How does Alzheimer’s affect the youngest among us?

My name is Emily, and I am the Development Associate and resident blogger at AGE. And I am a grandchild of Alzheimer’s Disease.

Or rather, I am a grandchild of a woman with dementia, likely caused by Alzheimer’s. It started when I was just 10 years old, and it has been over 15 years since my grandma started disappearing. It is no easier now than it was as a child.

First, she stopped cooking. It was how she showed her love and doted on us. I knew something was really wrong when my Grandpa, who had never really cooked, took over what had once been Grandma’s domain.

Then the more bizarre behaviors began- things that really mortified the kid I was at the time. Grandma would take out her dentures at the most inappropriate places to clean them, or she’d ask for ketchup at a Mexican restaurant because she couldn’t differentiate that from salsa, or she started to lose her ability to know when she should whisper in church or the movie theater instead of loudly observe things that you don’t say aloud in public.

And, of course, in crept the tell-tale sign of asking the same exact questions over and over and over again.

Grandma had an ‘angry’ period where she was occasionally physically and verbally violent, mostly towards my Grandpa. Then after a while, she became more and more juvenile- in the most joyful way. She became so affectionate, always reaching for a hand to hold.  And then, she became too affectionate, even with strangers. She has been known to sneak a kiss when a friend would try to just give her a hug, and since she’s in a wheelchair it’s quite easy for her hands to wrap around and give someone a little squeeze on the behind- it’s even happened to our pastor.

Mood swings and personality changes are common for those with dementia, but that was difficult to understand as child and even as a teenager. I sometimes felt annoyed at her behavior, angry at her outbursts, indifferent, confused, sometimes amused, and so very often deeply sad. Most of all, I felt beyond guilty for feeling anything but pure love and gratefulness for this woman.

As for the rest of the family, there have been stages of grief, denial, and bargaining for my parents and my aunt as they transitioned from being this woman’s children to being her caregivers. It has been an incredible journey of highs and lows, questions and transformations that have all fundamentally altered what my family looks like. Dementia changed my Grandmother, but it also changed us.

The irony is that she’s almost as fit physically now as she was five years ago. There’s no indication that she’s giving up yet, even if her mind has. The grandma I once knew has been almost completely devastated by whatever has taken residence in her brain. It has been a long progression. She hasn’t been able to walk for a few years now. She doesn’t really recognize any of us anymore. I don’t think I’ve heard a purposeful sentence from her in over a year. And these things can be hard for a child to witness and accept. “She looks fine, why won’t she talk to me? Why doesn’t she know you, Mom? How can she forget that she’s married?

I know my experience is not special or unique:  1 in 8 older Americans have Alzheimer’s disease. And there are over 15 million Americans providing unpaid care for a person with Alzheimer’s or other form of dementia (Alzheimer’s Association). That is a massive amount of individuals, spouses, children, and grandchildren being dragged through the mud of this disease. You are not alone. We can learn from our shared experiences. It’s important to tell your story. And it’s important  to include the children of your family in discussions about what’s going on with your loved one with dementia.

For those of you who have a child facing the immediate reality of dementia in either a parent or grandparent, there are some lots of resources out there to help you talk about dementia or Alzheimer’s. This disease is a bit different from others in that Grandma, or your uncle, or your Mom may look perfectly healthy on the outside. Kids need some help understanding the mechanics of this disease and that you can’t always see that something is wrong when someone is sick in this way. The two resources listed below have great information ranging from how to make the conversation developmentally appropriate to concrete tips and talking points:

Ultimately, I do not want to detract from unbelievably heartbreaking experience of those, like my Grandma, who are dealing with dementia themselves. Because it isn’t really about the pain of the rest of the family at all, it’s about allowing your loved one to experience the rest of their life with as much dignity and vitality as possible. Helping the children in your life understand what Alzheimer’s is doing to their loved one will make it easier for them to continue to see the person instead of the disease.

Reflecting back on the beginning years, Grandma never once talked about being aware of her diagnosis or what it was like for her. She sort of just slipped from the beginning stage where she was just ‘mildly’ forgetful to a place where she could no longer contemplate a question about her state of mind if she tried. I wish I knew what it was like for her. This journey has shown me that there many things I don’t know, and that there’s no ‘right’ way to be a supporter for someone with dementia. What I do know, Grandma, is that I will continue to love you wherever else this road takes us.

For those in the greater Austin area, AGE of Central Texas has a number of resources for caregivers and for those experiencing dementia. Click here to visit our website for more information.

KUT: UT-SOUTHWESTERN RESEARCHERS DISCOVER BRAIN COMPOUND

Interesting news and great research coming from our own Texas university research centers!

Researchers at UT-Southwestern Medical Center in Dallas think a therapy they’ve discovered can help patients with Alzheimer’s Disease and similar ailments.

UT-Southwestern Medical Center researchers have discovered a compound that may someday lead to improved memory for people with Alzheimer’s or neurodegenerative problems. Shelley Kofler of KERA in Dallas reports the scientists may have been working with mice but they had humans in mind all along.

Researchers Steven McKnight and Andrew Pieper discovered the P7C3 compound after introducing 1,000 different chemicals into the brains of mice. The compound seemed to allow new neurons to form in a part of the brain critical for memory. Older rats exposed to the compound showed a new ability to learn and remember tasks.

The scientists began their research about five years ago. McKnight, chairman of biochemistry at UT-Southwestern, says they had big goals right from the start.

“If we could be the people who could help stumble onto a way to keep cognitive capacity up, it would be spectacular for Andrew and me,” McKnight said. “That’s our aspiration.”

Pieper, an assistant professor of biochemistry and psychiatry, says the researchers took big risks to get big results.

Read more and listen at KUT.org.

Research: Case study on Alzheimer’s disease looks at progression before and after death

A case study from the Swedish medical university Karolinska Institutet sheds light on the pathological course of Alzheimer’s disease. The brain of the first Alzheimer’s patient to display amyloids demonstrable with a PET scanner has been studied both during progression of the disease and after death.

One pathological characteristic of Alzheimer’s disease is the accumulation in the brain of beta-amyloid proteins to form amyloid plaques. However, it is not known how early the plaques forms in the brain, whether they are the primary cause of the disease or what pathogenic role is played by other changes in the brain.

The very first PET scan in the world of amyloid plaque in a living patient with the amyloid-binding compound 11C-PIB was performed in 2002 by Professor Agneta Nordberg at Karolinska Institutet on a 56-year old Alzheimer’s patient. The researchers then monitored the patient as the disease progressed with regular PET scans and memory tests. After the patient died, the team carried out pathological and neurochemical analyses of the brain tissue.

The combined result analyses, which are now published in the renowned neurological journal Brain, give a detailed picture of how Alzheimer’s disease develops. For example, the results show that high concentrations of amyloid plaques were discovered at an early stage of the disease when the patient suffered slight memory loss. The levels remained unchanged during the course of the disease, in contrast to the increasingly declining energy metabolism in the brain, which was also measured using PET as the patient’s memory gradually deteriorated.

Read the full article at Physorg.com

NYT: Insights Give Hope for New Attack on Alzheimer’s

By GINA KOLATA

Alzheimer’s researchers are obsessed with a small, sticky protein fragment, beta amyloid, that clumps into barnaclelike balls in the brains of patients with this degenerative neurological disease.

It is a normal protein. Everyone’s brain makes it. But the problem in Alzheimer’s is that it starts to accumulate into balls — plaques. The first sign the disease is developing — before there are any symptoms — is a buildup of amyloid. And for years, it seemed, the problem in Alzheimer’s was that brain cells were making too much of it.

But now, a surprising new study has found that that view appears to be wrong. It turns out that most people with Alzheimer’s seem to make perfectly normal amounts of amyloid. They just can’t get rid of it. It’s like an overflowing sink caused by a clogged drain instead of a faucet that does not turn off.

That discovery is part of a wave of unexpected findings that are enriching scientists’ views of the genesis of Alzheimer’s disease. In some cases, like the story of amyloid disposal, the work points to new ways to understand and attack the disease. If researchers could find a way to speed up disposal, perhaps they could slow down or halt the disease. Researchers have also found that amyloid, in its normal small amounts, seems to have a purpose in the brain — it may be acting like a circuit breaker to prevent nerve firing from getting out of control. But too much amyloid can shut down nerves, eventually leading to cell death. That means that if amyloid levels were reduced early in the disease, when excess amyloid is stunning nerve cells but has not yet killed them, the damage might be reversed.

Read more at The New York Times website

News: Young Adults At Future Risk Of Alzheimer’s Have Different Brain Activity, Says Study

Brain maps showing increased brain network activity for the APOE4 carriers relative to non-carriers while at rest and while conducting a task. (Credit: Image courtesy of Imperial College London)
Brain maps showing increased brain network activity for the APOE4 carriers relative to non-carriers while at 'rest' and while conducting a task. (Credit: Image courtesy of Imperial College London)
ScienceDaily (Apr. 14, 2009) — Young adults with a genetic variant that raises their risk of developing Alzheimer’s Disease show changes in their brain activity decades before any symptoms might arise, according to a new brain imaging study by scientists from the University of Oxford and Imperial College London. The results may support the idea that the brain’s memory function may gradually wear itself out in those who go on to develop Alzheimer’s.

Click here to read the full article.