear of being judged, negatively evaluated, or rejected in a social or performance situation, according to the Anxiety and Depression Association of America. It affects about 15 million American adults, the ADAA says, and is the second most commonly diagnosed anxiety disorder, after having a specific phobia.

Paege tells SELF that she decided to write her tweet to try to help educate people, especially those who throw the phrase “social anxiety” around without understanding it.

She grew up with severe social anxiety and went to several special education pre-schools as a result of her condition. “It was incredibly difficult and the topic of social anxiety is still very painful for me,” she says.

Paege says that she hopes her tweet clears up misconceptions about social anxiety disorder. “Mental illness terminology is thrown around too often,” she says. “I also hope this helps people respect those with social anxiety. Whether it’s a teacher that has a student that needs accommodations or a friends that’s bullying, social anxiety is serious and isn’t something people should throw around in an attempt to be ‘relatable’.”

The tweet exploded online, with many people weighing in with their own experiences with social anxiety and how, unfortunately, many people who don’t experience from the condition just don’t get it. Here are just a few things they want everyone else to know about social anxiety:

1. You can’t just turn it off or “get over it.”

Social anxiety is a legitimate mental health condition and medical diagnosis. Telling someone with social anxiety to “get over it” is like telling someone with diabetes that they can just will it away—it’s ridiculous and unhelpful.

2. You constantly obsess over what you could have done or said differently in social interactions.

People with social anxiety are often very self-conscious in front of others, and feel embarrassed and awkward, the National Institute of Mental Health (NIMH) says. They’re also very afraid that others will judge them, and may spend weeks worrying about social interactions.

3. It can bring on physical symptoms, too.

Many people with social anxiety can have a rapid heart rate, nausea, sweating, and even full-blown panic attacks when they have to go into a social situation they’re worried about, the ADAA says. People with the disorder often know that their fear is unreasonable, but still feel powerless to do anything about it, the organization says.

4. Public speaking can be terrifying.

Sure, most people aren’t exactly stoked to get up in front of their colleagues and give a presentation, but it can be debilitating for people who struggle with social anxiety disorder. Some social anxiety sufferers don’t have anxiety in social situations but have it only when it comes to performances, like giving a speech, playing a sports game, dancing, or playing a musical instrument on stage, according to the NIMH.

5. Even an activity that seems simple, like making a phone call, can trigger anxiety.

Any kind of social interaction can make someone with social anxiety disorder feel anxious, the NIMH says. That includes everyday things like meeting new people, going on dates, doing job interviews, answering a question in class, talking to a cashier at a store, talking on the phone, or using a public bathroom.

6. But the level of anxiety someone experiences on a given day can vary widely.

As with many health conditions, social anxiety is different for everyone—and one person’s experience with it may change from day to day.

But it is possible to feel better. If you feel like your anxiety is interfering with you ability to live your life—including your social life—that’s a sign that it’s time to check in with a mental health professional.

Celiac Disease Linked to Increased Risk of Pneumococcal Infection

Patients with celiac disease may have a significantly increased risk of pneumococcal infection, according to a new study published in The American Journal of Medicine.

Researchers conducted a systematic review of three manuscripts, with a final analysis including a total of 50,547 celiac disease patients.

After adjusting for socioeconomic index, diabetes, level of education, sex and age, an increased risk of pneumococcal infection among celiac disease patients was noted. Only one cohort compared the risk of pneumococcal infection in celiac disease to that of the general population, confirming a higher risk of infection among those with celiac disease (HR=3.90, 95% CI=2.20, 7.00). This persisted when the analysis included only biopsy-proven celiac disease (HR=1.46, 95% ci=1.05, 2.03).

Pooled data from the three cohorts found an overall odds ratio of 1.66 (CI 95% 1.43, 1.92) for pneumococcal infection among celiac disease patients compared to inpatient references.

The authors note that post-1998 data, after the pneumococcal vaccine was widely available, showed a lower risk of pneumococcal infection among celiac disease patients. This result, write the authors, supports the prophylactic use of pneumococcal vaccination.

There is currently no vaccine recommendation in place in the US for celiac disease patients. The study authors suggest this is “potentially missing a crucial opportunity to intervene and protect patients with celiac disease.” The authors conclude that, “vaccination against pneumococcal infection in celiac disease should be strongly recommended for all age groups.”

This drug helps babies with rare form of epilepsy. But its maker is no longer selling it.

For the first six months of Christian Mumm’s life, his family lived on high alert. Christian, who has a genetic disease that causes severe epilepsy, experienced frequent seizures – at his worst, one every 10 minutes – that left him depleted and jumpy. His three older brothers and sisters tiptoed around the house in New Hartford, Connecticut, afraid that if they breathed the wrong way or clinked a dish too loudly, it would set off a storm in his brain.

Christian’s mother, Erica Mumm, recalled one heartbreaking day when her 9-year-old daughter came to her in tears.

“I kissed him, Mommy, and he had a seizure,” her daughter said. “I can’t kiss him anymore.”

After a half-dozen drugs failed to help Christian, doctors suggested the family try one called Potiga.

The medicine has had a powerful effect. Seizures that once struck multiple times an hour now come once every five or six days. But the drug came with a deadline: At the end of June, GlaxoSmithKline, the British drug company that sells Potiga, pulled it off the market because of declining sales, forcing families to stockpile supplies or wean their children off a drug that dramatically improved their quality of life.

The dilemma faced by parents whose children benefited from Potiga – and future families who potentially may never have access to the drug – highlights the limitations of drug companies’ business model.

Drug companies’ investor-driven business model allows them to make risky research bets to develop innovative drugs. But at the end of the day, it means products that are essential to sick people are being made by businesses.

That may leave few options to small patient populations who depend on a drug.

“There are people who’ve already been taking the drug, and based on their perceptions, it’s helping. I actually find this one more heart-wrenching,” said Alison Bateman-House, an assistant professor in the division of medical ethics at NYU Langone Health. “Yes, we realize you were getting benefits, but because of financial realities, and just what we choose to do with our business, we’re not going to make the drug anymore.”

GlaxoSmithKline said it has recently been in touch with two families, including the Mumms, to find a way to make the drug available. But the company is not presently making commitments to future patients, and its ability to supply the drug is not indefinite, because the remaining supply will eventually expire.

“We care deeply about patients and realize that any time a medicine is removed from the market it can be challenging,” GSK spokeswoman Sarah Spencer said in an email. “At this time, our focus is on the very small number of patients who are currently receiving the product.”

Christian’s severe form of epilepsy stems from a mutation in a gene called KCNQ2. That mutation causes electrical signaling in Christian’s brain to go haywire, and Potiga – though it was approved as a general seizure drug for adults – had a unique mechanism among epilepsy medications. It worked by targeting the precise biological defect that was at the root of Christian’s disease.

Christian still suffers developmental delays, but his quality of life is vastly improved. On the drug, he can interact with his siblings. He babbles and can learn and build on simple abilities, such as eating by mouth and smiling.

Physicians who treat and study patients like Christian say Potiga is a quintessential example of how 21st-century medicine is supposed to work. As scientists learn more about the biological causes of disease, they will be able to design drugs or rediscover old ones that treat not just symptoms but also the root causes of illness. Potiga was developed and approved to control seizures in adults with epilepsy, but it came with a bonus – it worked in a new way, by targeting potassium channels in the brain.

“Here we have 30 years of NIH-sponsored and industry-sponsored research leading to the specific understanding of a catastrophic illness. We have a drug that acts on that mechanism,” said Edward Cooper, an associate professor of neurology and neuroscience at Baylor College of Medicine. Taking it off the market “goes exactly against what our policymakers are explicitly trying to do, which is make available precision medicines to address unmet medical need.”

According to a 2011 study in Pharmacoepidemiology and Drug Safety, 118 novel drugs were withdrawn from the market between 1980 and 2009. Only a fifth of them were withdrawn primarily because of safety issues.

The plight of families who depend on Potiga is far from common, but it could become more so with the increasing recognition that a medicine that fails one group of people may be critical for another subgroup. There’s a major push in medicine toward using science to identify the set of people for whom a drug works.

But when drugs live or die depending on commercial viability, mass-market drugs that don’t fulfill their initial purpose may not be available.

From another point of view, Potiga is simply not a very good drug – an epilepsy medicine that was only ever approved for adults and turned out to have a big safety downside.

After it was approved in 2011, a scary side effect that caused blue-tinged skin and possible vision problems was uncovered, leading to a severe “black box warning” on the drug’s label. The safety problems made Potiga considerably less attractive than the other options available to the people it was approved to treat – adults with epilepsy. The drug was never tested in children because of the safety concerns and a hold on trials by federal regulators, according to Spencer, the GlaxoSmithKline spokeswoman.

“No neurologist has become dehydrated for weeping tears over the removal of a drug with so much promise and so little performance!” Robert Clancy, a professor of neurology at the Children’s Hospital of Philadelphia, wrote in an email.

Potiga sales peaked in 2013, at $14 million in U.S. sales, according to data from QuintilesIMS, a company that tracks health-care data – far from analysts’ original estimates that it could reach more than $200 million per year. When GSK announced it would discontinue the drug last summer, there were fewer than 500 prescriptions per month.

The Mumms have stockpiled as much of the drug as they could, spending about $1,200. They have about three months left. In late July, they finally got word that the company would help them get access to the medicine, but they have no idea how long the commitment will last.

“If they can do this to my kid, they can pull any other drug off the shelf of your medicine cabinet and do this to anyone else, without a second glance,” Erica Mumm said. “These companies have great power, and they shouldn’t be driven solely by profit. They do have an ethical responsibility to the patient.”

Spencer said that GSK is open to discussions with other companies that may want to acquire Potiga but has not seen significant interest in the drug. She also noted that if a company acquires the rights to Potiga, it would still be approved only for use in adults.

Doctors can prescribe drugs for off-label use as they see fit, but if the company wanted to market Potiga specifically for a rare disease, it would need to conduct a trial to get approval. It would have to get the hold on pediatric research lifted.

Other than selling the drug to another company, there may be other options.

“There are these really niche markets in the corners of the pharmaceutical marketplace that need extra attention,” said Aaron Kesselheim, an associate professor of medicine at Harvard Medical School. “If there was a nonprofit pharmaceutical manufacturer that wanted to jump in, this is the sort of place that could be a good possibility.”

The current solution is a piecemeal approach.

Amy Buches has been told the company will find a way to provide the drug to her son, Stephen. The Bucheses are one of the two families that GSK has agreed to help get the drug.

Buches said that she is personally satisfied. “Yet, it is unsettling to know that there could be an infant born in the world this very moment that would benefit from Potiga, but will not be able to use it,” she said in an email.

Mumm knows firsthand what it would mean to lose access to the drug.

In May, the Mumms – having heard that the company would not be making the drug available – began to wean Christian off Potiga. His seizures started up right away, multiple times an hour.

Mumm was in despair. Without the ability to control his seizures, the doctors were sedating her son. She emailed his palliative-care doctor. What was she supposed to do? Bring her son home in a fog of medicine and watch him disintegrate?

Just a few weeks earlier, Mumm had been hopeful, thinking about starting a new kind of therapy that could aid Christian’s development, thanks to the improvements she had seen while he was on the drug.

Instead, she found herself asking if there would be a way to ensure her son had a peaceful death.

“I want to get all my ducks in a row with knowing options,” Mumm wrote.

Mumm demanded that the doctors stop tapering his medicine, and her family went about securing as much of the drug as they could stockpile.

In July, company representatives got on a conference call with the family and Christian’s medical team to find a way to give him access to the drug.


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New pill could help Alzheimer’s patients


PHOENIX – It was just last week that the world said goodbye to the Rhinestone Cowboy. Country music star Glen Campbell passed away after a long battle with Alzheimer’s Disease. For the millions of Americans with the same diagnosis, there’s not much the medical world can do to help, but there’s a new drug being tested right now that could change lives.

On a Thursday afternoon, Doctor William Burke is making his rounds at the Banner Alzheimer’s Institute in Phoenix. One of his patients is Diane Scheel. She was diagnosed with the disease in 2012.

“It was really hard on me,” says Scheel. She’s 61. She’s already stopped driving and even had to give up being a dental hygienist – a career she had for 30 years.

“I was always active and everything like that and I never would have thought in a million years that I would have it – but it was there.”

The fact is, there are five million Americans right now living with Alzheimer’s. About 130,000 are right here in Arizona. This year the disease will cost the nation $259 billion. By 2050 the cost will go up to $1.1 trillion according to the Alzheimer’s Association.

Right now there are two FDA-approved drugs that help control the disease. You take them at the same time. Banner is testing a third pill to see if it will help those other drugs work better.

“It has been a decade since there’s been anything new approved so this would be the third medication,” said Dr. Burke.

According to the Alzheimer’s Association, since 2000, deaths from heart disease have decreased by 14 percent while deaths from Alzheimer’s have increased by 89 percent.

Scheel is on the clinical trial and is hoping the new drug will work for her and everyone else battling the same thing. “I’m stronger than I thought I was,” said Scheel. “But it was hard because there was a lot of tears – but I think I can handle it.”

Interested people and caregivers interested in participating in the SUVN-502 study can contact Banner Alzheimer’s Institute in Phoenix by calling 602-839-4894, or Banner Sun Health in Sun City at 623-832-6530.


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Losing sense of smell could signal Alzheimer’s: McGill researchers

If you have a hard time identifying specific smells, it could be a sign that you are at risk for developing Alzheimer’s disease, a group of McGill researchers has found.

The study, published in the journal Neurology, looked at whether a simple smell test could reveal someone’s susceptibility to the disease.

“Despite all the research in the area, no effective treatment has yet been found for Alzheimer’s disease,” John Breitner, one of the study’s authors, said in a statement. He is the director of the Centre for Studies on Prevention of Alzheimer’s Disease at the Douglas Mental Health Research Centre of McGill University.

“But, if we can delay the onset of symptoms by just five years, we should be able to reduce the prevalence and severity of these symptoms by more than 50 per cent,” Breitner added.

The study looked at nearly 300 people, with an average age of 63, who were considered at risk of developing Alzheimer’s because they had a parent who had the disease. Of those, 100 volunteered to have regular lumbar punctures to measure the levels of Alzheimer’s-related proteins in the cerebrospinal fluid.

The participants were given multiple-choice scratch-and-sniff tests and asked to identify such scents as bubble gum, gasoline or lemon.

Researchers say the tests revealed that those who had the hardest time correctly identifying the smells also had the more evident biological signs of Alzheimer’s.

“This is the first time that anyone has been able to show clearly that the loss of the ability to identify smells is correlated with biological markers indicating the advance of the disease,” Marie-Elyse Lafaille-Magnan said in a statement. She is a doctoral student at McGill and the first author on the study.

“For more than 30 years, scientists have been exploring the connection between memory loss and the difficulty that patients may have in identifying different odours. This makes sense because it’s known that the olfactory bulb (involved with the sense of smell) and the entorhinal cortex (involved with memory and naming of odours) are among the first brain structures first to be affected by the disease.”

Despite the results, researchers say that more work must be done to see how the loss of the sense of smell relates to the progression of Alzheimer’s.


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Alzheimer’s disease: Targeting enzyme may reverse memory loss

After many years of research, scientists have found that by blocking one specific enzyme, Alzheimer’s-related memory loss could be reversed or prevented.

A new study has suggested that it may be possible to reverse the memory loss that occurs in Alzheimer’s disease with drugs that selectively block the ability of the HDAC2 enzyme to interfere with the communication between brain cells.

Previous attempts to target HDAC2 have not been satisfactory because the drugs that were used also disrupted other functions of the enzyme, producing toxic side effects.

Now, research has shown that blocking a molecule called sp3 that binds to HDAC2 might be a way to stop them both from disrupting synaptic function, or the communication between brain cells that is important for memory.

A report on the study, led by researchers from the Massachusetts Institute of Technology (MIT) in Cambridge, is published in the journal Cell Reports.

Senior author Prof. Li-Huei Tsai, director of the Picower Institute for Learning and Memory at MIT, says that they believe that HDAC2 is a master regulator of genes that control memory and that because its levels are raised in Alzheimer’s disease, it blocks the expression of those genes.

“If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels,” Prof. Tsai explains, “then we can remove the blockade and restore expression of all these genes necessary for learning and memory.”

Growing number of people with Alzheimer’s

Alzheimer’s disease is the most common form of dementia, a progressive brain-wasting condition that gradually diminishes people’s ability to think, remember, reason, and make decisions.

As the symptoms worsen, people lose the ability to hold a conversation and respond to what is happening around them.

Experts do not yet know exactly what causes Alzheimer’s disease, but they say that it could be due to several factors that arise differently in different people.

Although it can affect younger people, Alzheimer’s disease is more common among adults aged 60 and older.

Around 5 million people are thought to be living with Alzheimer’s disease in the United States, and this number is expected to rise to 14 million by 2050.

Synaptic plasticity

The new study concerns the disruption of a biological process called synaptic plasticity, which is thought to be important for learning and memory.

Research on what happens at synapses – which are the junctions between brain cells – has revealed that they are “plastic” and not fixed as the soldered joints in electronic circuits are.

Synaptic plasticity is defined as a biological process whereby synapses change over time, depending on specific patterns of activity.

The synaptic changes affect various properties, including the strength of communication between brain cells, which impacts memory.

Prof. Tsai has been researching the role that enzymes called HDACs play in memory loss for over a decade. In 2007, she discovered that blocking HDAC activity in mice could reverse memory loss. There are around a dozen types of HDAC in humans.

HDAC2 blocks memory-related genes

HDACs affect memory by altering histones, which are the proteins that help to package DNA into a structure called chromatin. The effect of HDAC is to condense chromatin, which, in turn, reduces the expression of some genes in the DNA.

In later research, Prof. Tsai found that a particular HDAC in humans called HDAC2 blocked some genes that are important for memory, and that levels of the enzyme are higher in people with Alzheimer’s and also in mouse models of the disease.

Compounds that inhibit HDAC2 have already been tested, but most of these have undesirable side effects. For example, they interfere with HDAC1, which is important for cell proliferation, especially in white and red blood cells.

Therefore, Prof. Tsai and colleagues set out to find a way to target only the activity of HDAC2 that interferes with memory by searching for proteins that help the enzyme to bind to the relevant genes.

Gene expression data from post-mortems of people who did not have Alzheimer’s disease – some whose brains had high and some whose had low levels of HDAC2 – helped the team to find more than 2,000 genes that might be involved with HDAC2 activity.

Sp3 helps HDAC2 to block memory genes

Using other information that they already had about how the genes behave with HDAC2, the team whittled down the candidates to three.

Further tests on these three led them to Sp3, a “transcription factor” molecule that helps HDAC2 to alter chromatin and block the memory genes on the DNA.

Gene expression data from post-mortem samples taken from brains of people who died with Alzheimer’s disease revealed a strong link between levels of HDAC2 and Sp3.

The researchers then showed that reducing sp3 expression in a mouse model of Alzheimer’s disease restored the animals’ ability to form long-term memories.

Our findings indicate that targeting the HDAC2-Sp3 complex could enhance cognitive function without affecting HDAC2 function in other processes.”

The team also found a molecule that might serve as a basis for developing a drug that prevents sp3 from binding to HDAC2 to free up the memory genes. They showed that the molecule does not interfere with cell proliferation, as some other HDAC inhibitors do.

Prof. Tsai says that there is further work to do – such as finding a smaller version of the molecule – before they can settle on a suitable experimental drug candidate.

She also wishes to find out how many other genes might be teaming up with HDAC2, which could lead to other drug targets.


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What causes seizures in sleep? Nocturnal epilepsy explained

Epilepsy is a serious condition that is characterised by uncontrollable limb twitching, jerking, and in many cases, loss of consciousness.

Caused by abnormal activity in brain cells, seizures can affect brain processes and lead to symptoms such as confusion, a lack of awareness, staring into space and loss of bodily control such as bladder function.

Symptoms vary according to the type of seizure, and some will only suffer from seizures while sleeping – this is called nocturnal epilepsy.

Here is everything you need to know about the condition.

What is nocturnal epilepsy?

Man in pajamas is sleeping. An alarm clock is standing next to his head.

A seizure disorder where seizures only occur while sleeping. Epilepsy is categorised as nocturnal if it’s triggered only while one is sleeping.

However, if someone is awake during a time they’re normally sleeping, a seizure can be had while awake.

What are the symptoms?

People who have nocturnal seizures may notice unusual conditions around them when they wake up, such as having a headache, bedwetting, discovering they’ve bitten their tongue, muscle strain, weakness or fatigue, lightheadedness, and bone or joint injuries.

They may wake up on the floor, or find objects near their bed have been knocked to the ground.

When do the seizures happen?

Most nocturnal seizures take place during light sleep – either soon after falling asleep, before waking or during arousal over the course of a night.

Early nocturnal seizures take place within the first or second hour of going to sleep, early morning seizures happen one or two hours before the usual time of awakening, and they can also occur an hour or two after waking up.

They’re not limited to just night time, either – nocturnal seizures can happen during an afternoon nap, too.

What causes nocturnal seizures?

The cause of seizures are often unknown, but can be linked to unusual brain development, stroke, brain tumours, serious head injury or reduced levels of oxygen reaching the brain.

Certain seizure conditions are more likely to result in nocturnal seizures. These include frontal lobe epilepsy, awakening tonic-clonic seizures, juvenile myoclonic epilepsy, Landau-Kleffner syndrome and Benign Rolandic epilepsy.

How is it diagnosed?

Such a condition can be difficult to diagnose, purely because the symptoms take place while the patient is unconscious.

Because of this, it can also be hard to know how long they’ve been present, or the average duration of each seizure.

Can it be treated?

When a patient suspects they have nocturnal epilepsy, a doctor can treat the condition with anticonvulsants.

It’s important to find the right type of medication, as anticonvulsants can disrupt a person’s sleeping structure – and a regular sleep cycle is essential, as undisrupted sleep will lower the likeliness of symptoms appearing.




































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