Aricept Losing Efficacy (was: Re: Loss of weight)

[Guest guest]

, I was under the impression that AD had tangled neurons, with lack of

proper transmission, and LBD had cell death.

Please advise.

Imogene

In a message dated 3/7/2007 3:31:18 PM Central Standard Time,

ericbls@... writes:

Something to think about when deciding whether or not to restart/keep

using Aricept/Reminyl/Exelon...

Aricept and Reminyl are not approved in LBD/PDD - so the data that

shows the " falloff " in efficacy in N years is really talking about the

large group that it's approved for, AD patients. AD is a disease of

broad-based brain death - cells die. Nothing is going to bring them

back to life.

In LBD, the issue is a deficit in neurotransmitters so cells can't

communicate well - specifically, loss of acetylcholine-manufacturing

neurons in one brain region that make the acetylcholine supply for the

whole brain. Anything you can do to keep the acetylcholine around

longer after manufacture is probably helpful in LBD.

LBD is so different than AD in this regard - these drugs are modestly

good at slowing decline in AD, they can really turn things around for

people with LBD. It's because AD brains don't lack the chemical so

much as lacking the cells to signal.

I haven't spent a lot of time with the Exelon information in PDD,

which it is approved to treat. I suspect that the functional decline

over time in Exelon-treated PDD patients looks quite different than

that of AD patients. Perhaps someone more familiar with the data can

offer a different perspective there.

Nobody wants to give people more medicine than they need, but this is

one of those agents where the differences may be subtle-but-meaningful

- they're able to cooperate with positioning a bit longer, able to

express pain origins a bit more precisely. That kind of incremental

stabilization or improvement might be well worth the cost.

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[Guest guest]

Have I misunderstood AD and LBD for a couple of years now? I explained the

differences several times to others on another List, and have never been

corrected. Now, I need to know.

Imogene

In a message dated 3/7/2007 3:43:52 PM Central Standard Time, o

ctoryrose@... writes:

-- you're so smart... We're so lucky to have you here...

Will keep this in the links section... PS I've been meaning to research

a couple new drugs that are coming out for memory loss. Thanks for the

reminder... (read something about that when they're on the market they

are going to take over the sales of the other 3 meds...) Will post what

I find...

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[Guest guest]

My dear , I am on the high side of average intelligence, and this is way

over my head. I have read a lot of Medical, but this is just to deep.

We love you, even if we don't understand you. (grin)

Imogene

In a message dated 3/8/2007 12:00:56 AM Central Standard Time,

ericbls@... writes:

I'm a ba-ptist when it comes to AD; I believe that Beta Amyloid

aggregation causes calcium imbalances in the cell, which leads to cell

death. This is one of three theories of AD - the cholinergic deficit

theory (largely off the table), ba-ptists, and tau-ism, whose

adherents believe that misfolded tau protein causes cell death.

LBD is not a disease of generalized neuronal death so much - the major

problem is acetylcholine-producing cells buying the farm, in the

nucleus of Meynert. This is why aggressively treating the

acetylcholine deficit is so important, and why anticholinergic drugs

are such bad news. The brains of LBD patients look dramatically

different on MRI than AD brains. Mayo has recently published on this

- The atrophy is quite characteristic in late-stage AD.

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[Guest guest]

Bless your heart , Thank you for helping us normal people. You are not

normal. Anyone that knows all those big words and what they mean is not

normal. All joking aside, thank you. I want to go back and read all the material

I

studied so diligently when my husband first became ill. I want to know where I

learned that AD was tangled neurons, and LBD was the death of cells.

But, the way you explain it, and as I watch my husband and my AD sister,

your explanation

holds more water than mine.

Thank you,

Imogene

In a message dated 3/8/2007 12:21:57 AM Central Standard Time,

ericbls@... writes:

*chuckle* One of my projects this year, after I finish the drug

review process, is to come up with a clever animation that explains

all this - AD vs LBD vs. vascular/multi-infarct dementia.

The shortest answer:

AD = brain cells dying everywhere because goo gets in them. The goo

is either directly toxic or messes with a signaling pathway that

causes the cell to die a hasty death. Debate continues on which of

the two it could be.

LDB = specialized brain cells that make neurotransmitters die, so

communication between all brain cells falters. The problem is evident

in the early stages not because so many brain cells handling cognition

die, but because all of the cells of the brain rely on the messenger

chemicals produced in the specialized center. Boost levels of the

messengers, the brain can continue to function more like normal.

Vascular/MID = brain cells die from lack of oxygen.

<BR><BR><BR>**************************************<BR> AOL now offers free

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[Guest guest]

i agree with eric about what he says about dementia meds but everyone please

keep in mind two things, dementia meds for lbd are to slow down the progression

of the disease not to stop or prevent the disease. and most important, just

becuase it doesnt work ofor one lbd'er doesnt mean that it wont work for another

lbd'er, everyone seems to react different to meds and treatments, the rule of

lbd is go low, go slow, one change at a time and stay that way for a wh\ile then

the change/add/take away another.

good luck hugs, sharon m

---- epthompson wrote:

Something to think about when deciding whether or not to restart/keep

using Aricept/Reminyl/Exelon...

Aricept and Reminyl are not approved in LBD/PDD - so the data that

shows the " falloff " in efficacy in N years is really talking about the

large group that it's approved for, AD patients. AD is a disease of

broad-based brain death - cells die. Nothing is going to bring them

back to life.

In LBD, the issue is a deficit in neurotransmitters so cells can't

communicate well - specifically, loss of acetylcholine-manufacturing

neurons in one brain region that make the acetylcholine supply for the

whole brain. Anything you can do to keep the acetylcholine around

longer after manufacture is probably helpful in LBD.

LBD is so different than AD in this regard - these drugs are modestly

good at slowing decline in AD, they can really turn things around for

people with LBD. It's because AD brains don't lack the chemical so

much as lacking the cells to signal.

I haven't spent a lot of time with the Exelon information in PDD,

which it is approved to treat. I suspect that the functional decline

over time in Exelon-treated PDD patients looks quite different than

that of AD patients. Perhaps someone more familiar with the data can

offer a different perspective there.

Nobody wants to give people more medicine than they need, but this is

one of those agents where the differences may be subtle-but-meaningful

- they're able to cooperate with positioning a bit longer, able to

express pain origins a bit more precisely. That kind of incremental

stabilization or improvement might be well worth the cost.

--

I am daugher of Leonard, diagnosed May 2004, probably had lbd since 1993,.Dad

had a serious fall in 7/05 causing him to hav hip surgery .After that he

developed aspiration pneumonia 7/05 with pulmonary embolyis, which he almost

died from. He had a 2nd bout of aspiration pneumonia and uti 8/05. He died when

his blood pressure fluctuations started dropping without coming back up on

9/25/05,

may he rest in peace with his mom and dad,

a smile a day keeps the meanies away

[Guest guest]

<snip>and most important, just becuase it doesnt work for one lbd'er

doesnt mean that it wont work for another lbd'er, everyone seems to

react different to meds and treatments, the rule of lbd is go low,

go slow, one change at a time and stay that way for a while then the

change/add/take away another.<snip>

And I'll further comment that the 3 similiar meds must not work

entirely the same. Because Aricept didn't work for my mom at all

(although this was before we knew she had LBD and maybe she didn't

start at the lowest dosage as suggested for those w/ LBD)... But even

though Aricept didn't work for her (actually made some of her

symptoms worse), we took the chance of starting her on Exelon -- and

the NARANJA! moments is proof enough to know that IT WORKED! :)

And as you may or may not know... her doctor at the NH didn't want to

start her on ANYTHING... (apparently he sees all dementia the same -

THAT's a big NO-NO IMHO)... and it wasn't until after I became his

squeaky wheel that he listened to me and had her start it...

[Guest guest]

THANK YOU, ERIC!

" epthompson "

<ericbls@spintell

igentlabs.com> To

Sent by: LBDcaregivers

LBDcaregivers@yah cc

oogroups.com

Subject

Aricept Losing

03/08/2007 12:00 Efficacy (was: Re: Loss of weight)

PM

Please respond to

LBDcaregivers@yah

oogroups.com

Excellent point that they're not all the same.

Aricept and Reminyl are more alike than Exelon; regardless of what

insurers (the worst offenders) think, they're not completely

interchangable. If one doesn't work for you LO, push for a trial of a

different one. Just recognize that " work " can be a subtle

improvement or stabilization, and that it takes anywhere from four to

six weeks to get to the therapeutic dose and let blood levels stabilize..

E

[Guest guest]

..looking forward to that..thanks for all your input..Meg

Aricept Losing Efficacy (was: Re: Loss of weight)

*chuckle* One of my projects this year, after I finish the drug

review process, is to come up with a clever animation that explains

all this - AD vs LBD vs. vascular/multi- infarct dementia.

The shortest answer:

AD = brain cells dying everywhere because goo gets in them. The goo

is either directly toxic or messes with a signaling pathway that

causes the cell to die a hasty death. Debate continues on which of

the two it could be.

LDB = specialized brain cells that make neurotransmitters die, so

communication between all brain cells falters. The problem is evident

in the early stages not because so many brain cells handling cognition

die, but because all of the cells of the brain rely on the messenger

chemicals produced in the specialized center. Boost levels of the

messengers, the brain can continue to function more like normal.

Vascular/MID = brain cells die from lack of oxygen.

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