Monday, September 26, 2011

Friends that won't stay

This next piece really hit home for me.  My parents had a lot of friends and there were more that stayed around after my dad's diagnosis came out in the open, then didn't stay, but there were those ones that just never came back around.  Some would still come by to ask my dad to help them with their car or borrow a tool, but when they started seeing changes in him they ran for the hills.  This story tells how it feels to the one that has this disease that some people just don't really know anything about, and can't face the hard core truth.  I'm so thankful for the friends that stuck by my parents and held my dad's hand right up until the end.  True friends!!

Why the Stigma?
This is a question I have been asking myself for nearly two years now.  I have experienced firsthand how many "Friends" I have lost since announcing my early onset and have also been abused just for being me?  All this I don't understand.  (I would just like to say that the support I have had from family, a few friends, and complete strangers has been overwhelming and far outweighs the negative comments, but hey!! Everybody is entitled to an opinion.)

It's the two words Alzheimer's and Dementia that seems to start some kind of mental chain reaction where people's minds go into overdrive and imagine God knows what??  Do I sound insane?  Are my writings the work of someone like a literary Picasso?? I certainly hope not.  So, what is it that sparks such a bad reaction?
I have tried to figure a few things out and come to a couple of conclusions.
Fear of the unknown is almost certainly one of the reasons.  I myself don't like unpredictability so I can sort of understand where that is coming from but yet am I alone in wanting to find out all about something I don't know?  Especially when it involves a friend?  Surely I can't be? As must it help a friend so much if I understood the illness better, which brings me onto my next point.
Not understanding the illness.
Why is it that when I tell people I have Alzheimer's they either "Laugh" thinking it's a joke?  Or cock their head to one side (No idea what that's supposed to achieve but it actually does happen lol!)  and start to look you up and down.  Quickly followed by a sharp exit after the lamest excuse you can imagine. 
Do they not understand how hurtful this is? Especially when it is someone you know or have known for years?  Yes!!! I have Alzheimer's:  Yes: there is no cure: and YES: I am frightened half to death, BUT!!! I am still the same person, with the same feelings.  I eat the same as you; I breathe the same as you and I love my family and friends the same as you, I AM THE SAME PERSON!!!
This terrible illness knows no rules and is indifferent to age, race, or creed so this is a plea from an early onset sufferer, who by the grace of God, a loving family and a very good consultant.
I am still able to Blog, talk for ages (most days), write, and play with my grandchildren.  I am no different to you really, just a bit forgetful at times but hey!! Who isn't??.

-Norman McNamara

I Haven't Got the Plague
As I walked through town today,
I saw a friendly face,
But as he walked toward me,
He then walked past with pace,
Im sure that he had seen me, and saw my friendly wave,
Ive only got Alzheimer's and not Bubonic plague,
Why do people treat me so, why are they so cruel,
I'm just the same as them, not some bumbling fool,
Some are freinds I have known, all my working life,
Who used to chat and laugh, to both me and my wife,
But now most of them act, as if I don't exist,
And all the good times that we had, are just a mistant mist,
I still laugh and I still cry, and still know that they're there,
Even when they ignore me, without a gleeting care,
But at least I known now, who really are my friends,
And one that I can trust, right up to the end,
So those friends I have lost, I say to one and all,
I hope the dementia demon, never comes to call.

Granddads words

My children were to young to remember my dad, but my nieces were older and have memories of him.  Their J-Pa.  This piece of a story reminded me of him with them and I know he would have said in his own words the same thing.  His speech was one of the very first things to go, way before he even got farther along in the stages. So he couldn't tell us what he was feeling, so I think a lot got unnoticed.

"Is that the grandkids?? Hello my lovelies!! Your granddad is still here even though he's more grumpy these days not like he used to be. I've sat here for quite a while now and watched you all grow into your own persons.  I just want you to know how proud I am of you all.  I hear you asking grandma  "Why does granddad not speak anymore?"  And "Will granddad ever get better?"  I just want you to know that while you keep coming round and seeing grandma and me we appreciate it very much, even though I do sometimes jump a mile when you make a loud noise!  Don't worry, children are supposed to be noisy. (just don't tell your gran I said that)"

Now talking to his wife
"As I look around I see all the home made Easter Eggs are as beautiful as ever.  I am so pleased you have kept that tradition up, I wouldn't have liked it if you hadn't.  I haven't gone anywhere yet, I'm still here my love, you just can't hear me.  But when you talk to me so gently and look into my eyes I will blink two or three times just to show you I'm listening, or I will try anyway.  Just wanted you to know I am listening to what you say and love hearing the latest news from the family. "

- Norman McNamara

Sunday, September 25, 2011

A forgotten thought

I wanted to share this.
Today I was outside, enjoying the cool breeze that Oklahoma seldom has.  I love this time of year so much.  I thought of something, and came in to do it, but I was approach by one of my daughter's telling me something that she was doing with her friends outside as our dog is having some kind of anxiety attack, I call it,  because she wants to be outside with the kids and she can only stay in her fence. (very protective, and Playful Mastiff)  Then I noticed the dryer had stopped so it was time to rotate the laundry.  As I was folding clothes I realized I had no idea what I had came in to do.  This was certainly not it, and my thoughts began to spiral as I tried to remember what it was.  What was I thinking about, what made me think of this "something"?  I couldn't think of it and it was driving me crazy trying to remember what it was.    
If I had no idea I had an Alzheimer's gene in my family I wouldn't think twice of me forgetting this thought being anything other than having a lot going on all at once.  Which is very normal for me.  But because I do and I'm not 100% sure I don't have the disease, I automatically think I am starting to show signs.    
Then, I made myself stop.  I thought,  "You can not start this because if you start thinking every time you forget the littlest thing means you have Alzheimer's, then it will ruin your life."   Every one forgets things here and there, and I'm not going to give in even if I find out I do have it.  I'm not going to let "maybe" or "definitely" ruin my life.  I'm not going to stop fighting until I'm completely unconscious of everything around me.  Even then I hope I still have it in me to keep fighting. 

Just something I wanted to share for those of us with the demon gene in our DNA.  Don't give up while you still are able to make a difference.  Don't give up when there still isn't a cure.  We gotta keep on fighting!

Tuesday, September 20, 2011

Go Purple on September 21st!

September is World Alzheimer's Month (WAM). Join us in the fight against Alzheimer's by honoring the heroes that fight against the disease every day — and become a hero by helping to raise awareness. 
September 21st is Alzheimer's Action Day.  Wear purple to raise awareness.  My children are wearing their purple shirts to school that they wore to the Walk to End Alzheimer's.  

Tuesday, September 13, 2011

Dementia Awareness Day. September 17th

This is Norm's videos and links to his books.  I am planning on putting some of his amazing work on here.  Please come back for more.

Here is his wife's story.  You go girl!!

Here are his books.  I have read the first one "Me and my Alzheimer's".  I would recommend these to anyone, even those that are not personally effected by the disease.  It is such a great insight to what a person suffering from Alzheimer's is feeling and goes through on a day to day basis.  Huge eye opener for me.

Saturday, September 10, 2011

Needing a push in the right direction.

   Any type of Alzheimer's is gut wrenching and means the person diagnosed is going to die.  No matter if you are 70 or 40 when diagnosed.   The gene my family carries does effect individuals at a lot earlier age and has a specific name, but it doesn't mean I feel like ours is any worse than those that are diagnosed at a later age.  I sometimes think people think that the elderly just don't matter anymore.  "They are old, they have lived their lives, why try and find a cure for whatever they have, they can't benefit the world anymore."   If everyone felt this way, then why try to fight for anything.  These "Elderly" are part of our heritage, our family tree, our whole being of existence.     ( God is first, but you get what I'm saying)  So, if you give up on them, are you saying you give up on yourself as well?
My type of Alzheimer's ( I still do not know if I carry the gene, but family members of mine do)  was given to me while I was growing in my mother's womb.  I will carry this gene, part of my DNA, all throughout my life.  My dad was one of the first to be tested within this type of research for Early On-Set Alzheimer's, and since the 1990's scientist have progressed so much with the facts and diagnosis for people with Early and Late on-set Alzheimer's.  This type doesn't sneak up on you gradually when you are 65 or older.  This type hits you unexpectedly in your 30's to 40's. Yes, I'm sure there are signs something may be wrong before, but the whole horrible disease hits you as a young adult.  (Most people I know still have young children living at home at this age. I have four, ages 9-3 and I'm 29.) That is just four more reasons I want a cure.  If I do have the gene each one of children have a 50/50 chance of having it as well.  If researchers, scientists, and doctors know so much more then they did ten years ago, I'm certain within the next ten there will be something to stop the disease.  I pray sooner, but this is where we step in as being advocates, caregivers, volunteers, donators, victims, ANYTHING to find a cure.
I may have this disease, I may not.  If I don't, THANK THE LORD.  I am NOT going to stop fighting though.  I have decided to dedicated my life to this disease. (to find a cure)  
If I do have it, and I am going to find out when I do go do the testing. (Still details to be prepared)
You better get ready.  I'm not going to wither away, feel sorry for myself, or hide.  I've been given this life, and I intend on living it to the fullest. I went through this horrid disease with my father, and so many of my family members are going through it as we speak.  Why wouldn't I do this?  I want to help anyone and everyone.  I certainly don't want to just find a cure for AD.  I would love to help with every disease and illness that doesn't have a cure.  This one is just very personal to me.
I've been at a stand still lately on what to write, and what I can do next.  I've been very busy lately with my kids, so time on here is pretty limited.  I can't stop thinking about it, and it consumes my every thought.  I just don't know what my next step needs to be.  For anyone reading please give me ideas if you have any.  I would greatly appreciate any. 

Sunday, September 4, 2011

Some Scientific Background

These are some facts I found on Familial Early On-set Alzheimer's.  The presenilin 2 gene is what the DeMoe's carry.  

Alzheimer's is the opposite of cancer.
Cancer is runaway cell growth.
Alzheimer's is runaway cell death.
—SANDRA STEINGRABER, Origins of Dementia, Part 2

Alzheimer's disease is classified in two ways: by heritability and by age of onset. Familial AD (FAD) follows a certain inheritance pattern, whereas sporadic AD, according to current research, does not show an inheritance pattern.

Alzheimer's disease is also classified as either early-onset or and late-onset. Early-onset AD occurs in people younger than 65 and is called pre-senile dementia. Late-onset AD, the most common form of the disease, occurs after age 65 and is referred to as senile dementia Alzheimer's type (SDAT). Fortunately, early-onset AD is rare (about 5% to 10% of cases) and affects people between the ages of 30 and 65. It often progresses more rapidly than late-onset AD. Some forms of early-onset AD are inherited.
Research to date indicates that most familial AD has an early onset and that about half of all cases of FAD are known to be caused by mutations (defects) in three genes located on three different chromosomes:

    Mutations in the APP gene on chromosome 21
    Mutations in the presenilin 1 gene on chromosome 14
    Mutations in the presenilin 2 gene on chromosome 1

Everyone inherits two copies of each of these genes—one from each parent. A parent carrying a defective version of one of these genes has a 50-50 chance of transmitting the defective gene to each of his or her children. A single defective version of any one of these three genes will cause early AD nearly 100 percent of the time.
This type of inheritance pattern is called autosomal dominant inheritance. The total known number of these cases is small—between 100 and 200 worldwide. There is no scientific evidence that links these mutations with the more common sporadic, late-onset AD.

Presenilin 1 is a protein found in brain cells. Its function is unknown. However, it may be involved in protein production and trafficking, especially during early development. More than 40 different mutations have been found in the presenilin 1 gene, and these mutations associate with early-onset familial alzheimer's disease. The disease strikes as early as 28 and as late as 62, with an average age of onset in the mid-forties. Mutations in presenilin 1 tend to elevate levels of amyloid beta in the blood, cerebrospinal fluid, and brains of those affected by mutations. Again, mutations in the presenilin 1 gene are dominant. This means that if a mother or father has the mutated presenilin 1 gene that causes alzheimer's disease, then each of their children has a 50-50 chance of having the mutation. Those children with the mutation have an almost virtual certainty of developing the disease.

Nearly 5.2 million Americans are living with Alzheimer's disease; although most of them are older, about 5% have a form of the disease called early-onset Alzheimer's. This condition can be diagnosed in people in their 30s, 40s, and 50s.
Although early-onset Alzheimer's disease is rare, those who suspect that they or a loved one have it should seek the advice of a physician immediately, regardless of age. New medications show promising results in slowing the progression of the disease. And although the diagnosis is certainly scary, a proactive approach is not only practical but can give those affected some sense of control over what lies ahead.

All Alzheimer's disease involves the progressive degeneration of the brain cells, beginning with the hippocampus, the area of the brain that processes memories, and the cerebral cortex, which is responsible for decision making and thought processes. Scientists aren't certain what causes the degeneration or why the progression of the disease varies tremendously among individuals. Most cases of late-onset Alzheimer's disease, usually diagnosed in people over the age of 65, are what researchers call "sporadic" or not necessarily hereditary, although the trigger hasn't been identified. However, researchers agree that almost all early-onset Alzheimer's disease is inherited.

A Strong Genetic Link
Inherited Alzheimer's is also referred to as familial Alzheimer's disease (FAD). According to the National Institute on Aging, if a parent has the familial form of early-onset Alzheimer's disease, his children have a 50% chance of developing the condition.
Mutations on three genes have been linked to familial, early-onset Alzheimer's disease. These genes have been labeled PS1, PS2 and APP by researchers.

Research from the 1990s indicates that mutations on a gene labeled PS1 may be responsible for 30% to 60% of early-onset Alzheimer's cases. Newer research is inconclusive regarding the exact prevalence of specific mutations, but confirms that a PS1 gene is the mutation most commonly linked to FAD.
It is possible to undergo genetic testing for these gene mutations, but there are many pros and cons to doing so, ranging from being able to provide this important health information to your children to coping with the knowledge that Alzheimer's is inevitable. A trusted doctor or genetic counselor can help you decide whether genetic testing is right for you or a loved one. Be sure to check with your insurance company before pursuing testing, because the coverage for costs of testing varies, and some policies don't pay for any of it.

ScienceDaily (June 11, 2010) — Researchers have discovered how mutations in the presenilin 1 gene cause early-onset Alzheimer's disease (AD). The finding, reported online in the journal Cell, opens the door to developing novel treatments for this form of the mind-robbing disease and for the more common, late-onset form that develops later in life and affects millions of people worldwide. 
The presenilin gene is most commonly associated with the early-onset familial form of Alzheimer's, which runs in families and can strike people in their 30s. The gene was discovered 15 years ago, but until now no one understood how mutations in the gene caused the disease.

The researchers led by Ralph Nixon , MD, PhD, professor in the Departments of Psychiatry and Cell Biology at NYU Langone Medical Center and director of the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research, discovered that the presenilin 1 gene performs a crucial biological function that enables cells to digest unwanted proteins and is essential for brain cell survival. The mutations, they report, disrupt this cellular protein-recycling process, killing nerve cells.

"In mouse models of Alzheimer's disease and in skin cell of patients with Alzheimer's disease caused by presenilin mutations, we observed that the ability to break down and reuse normal proteins and to remove potentially toxic damaged proteins and organelles is severely impaired," says Dr. Nixon who is also director of the Center of Excellence on Brain Aging and the Silberstein Alzheimer's Institute at NYU Langone Medical Center. The impairment can kill nerve cells, and the loss of neurons does not appear to be dependent on amyloid beta, the plaque-forming protein found in the brains of patients.

"Most of the drug development for Alzheimer's has been focused on removing amyloid from the brain," says Dr. Nixon. "Our findings strongly suggest that there are alternative pathways that can be targeted as well. For example, therapies could be aimed at repairing the cellular mechanism that eliminates toxic proteins before they damage the brain."

Preliminary observations from ongoing studies at the Nathan Kline Institute, says Dr. Nixon, indicate that similar disruptions of the cellular protein-recycling process occur in neurons affected by late-onset Alzheimer's, suggesting that factors other than mutations in the presenilin gene can also impair this process.

More than 160 rare mutations in the presenilin 1 gene and two others have been found to cause early-onset familial Alzheimer's disease. Only a few genes associated with late-onset form of Alzheimer's, the most common form of senile dementia, have been identified so far.

"Presently, no effective treatment exists to either slow or prevent the progression of Alzheimer's disease," says Dr. Nixon. "There is urgent need to see Alzheimer's disease as multi-factorial and to approach the treatment from that perspective."

Funding for this research was provided by the National Institutes of Health (NIH) and the Alzheimer's Association. The study was done in collaboration with NYU Langone's Silberstein Alzheimer's Institute and the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research (NY); The Marion Bessin Liver Research Center at Albert Einstein College of Medicine (NY); Osaka University Graduate School of Medicine (Japan); University of Alberta, Edmonton (Canada); and the University of Chicago (Illinois).

Co-authors include Ju-Hyun Lee, Haung Yu, Asok Kumar, Sooyeon Lee, Panaiyur S. Mohan, Corrinne M. Peterhoff and Devin M. Wolfe of NYU Langone Medical Center. Dr. Yu is presently at the Taub Institute, Columbia University.

Thursday, September 1, 2011

Walk to End Alzheimer's a success

Here is our team from the 2011 Walk to End Alzheimer's in Tulsa, Oklahoma.  There are a few more that aren't in the picture.  It was so much fun, and there were so many people that came to walk and show their support.  I am so happy to have been apart of this great fundraiser.  I am already looking forward to next year, and hopefully get more members to walk with us.  I just hope it isn't as hot next year.  wooo!!  Even at 9:30 A.M. is was a scorcher.  Good ol' Oklahoma!
I can not Thank You enough to all of you that came, to those that donated, and even the ones of you that couldn't do either, but verbally gave us your support. 

This is the Memory Garden.  We could write a message on the pedals, whatever we wanted, and while we were walking the staff "planted" our pinwheel flowers.  It was so pretty. Although the wind only caught the wheels a few times, when it did it was beautiful.
The yellow ones stood for caregivers, the blue were for those suffering with Alzheimer's, and the purple were for In Memory Of the loved ones already gone.

   This is the back of our shirts.  DeMoe because that is why we are walking and #40, because it was my dad's football number in high school.  My son and husband had to miss the walk because my son had his first football game of the season.  I knew he would appreciate having something to do with football and his J-pa.  (He is a very sentimental child, and adores everything that my dad was about.  That in its self is a different story that I will post later.)

This is the front.  I saw this design on a different shirt and loved the meaning.  Hope, always there.  Love, because we all love. And Cure, because there needs to be one for this disease.

Our neighbor, and friend, made these shirts.  It was a very last minute idea, and next year I am going to have many made to supply everyone that wants to come walk for our team.  He did a terrific job!  If anyone wants this design, or any other shirt, you can contact him,
He graciously made these last minute for us, and gave us a huge discount because it was for this cause.