Nicotine, Parkinsons and Dementia

[Vocalek]

I finally got a definitive diagnosis on my mother today. Lewy Body Disease, aka Dementia with Lewy Bodies. It is like a cross between Parkinson's (problems with gait and balance, stiffening up) and Alzheimers, with one not-very attractive addition, hallucinations and even delusions. I found this information at Welcome to Neurology | Neurology

Cognitive Profile of Dementia with Lewy Bodies and Parkinson’s Disease Dementia
In both DLB and PDD, the cognitive profile includes problems with attention, executive functions, and visuospatial function. Much of the literature on the neuropsychology of DLB compares DLB versus AD, consistently finding that higher-order attention and visuospatial function are more impaired in DLB than in AD, and that episodic memory and language function are more impaired in AD than in DLB.4,5 The impairment in attention in DLB may relate to the fluctuations that are characteristic of the disorder. However, examination of the nature of attentional impairment in DLB reveals that simple attention (e.g. digit span) is less impaired than higher-order attention (visual search and set shifting, Wechsler Adult Intelligence Scale [WAIS] digit symbol).4 Some have suggested that the attention deficits in DLB and PDD reflect the executive demands of the tests.6 Executive function comprises a group of cognitive operations that encompass planning, anticipating, sequencing, and monitoring complex cognitive operations. Executive function is consistently found to be impaired in DLB and PDD.5

OK, when I am totally off nicotine, my problems are well described by the first sentence above.

The article discuses Nicotine as treatment:

Trials of cholinergic agonists are also rational in PDD and DLB. Studies showing that transdermal nicotine improves attention in healthy nonsmokers24 implicates nicotonic receptors in the cognitive domain that is most impaired in PDD and DLB. Nicotine has also been shown to improve attention in healthy elderly with memory loss25 and even in AD.26 Nicotine has also been shown to improve attention in patients with PD.27 Although nicotine is not a viable therapeutic option itself, nicotinic agonists in development may be viable agents for DLB and PDD.

I must write to the authors to ask them "why" regarding the final sentence above.

 

[markarich159]

I finally got a definitive diagnosis on my mother today. Lewy Body Disease, aka Dementia with Lewy Bodies. It is like a cross between Parkinson's (problems with gait and balance, stiffening up) and Alzheimers, with one not-very attractive addition, hallucinations and even delusions. I found this information at Welcome to Neurology | Neurology

Cognitive Profile of Dementia with Lewy Bodies and Parkinson’s Disease Dementia
In both DLB and PDD, the cognitive profile includes problems with attention, executive functions, and visuospatial function. Much of the literature on the neuropsychology of DLB compares DLB versus AD, consistently finding that higher-order attention and visuospatial function are more impaired in DLB than in AD, and that episodic memory and language function are more impaired in AD than in DLB.4,5 The impairment in attention in DLB may relate to the fluctuations that are characteristic of the disorder. However, examination of the nature of attentional impairment in DLB reveals that simple attention (e.g. digit span) is less impaired than higher-order attention (visual search and set shifting, Wechsler Adult Intelligence Scale [WAIS] digit symbol).4 Some have suggested that the attention deficits in DLB and PDD reflect the executive demands of the tests.6 Executive function comprises a group of cognitive operations that encompass planning, anticipating, sequencing, and monitoring complex cognitive operations. Executive function is consistently found to be impaired in DLB and PDD.5

OK, when I am totally off nicotine, my problems are well described by the first sentence above.

The article discuses Nicotine as treatment:

Trials of cholinergic agonists are also rational in PDD and DLB. Studies showing that transdermal nicotine improves attention in healthy nonsmokers24 implicates nicotonic receptors in the cognitive domain that is most impaired in PDD and DLB. Nicotine has also been shown to improve attention in healthy elderly with memory loss25 and even in AD.26 Nicotine has also been shown to improve attention in patients with PD.27 Although nicotine is not a viable therapeutic option itself, nicotinic agonists in development may be viable agents for DLB and PDD.

I must write to the authors to ask them "why" regarding the final sentence above.

I remember hearing and reading about this while I was in Pharmacy school over a decade ago. Apparently, a few clinicians, at the time, were actually discussing the prospect of suggesting that individuals with a positive familial history of Alzheimer's start smoking later in their lives to reduce the chances of developing the disease. The thinking was, if you would start smoking(remember, vaping did not exist, nor did Nicotine analogue drugs-although NRT's did) late enough in life, the pulmonary and Cardiovascular damage would be minimal as compared to the Neurological benefits. But I agree with your last statement, I suppose the updated viewpoint is that the cardiovascular(hypertensive) effects of nicotine outweigh the benefits.

 

[TheLizinator]

Not familiar with this diagnosis, but Parkinson's has been linked to a deficit of dopamine (or at least a lessening of the effect of dopamine on receptors). Schizophrenia has been linked (don't know how definitively with more recent research) with an excess of dopamine excitation of neural receptors. Made sense to me that one was marked by flat affect and the other by an overabundance of neural excitation. I would love to read more on dopamine/nicotine connections as nicotine does have some positive contributions to our neurochemistry; probably far more than is recognized (nicotine sure has had a bum rap due to its unavoidable relationship with tobacco-smoking). Every drug ever used has potential for great help and serious harm. Let's see....toenail fungus or death? Gimme a second to think about it...

 

[Vocalek]

Is that your photo Linz? You look remarkably good for a smoker!

 

[TheLizinator]

Is that your photo Linz? You look remarkably good for a smoker!

Hahaha no that's not me but I thought the pic was just priceless. The woman does look great for her age (assuming that's her cake she's lighting up from). So much for the theory that "clean living" leads to longevity, eh?

 

[Vocalek]

Yes, I was familiar with the dopamine deficit linked to Parkinsons. It is one of the reasons that I would not touch Chantix with a 100-foot pole. The last thing I want going on in my head is blocked dopamine receptors.

When will the "experts" get it through their heads that we don't use nicotine to "get high"? That was the theory underlying Chantix. Smokers get pleasure from nicotine. Block the receptors so that nicotine can't get through. Problem is that they ignored all the other functions of dopamine (and therefore the other reasons we use nicotine).

 

[Vocalek]

Can't get the table to render properly, but here is a link to the PDF for the entire article:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2046219&blobtype=pdf
Nicotinic receptors as CNS targets for Parkinson’s disease

Table 1
Summary of the studies testing nicotine or a nicotinic agonist in Parkinson’s disease patients

Study
Test agent
Type of study
# subjects
Duration
Final dose/day
Anti-parkinsonian effect
Dose titration
Dose maintenance
Ishikawa & Miyatake, 1993
Smoking and nicotine gum
Open-label
6
Chronic smoker
NA
Yes
Fagerstrom et al., 1994
Nicotine gum and patch
Open-label
2
≥ 7 mo
15 mg patch + gum
Yes
Clemens et al., 1995
Nicotine gum
Double-blinded placebo-controlled
48
ND
1 day
3 × 2 mg
No
Ebersbach et al., 1999
Nicotine patch
Double-blinded crossover
16
ND
12 hours
7 mg#
No
Kelton et al., 2000
Nicotine iv and patch
Open-label
15
2 wk
1 wk
14 mg
Yes
Vieregge et al., 2001
Nicotine patch
Double-blinded placebo-controlled
32
1 wk
2 wk
14 mg
No
Mitsuoka et al., 2002
Nicotine gum
Open-label
8
ND
1 day
NA
Yes
Lemay et al., 2004
Nicotine patch
Open-label
22
22 days
3 days
21 mg
No
Shoulson et al., 2006
SIB-1508Y
Double-blinded placebo controlled
77
2 wk
2 wk
10 mg
No​

#Used the 35 mg patch, of which 14 mg is absorbed over 24 h, or 7 mg over 12 h. ND – not done; NA, not available.

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#Used the 35 mg patch, of which 14 mg is absorbed over 24 h, or 7 mg over 12 h. ND – not done; NA, not available.​

Biochem Pharmacol. Author manuscript; available in PMC 2008 October 15.
Published in final edited form as:​

Biochem Pharmacol. 2007 October 15; 74(8): 1224–1234.​

Published online 2007 June 17. doi: 10.1016/j.bcp.2007.06.015.

Nicotinic receptors as CNS targets for Parkinson’s disease

 

[dragonpuff]

Not familiar with this diagnosis, but Parkinson's has been linked to a deficit of dopamine (or at least a lessening of the effect of dopamine on receptors). Schizophrenia has been linked (don't know how definitively with more recent research) with an excess of dopamine excitation of neural receptors. Made sense to me that one was marked by flat affect and the other by an overabundance of neural excitation. I would love to read more on dopamine/nicotine connections as nicotine does have some positive contributions to our neurochemistry; probably far more than is recognized (nicotine sure has had a bum rap due to its unavoidable relationship with tobacco-smoking). Every drug ever used has potential for great help and serious harm. Let's see....toenail fungus or death? Gimme a second to think about it...

As far as i know, there haven't been any studies done on how nicotine may benefit those with severe mental illnesses (if there have been any since i last checked, please let me know as i am a sucker for this stuff ). However, they have found that approximately 80% of schizophrenics and 60-70% of bipolars smoke. The rate in the general population is only 20-25%. Obviously it must be doing something for them.

And yet, because hospitals are non-smoking and many doctors are ignorant to these effects, most patients are forced to quit all forms of nicotine upon being admitted, when they are clearly at their worst. Yes, NRT's are "available," but most psychiatrists only hand these out to patients who ask for it, i.e. only those of most sound mind will receive it. But i suppose its ok because the nicotine usually winds up replaced by something like Haldol anyways.

 

[mlady]

As far as i know, there haven't been any studies done on how nicotine may benefit those with severe mental illnesses (if there have been any since i last checked, please let me know as i am a sucker for this stuff ). However, they have found that approximately 80% of schizophrenics and 60-70% of bipolars smoke. The rate in the general population is only 20-25%. Obviously it must be doing something for them.

And yet, because hospitals are non-smoking and many doctors are ignorant to these effects, most patients are forced to quit all forms of nicotine upon being admitted, when they are clearly at their worst. Yes, NRT's are "available," but most psychiatrists only hand these out to patients who ask for it, i.e. only those of most sound mind will receive it. But i suppose its ok because the nicotine usually winds up replaced by something like Haldol anyways.

as a bipolar with pmdd ... quitting the damn cig has been a constant struggle. i tried with e cigs about a year ago with disastrous results. i blame the company, not the product. so i went back to smoking, and reading up on the e cigs again.

the craving for a smoke has gone away since i have been puffing on a regular basis. i had a craving creep towards me today, but it went away when i vaped like a mad woman (no pun ....?)

 

[dragonpuff]

I'm in the same canoe as you mlady, and i learned the painful way not to even try to quit nicotine. I've worked very hard to get to where i am now, i'm not gonna throw all that away because someone else thinks they know what's best for me.