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 Notes and Caregivers' FAQ from 6/15/09 DLB webinar 
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Joined: Fri Aug 11, 2006 1:46 pm
Posts: 4811
Location: SF Bay Area (Northern CA)
Post Notes and Caregivers' FAQ from 6/15/09 DLB webinar
MM passed on some info she had received from Dr. Brad Boeve, an LBD expert at Mayo Rochester, about the Alzheimer Research Forum having a webinar on LBD next week.

The details are:
Dementia With Lewy Bodies — Dreadful, Common, Understudied?
A series of expert presentations on dementia with Lewy bodies (DLB), the quintessential overlap disease between Alzheimer (AD) and Parkinson diseases (PD)
Monday, June 15, 2009
9-10am California time (noon-1pm EDT)
Register here:

This webinar will feature short slide presentations by Ian McKeith, Brit Mollenhauer, James Galvin, James Leverenz, and Walter Schulz-Schaeffer, with audio provided via a telephone line. Following the talk, the panel will take audience questions submitted in writing both in advance and during the live hour.

Shortly before 9am on 6/15, you will join the audio portion of the seminar by calling 800-658-3095, with these codes handy:
Access Code: 914559771#
Webinar ID: 110-430-515

Once you register for the webinar, you'll be sent a web address (link) that is unique to you.

If this works like other GoToMeeting webinars I've attended, you can actually listen in by phone if you don't have a computer available to you at that time. You won't be able to see the slide presentations.

If anyone attends next Monday's webinar, please take notes and share here!

You can find additional background on LBD and this webinar on this Alzheimer Research Forum webpage: ... liveID=175
I've copied the text from that webpage below.

The Alzheimer Research Forum is the same organization I mentioned in a post last week that has been posting reports on a recent DLB/PDD conference. The most readable of those conference reports is Part 3, available here:
Part 3 is about the challenges of diagnosing and researching DLB. I've posted what I thought were the best excerpts of Part 3 here:

Robin ... liveID=175

Live Discussion: Betwixt and Intermixed—Dementia With Lewy Bodies

This live discussion will be carried out in Webinar format and will feature short slide presentations by Ian McKeith, Brit Mollenhauer, James Galvin, James Leverenz, and Walter Schulz-Schaeffer, with audio provided via a telephone line. Click here to register.

Contact Us: Please send us technical questions submitted in writing both in advance and during the live hour. (Select "Live Discussions Login/Technical Help" in the dropdown menu on the Contact Us form.)

Background Text
By Gabrielle Strobel

Dementia with Lewy bodies (DLB)—a disorder at the interface of AD and PD—competes with vascular dementia for second spot (after AD itself) on the list of most common causes of dementia among the elderly. If you just said “Huh!” to yourself, you are not alone. Most people wouldn’t know how frequent DLB is, judging by the vastly smaller amount of attention it receives across the board, from neurologists, psychiatrists, scientists, and funders. But this may be changing. Twenty years after DLB came to be recognized as a clinical and pathological category in its own right, a growing number of researchers from both the dementia and the movement disorder fields believe that AD and PD—formerly viewed as separate domains—are connected across a spectrum, and that DLB links the two. Investigators who formerly focused on one of the two established diseases at either end of the spectrum are now developing an active interest in this mixed disease. In DLB, patients suffer from various combinations of Alzheimer and Parkinson signs, which are compounded by frustrating fluctuations in symptoms, visual hallucinations, visuospatial impairments, and, in many cases, rapid decline. “DLB may provide a link between AD and PD that will help us understand both disorders better,” said Ian McKeith of Newcastle University, UK.

Since 1995, a series of targeted workshops have focused on DLB, and on its neighbor on the PD end of the spectrum (Parkinson disease dementia, aka PDD). The workshops have sharpened the clinico-pathological picture of these diseases to crisper definitions that are applicable in the clinic. Clinicians know now that DLB and PDD patients respond especially favorably to cholinesterase inhibitors as was predicted from their postmortem neurochemical pathology. This past March, the latest in this series of small meetings, held in the German city of Kassel, broke new ground by proposing working groups that are charged with hammering out a collaborative research agenda for both biomarker development and presymptomatic diagnosis. Another priority the scientists set is molecular pathogenesis research that aims to unravel how the three main proteins known to underlie this disease spectrum—amyloid-?, tau, and ?-synuclein—conspire in various ways to drive an individual person’s disease. What’s more, a new player on the DLB/PDD/PD end of the spectrum recently burst on the scene in the form of glucocerebrosidase, an enzyme of lipid metabolism whose gene appears to underlie a significant number of cases, and whose modus operandi in disease urgently needs to be figured out.

The Alzforum this past week began an ongoing series of daily stories that summarize recent advances on this topic. They form the background material for this Webinar discussion. So that you can come armed with questions about the latest and greatest, consider reading the introduction about spectrum neurodegeneration, tau in Parkinson’s, dementia with Lewy bodies, oligomers in DLB, AD, brain imaging markers, fluid ?-synuclein markers, fluid progranulin markers, Parkinson’s gene reshuffling (to be published Monday), GBA as DLB and PD gene (Tuesday).

Buoyed by such and other advances, the DLB/PDD scientists hope to disabuse the field at large, as well as physicians who see these patients, of the entrenched but quite possibly outdated notion that DLB is rare (they say it’s not), vague (ditto), of indeterminate relationship to AD and PD (ditto), and complex (yes, but tractable). Join us for slide presentations and subsequent discussion. Send in your questions and comments before the live hour by typing into the comment box below. During the live event on 15 June, type into the GoTo Webinar comment field on your screen and the moderator will pose questions to the panel.

Last edited by robin on Fri Aug 28, 2009 9:21 pm, edited 1 time in total.

Mon Jun 08, 2009 1:26 pm

Joined: Thu Aug 24, 2006 12:03 pm
Posts: 79
The 9 hour difference is too great for me to attend this discussion and I wondered if someone who is listening could take notes and summarize it for the forum. Thanks in advance, Dinny Wolff

Wed Jun 10, 2009 1:50 am

Joined: Fri Aug 11, 2006 1:46 pm
Posts: 4811
Location: SF Bay Area (Northern CA)
Hopefully several people will offer their notes!

The LBDA put out a note yesterday that they heard a transcript will be provided. Not sure how/when they'll do that but that might be one way of your getting notes.

Wed Jun 10, 2009 10:05 am

Joined: Wed Aug 06, 2008 2:24 pm
Posts: 40
Post Archive for the DLB Event
Hi Everyone -

I checked past events on the Alzheimer's Research Forum and those include both the audio of the event, the PowerPoint presentations and the transcript of the chat dialogue that followed.

As soon as that is made available from the DLB event, I will be sure to post the direct link here for everyeone's convenience.

Hope that's helpful,

Angela Taylor
Director of Programs
Lewy Body Dementia Association

Thu Jun 11, 2009 10:55 am
Profile WWW

Joined: Fri Apr 03, 2009 9:55 am
Posts: 61
That would be great! I wanted to sign up for it but I will be at work.

Fri Jun 12, 2009 9:59 am

Joined: Fri Aug 11, 2006 1:46 pm
Posts: 4811
Location: SF Bay Area (Northern CA)
I received this note via email from the LBDA:

The Alzheimer Research Forum,, is the web's most dynamic scientific community dedicated to understanding Alzheimer's disease and related disorders like Lewy body dementias.

Their upcoming event, Betwixt and Intermixed-Dementia With Lewy Bodies has generated a tremendous response from the caregiver community, including some 90 questions on LBD diagnosis and treatment submitted from caregivers.

With this event, the Alzheimer's Research Forum aims to increase awareness of dementia with Lewy bodies (DLB) among scientists and physicians, their primary audience. As such, the panel of LBD experts will focus largely on scientific research topics.

While the live event may address some clinical issues at a high level, at only one hour long it will be impossible to address the many caregiver questions that have been submitted. To ensure your questions receive the attention they deserve, the AlzForum editors have assembled them in a caregiver comment page and will be asking the panelists and the Lewy Body Dementia Association to respond offline to these questions
after the event.

Some of this information can be found on the LBDA website now. Visit to read our many publications or watch caregiver educational videos on LBD at ... ources.htm.

For those who are registered for this event, only questions on the scientific topics should be submitted DURING the actual event. If you are a patient or caregiver and have questions in addition to those already posted, you are invited to submit them ahead of time via the AlzForum website at

LBDA will work with the AlzForum editors to provide the fastest response to the most frequently asked questions so that LBD families now and in the future can all benefit from the answers. Due to the volume of questions, the reality of limited resources, and the availability of our LBD experts, there will be a modest delay before the answers are posted online.

We appreciate your patience while AlzForum and LBDA work together to develop the answers you need.

The LBDA Team

Fri Jun 12, 2009 7:24 pm

Joined: Fri Aug 11, 2006 1:46 pm
Posts: 4811
Location: SF Bay Area (Northern CA)
Please share what YOU got out of this morning's webinar!

Here are the notes I took. I missed most of Dr. McKeith's presentation (which was at the beginning) so perhaps someone else can fill that in! I put notes about questions and answers (in the Q&A portion of the webinar) under the answerer. (So, anything Dr. McKeith answered I put beneath the notes I took on his presentation.)

The only part of the webinar that was new to me (and understandable*) was Dr. Galvin's explanation of his recent work comparing those with AD, pure DLB, and mixed DLB/AD in terms of how well they do on specific tests over a several-year period. I look forward to the publication, hopefully this year, of Galvin's paper on his latest research.

Info on three of the research papers mentioned -- Norwegian study on Namenda** (2009), the Tsuang paper on visual hallucinations*** (2009), and the Galvin paper on clinical predictors**** (2006) -- has been posted here. I will find the Johnson 2008 paper, as that sounds interesting.


* Nearly all of the last two presentations on proteins was new to me but not understandable!




Betwist and Intermixed - Dementia with Lewy Bodies
Webinar by Alzheimer Research Forum

Ian McKeith
University of Newcastle upon Tyne

Why is DLB important?
* DLB causes significantly greater functional disability than AD
* Care costs of DLB are twice those for AD
* Quality of life for people with DLB is significantly worse than for AD with 1 in 4 caregivers rating it as worse than death!
* DLB is likely to be informative about the mechanisms of PD and AD

We've taken some of the understandings of AD and PD, and applied this to DLB.

Quite a lot of people who are diagnosed with AD have other pathologies!

Cognitive dysfunction in AD may be due to irreversible cell death. The fluctuation in DLB seems to indicate that sometimes neurons are working and sometimes not. (This speculation came from Walt's presentation at the end.)

Fluctuation can occur in AD. But we need to characterize the fluctuation. If we can do this, then we can narrow down who has DLB and who has AD. DLB patients can fluctuate by the minute; they fluctuate while taking a cognitive test. Brit indicates that fluctuations can occur in vascular encephalopathy. But those with vascular dementia may fluctuate between tests but not within a given test.

What makes DLB such a challenge? The unpredictability of it makes DLB very difficult for caregivers.

Perhaps the DLB diagnostic criteria will be revised after the 2010 biomarkers conference.

Does it make a practical difference to caregivers for the patient to be correctly diagnosed? Absolutely. Avoiding neuroleptics is a big issue.

Any promising drug treatments from the AD world that can help in DLB? Amyloid-based therapies may have a lot of promise in DLB. Animal models of anti-alpha-synuclein vaccines are promising. Memantine may have benefits for patients. Some optimism from the Norwegian study but it's not the answer.

He stated several times that Walt's research is very important.

Jim Leverenz
Assoc Prof, Neurology and Psychiatry and Behavioral Sciences
University of Washington (Seattle)

LRP = Lewy related pathology. Refers to both classic Lewy bodies and immunopositive lesions (positive for alpha-synuclein).

LRP in a community-based dementia sample: (Kraybill et al, Neurology, 2005)
* in Seattle, drawn from HMO
* looked at about 1K people with dementia
* of 226 autopsies, 126 are LRP positive (56%). (Breakdown of 126: 20 brainstem, 24 amygdala, 22 limibic, 55 neocortical.)

LRP frequency in AD:
* classic Lewy bodies: 21 to 55%
* all LRP (including amygdala): up to 60% of sporadic AD (40% excluding amygdala); up to 90% of familial AD (54% excluding amygdala)

Back to community-based sample:
AD: n=48
AD with LRP: n=65
LRP alone: n=22

In community-based sample:
AD with LRP: more rapid rate of cognitive decline (seen through DRS and MMSE)
VH associated with LRP

Study looks at VH in LRP and AD:
Tsuang et al, Am J Geriatri Psychiatry, 2009

LRP is common (about 50%) in dementia. "Pure LRP" (without AD) - about 15%
LRP in AD: about 40% of sporadic AD; associated with more rapid cognitive progression
LRP associated with VH, even in AD
Pure DLB and LRP/AD are significant portions of dementia cases

Lewy bodies in AD do have a clinical impact.

What makes DLB such a challenge? It has behavioral, movement, and cognitive components.

Does it make a practical difference to caregivers for the patient to be correctly diagnosed? Avoid traditional neuroleptics. (Many patients say that they are allergic to Haldol. Actually the patients have had extrapyramidal reactions to Haldol.) Patients and caregivers know that they are dealing with something different from AD (because they have family members with AD); so it can be a relief to patients to have a name other than AD given to their disorder. If clinicians know they are dealing with DLB, they can be sensitive to treating psychosis and sleep disturbances.

Try to get patients off of anticholinergics bladder meds as these can aggravate cognitive impairment.

Jim Galvin
Washington University (St. Louis, MO)

Development of cognitive profiles in dementia
Took about 3 years to develop this model
Johnson et al, Neurology 2008
12 tests = WAIS Information, WMS Associate Recall, Boston Naming Test, Logical Memory, Benton Visual Recall, WAIS Digit Symbol, Trailmaking A, WAIS Block Design, Animal Fluency, WMS Mental Control, Digit Span - Forward, Digit Span - Backward

Johnson and Galvin have submitted a paper (in 2009) on this

Sample: control = 192, AD = 130, mixed DLB = 84, pure DLB = 15
Controls actually get better taking test year to year!
With AD, only slight decline
Pure DLB: rapid decline after 2 years
Mixed DLB: rapid decline after 2 years; most rapid advancement of dementia

What clinical symptoms can help? Clinical predictors.
Galvin et al, Neurology (2006) 67:1605-1611
Greater chance of having LB pathology came with being male, having parkinsonism, and XXX.
There is a Lewy Body risk score based on clinical features. Good predictor of who will have LB pathology.

PIB imaging in DLB and PDD
MRI and PET scans
If you start out with PD and get dementia, you have a small amyloid burden.
If you start out with dementia, you have a large amyloid burden.
This just confirmed what we already knew.

But, when this MRI and PET data is combined with the clinical predictors, we have a better way to discriminate between groups We can correctly classify most of our dementia cases. We can figure out who has mixed DLB/AD, who has AD, and who has DLB. We are also able to make predictions as to who will develop dementia!

What DLB biomarkers tell:
* DLB has a more rapid progression than AD. Inflection points 2-3 years prior to clinical DX. Differences exist between mixed and pure forms.
* DLB (mixed and pure), AD and controls can be discriminated by combining biomarkers

All the dementias are "bad"; there are no "dementia survivors." (In contrast, there are heart attack survivors.) The dementing illnesses have different features. The course in DLB is faster than in AD. This could be related to the movement aspects or the mood aspects of DLB.

FDA doesn't recognize DLB as an "indication" or a separate disorder. So drug companies aren't willing to research DLB. This is a big issue.

Brit Mollenhauer
Georg August University Goettingen, Germany

The role of CSF biomarkers

Paper by Seubert, et al ("Isolation and quantification of soluble Alzheimer's beta-peptide from biological fluids") from about 15 years ago showed that Abeta42 could be isolated. It has taken us 15 years to make progress on this discovery! Now we can isolate tau protein in CSF.

NFT --> tau
Amyloid plaques --> beta-amyloid
Lewy bodies --> alpha synuclein is key component

Paper on alpha-synuclein in CSF: Moellenhauer et al, 2008
Decreased CSF alpha-synuclein in DLB (thirty-eight) and PD (eight) patients, compared to AD (13), control (13), and CJD (eight)

Speculative mechanisms of CSF alpha-synuclein reduction in synculeinopathies:
* lower expression of SNCA gene as a result of PD/DLB
* reduced exocytosis

Imaging data (which is biomarker data) is already part of the DLB diagnostic criteria. But we need a better biomarker for DLB.

Walter Schulz-Schaeffer
Georg August University Goettingen, Germany

Hypothesis: DLB/PD is a synaptic disease
Hypothesis: alpha-syn aggregates at the synpases are responsible for the neurodegenerative process

They developed a PET blot method for detection of aggregated proteins
PET = paraffin embedded tissue

The great majority of alpha-synuclein aggregates (90-99%) in DLB is NOT located in Lewy bodies
These aggregated are located as small particles in prasynaptic terminals of synapses.

Alzforum moderator = Gabrielle Strobel

Mon Jun 15, 2009 1:59 pm

Joined: Sat Jan 03, 2009 2:59 pm
Posts: 1978
The audio and .ppt from today’s Alzheimer’s Research Forum DLB webinar are already posted at the following link. ... liveID=175

Irene Selak

Mon Jun 15, 2009 9:38 pm
Profile WWW

Joined: Sun Oct 21, 2007 4:18 pm
Posts: 835
Location: Acton, MA
Robin & Irene, I did watch and listen for the 1 1/2 hrs. but most of it was over my head. I did gain a bit of knowledge form Jim Galvin, I don't know if it was his portion of material or the way he presented it but I could follow him. I was a disappointed, or maybe I missed the caregiver to expert question/answer section but I only heard "when do they think they will have the answer to these diseases" ? Any info is appreciated.

Thank you both for all the time you give to this forum.

Take Care, Gerry

Tue Jun 16, 2009 7:32 am

Joined: Fri Aug 11, 2006 1:46 pm
Posts: 4811
Location: SF Bay Area (Northern CA)
I also thought Dr. Galvin's presentation was the most understandable! I think it was both his style and the fact that he limited himself to talking about the findings of a fairly recent (unpublished) study.

Tue Jun 16, 2009 11:11 am

Joined: Fri Aug 11, 2006 1:46 pm
Posts: 4811
Location: SF Bay Area (Northern CA)
There were over 100 questions submitted by caregivers to the panelists during and after the 6/15 Dementia with Lewy Bodies webinar put on by the Alzforum. (The webinar is still viewable. See the link above.) The Alzforum asked the LBDA's help in answering these questions. Here's the first installment of the LBDA's answers to the most frequently asked caregiver questions, broken into seven categories -- symptoms and diagnosis, treatment, living with LBD, physician awareness, caregiver information, genetics, and research.


What is LBD?

Lewy body dementia (LBD) is a progressive neurological disorder. LBD is an umbrella term for two related diagnoses - Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB). The earliest symptoms of these two diseases differ, but reflect the same underlying biological changes in the brain. Over time, people with both diagnoses will develop very similar cognitive, physical, sleep, and behavioral symptoms.

Do all people with DLB hallucinate? My dad has a recent DLB diagnosis but does not hallucinate, thank goodness. Does this mean his diagnosis is wrong?

This is great question. Not everyone with LBD hallucinates, though many will at some point. Likewise, not all patients will exhibit the other clinical signs associated with LBD. The diagnostic criteria requires a person to have dementia plus only TWO of any of the following: hallucinations, parkinsonism, fluctuating cognitive abilities, REM sleep behavior disorder, a severe sensitivity to antipsychotic medications, or an abnormal result on a brain scan that detects levels of dopamine.

Are the hallucinations/delusions the main difference between DLB and Alzheimer's? And can people presenting with delusions otherwise score quite well on standard cognitive testing, like the MMSE?

The MMSE is a commonly-used test to detect a general decline in cognitive function and memory. Because people with LBD typically fluctuate in their cognitive abilities and often perform well on the MMSE early in the disease, the MMSE is not sensitive enough to diagnose DLB, nor is it adequate by itself to diagnose Alzheimer's disease (AD).

There are a number of distinguishing features that help differentiate DLB from AD. For example, the cognitive profile in DLB features deficits in executive functioning, such as problem solving, abstract thinking, and reasoning, while Alzheimer's features a predominant decline in memory. Hallucinations occur earlier in Lewy body dementia, while they appear later in Alzheimer's disease. Severe sensitivity to antipsychotic medications used to treat hallucinations is common in LBD, but not so in Alzheimer's disease. REM sleep behavior disorder is common in DLB, but not in Alzheimer’s. For a more detailed discussion, please visit LBDA’s webpage on LBD symptoms.

Could you address sleepiness? My husband is very tired during the day. Are there ways to combat these symptoms of the disease?

Sleep disorders like sleep apnea, restless leg syndrome and REM sleep behavior disorder are common in LBDs. Sleep disorders often prevent the person with LBD and their caregiver from getting sleep. Excessive daytime sleepiness, despite adequate rest at night, is also common in LBD. Ask your physician to order a sleep study to identify and treat ALL underlying sleep disorders. It is also important to review sleep hygiene such as use of alcohol, caffeine, chocolate or other substances late in the day. Many foods and over the counter medications can have effects on sleep. If excessive daytime sleepiness is a severe problem, a sleep specialist may recommend the use of medication such as a stimulant to promote daytime arousal.

Does anyone with LBD ever recoup mental capabilities?

There are a number of things that can impact cognition in LBD in the short run. Cognitive abilities fluctuate in LBD, making a person appear to function better on one day, and worse on another. Illness, pain, infection, sleep disruption and other medical issues can impact cognition negatively as well. Some people with LBD respond to treatment with cholinesterase inhibitors (originally intended for Alzheimer's disease) very positively. But because LBD is a progressive disease, there is irreversible long term cognitive decline.

Are we getting any closer to confirming diagnosis prior to autopsy?

Right now, 2 out of 3 cases of dementia with Lewy bodies go undiagnosed, and there are no widely-available tests to definitively diagnose it. There are some very promising biological indicators in development to identify LBD through cerebral spinal fluid, blood, and brain imaging; however these are still several years from being ready for clinical use.

My father passed away from DLB, or so we thought. We donated his brain for research and the autopsy came back as having no Lewy bodies. Do LBD and Alzheimer’s mimic each other?

Alzheimer's disease (AD) and Lewy body dementias are both neurodegenerative diseases and share many overlapping symptoms. The clinical criteria permit correct classification the majority of time however, the criteria are not perfect. Among the most common cause of disagreement between autopsy reports and clinical diagnosis is when an autopsied LBD cases was diagnosed with AD. Less commonly a clinically diagnosed LBD case will really be caused by AD. This highlights the need for more research to develop better clinical diagnostic tests.

How do I find a local neurologist who specializes in DLB?

Family physicians are a great, first-step resource if you are experiencing any cognitive, emotional, behavioral or physical changes. However, neurologists generally possess the specialized knowledge to diagnose specific types of dementia or movement disorders, as do geriatric psychiatrists and neuropsychologists. However, these specialists may require a referral from your primary care physician. Geriatricians, who specialize in treating older adults, are also frequently familiar with the different forms of dementia.

If you have access to a hospital affiliated with a medical school, the hospital may have a clinic specializing in dementia or movement disorders where you may find a high level of diagnostic and treatment capability.

The Lewy Body Dementia Association's Scientific Advisory Council is comprised of leading experts in Lewy body dementias. Click here to learn more.


What is the best treatment for DLB?

Right now, cholinesterase inhibitors are the gold standard in LBD treatment. People with LBD may obtain more benefit from these drugs than people with Alzheimer's disease. Treating sleep problems is also important, as any unresolved sleep disorders may increase confusion or behavioral problems. And very conservative treatment of parkinsonism or hallucinations is important in order to avoid medication side effects. Other symptoms, such as depression and changes in blood pressure regulation, should also be evaluated and treated.

Is DLB responding to any meds at this point? If so, which ones should be considered and what side effects are associated with them?

The symptoms of LBD are often quite responsive to treatment. Information on the most common LBD treatment options can be found at by clicking here.

Side effects vary for each person, but the most typical are as follows: Cholinesterase inhibitors, used to treat cognition, sometimes cause gastrointestinal upset. A recent report suggests that cholinesterase inhibitors may increase the risk of fainting spells (syncope). Levodopa, used to treat movement problems, can sometimes cause or worsen hallucinations. And many people with LBD are very sensitive to medications used to treat hallucinations.

NOTE: Up to 50% of patients with LBD who are treated with any antipsychotic medication may experience severe neuroleptic sensitivity, such as worsening cognition, heavy sedation, increased or possibly irreversible parkinsonism, or symptoms resembling neuroleptic malignant syndrome (NMS), which can be fatal. (NMS causes severe fever, muscle rigidity and breakdown that can lead to kidney failure.)

Is donepezil (Aricept) the best drug to counter memory loss in DLB? If not, what is?

There is no evidence that any one cholinesterase inhibitor is better than another for LBD cognitive symptoms.

Is Exelon likely to exacerbate hallucinations in DLB patients?

No, in fact, that class of drugs (cholinesterase inhibitors) has been shown to reduce hallucinations and other behavioral disturbances.

Does memantine (Namenda) have value for a DLB patient?

While there has been some conflicting data on memantine in LBD, new research from a small clinical trial shows memantine may be beneficial in LBD. Data from a larger trial is currently being analyzed and will provide a clearer picture in the near future.

It has been suggested to me that quetiapine (Seroquel) is the only medication that should be given to my husband who has DLB when he has “bad behavior.” What is your opinion and suggestion for the best medication for these behavioral problems? They make caregiving much harder.

The first course of treatment for LBD, cholinesterase inhibitors, has been shown to be effective in treating hallucinations and other psychiatric symptoms of LBD. However, the effect is not immediate. If hallucinations they are disruptive or upsetting, physicians may recommend a cautious trial of a newer antipsychotic medication.

Your doctor is showing caution for a good reason. Severe sensitivity to neuroleptics is common in LBD. Neuroleptics, also known as antipsychotics, are medications used to treat hallucinations or other serious mental disorders. While traditional antipsychotic medications (e.g. haloperidol) are commonly prescribed for individuals with Alzheimer’s with disruptive behavior, these medications can affect the brain of an individual with LBD differently, sometimes causing severe side effects. For this reason, traditional antipsychotic medications like haloperidol should be avoided. Some newer ‘atypical’ antipsychotic medications like risperidone may also be problematic for someone with LBD. Quetiapine is preferred by some LBD experts. If quetiapine is not tolerated or is not helpful, clozapine should be considered, but requires ongoing blood tests to assure a rare but serious blood condition does not develop. Hallucinations must be treated very conservatively, using the lowest doses possible under careful observation for side effects.


In what age range does DLB begin?

LBD is most often seen in the over-60 population, though like other neurodegenerative diseases, there is a small percentage of people who experience and earlier onset in their 40's and 50's.

What does the typical progression of DLB look like? Can you please describe the stages of the disease, so I know what to expect as it progresses?

Unlike Alzheimer's disease, which has clearly defined stages, LBD progression is much less predictable. Symptoms often appear in varying combinations and severity, making each person's experience unique. The prognosis is also different for each person and may be affected by your general health or the existence of unrelated illnesses. Because LBD progresses at varying rates for each individual, it is not possible to determine how long someone may live with the disease. The average duration of LBD is typically five to eight years after the onset of obvious LBD symptoms, but may range from two to twenty years. It is important to remember that this is a disorder that progresses gradually over years, not days or months.

My father was just diagnosed with DLB. It came on suddenly, though looking back we see other signs that we didn't realize at the time are a part of the disease. He doesn't know he has DLB. I don't want to tell him. Should I?

That decision may depend on the cognitive ability and temperament of the individual with LBD. While some people may find a dementia diagnosis distressing, a recent study indicates that most individuals actually find some relief in knowing the diagnosis and in understanding how this relates to their changing abilities.

My father has DLB. It wasn't until I went with him to a doctor’s appointment that he got diagnosed (turns out he wasn't telling the whole story to his doctor). What I find most difficult in caring for my father is his thinking he is all right and everyone else has a problem. Patience is a great asset for repeating directions, plans, and whatever comes up. Is there anything else we can do to help him keep focused and slow the disease?

Not everyone with LBD retains an insight into why they cannot do some of the things they used to do. So maintaining a meaningful and structured life may benefit both the person with LBD and the family caregiver. Encourage him to be an active partner with you in a comprehensive treatment program, especially by remaining socially and physically active, as they are both good for overall cognition. And treatment with a cholinesterase inhibitor is highly recommended.

My husband's cognitive abilities go up and down like a yoyo. Is this "normal"? He was diagnosed three years ago with Alzheimer's, but has since been told he has LBD with Parkinson's symptoms. He is sometimes better now than he was three years ago.

As opposed to calling something “normal” or “abnormal”, it is probably better to comment that the “yoyo-ing” or fluctuating course of your husband’s disease is consistent with the cognitive fluctuation feature of LBD. His partial improvement may be attributed in part to his early treatment when he was diagnosed with AD.

How do I get family members to understand that some of the behaviors from our mom is the disease and not mom?

The best thing you can do is to educate them about the disease. Send them to the Lewy Body Dementia Association's website to learn more about LBD and to hear the stories of other families like yours, posted at LBDA’s online community.

I have a family pattern of DLB. Can I prevent getting it?

Most dementias, including Alzheimer and Lewy body diseases are not genetic. Because research has not yet unlocked enough answers about LBD’s root cause, we do not know yet how to prevent it. Living a heart-healthy lifestyle has been shown to reduce the risk of all forms of dementia, as has staying cognitively and socially active and physically fit.

My wife is now diagnosed with DLB after having had PD for 11 years. I need to know what I am in for. Please describe "rapid decline" regarding future months or years.

Technically this would be a case of PD dementia (PDD). Both PDD and DLB are Lewy body dementias – the difference being largely what the first symptom presentation was. Most individuals experience a gradual disease progression lasting well over 5 years, though a small percentage of people experience the full disease progression in as few as 2 years.

My husband has had two quadruple bypass surgeries, the last one in 1994 at age 60. Months after the last surgery he went back to work but the math he had to do for his job was too much for him. He just couldn't do it. He had to give up a job he loved and had been doing for over 30 years. He also made a mess of our checkbook many times. He was most difficult to live with, as opposed to normally being a kind, loving, and gentle man. He had vascular surgery again four times in 1997 and was off-the-wall difficult to handle. He was semi-conscious for days and used his hands to write in the air. He had a nurse with him 24/7 the first few days. He saw cats in the register overhead, etc. It was also after that that he could no longer do things around the house that he had always done. He just couldn't figure out how to do them. He finally asked me to help. I believe he began having DLB in 1994, most definitely since 1997. Is it possible that his dementia could have begun so long ago?

Sometimes DLB can have a very slow, progressive path. An illness or surgery may reveal LBD underlying symptoms that were not apparent at a clinical level, leading to a new diagnosis. People with LBD also often respond to certain anesthetics and surgery with acute states of confusion or delirium, and may have a sudden significant drop in functional abilities, which may or may not be permanent.

In addition, cerebral vascular disease is commonly co-existent with cardiovascular disease. Open-heart surgery is a tremendous stress for the body and the brain in particular. Many patients have periods of post-operative confusion, most recover but not all do.

It is always difficult to pinpoint exactly when neurodegenerative diseases begin because there is probably a period of several years where brain changes are occurring yet patients do not yet exhibit symptoms.

My father was diagnosed recently with DLB. He was in and out of different hospitals five times, then ended up in a care facility where he got better. So mom took him home and now he doesn’t remember being sick. He seems fine. How can that be?

In all dementia, periods of time (particularly more recent events) may seem less clear or even forgotten. Some of these forgotten events can be quite climactic such as a recent hospitalization. In addition, certain medications can exacerbate LBD symptoms, as do pain, infection, and illness. In addition to addressing other underlying health problems, in-patient care sometimes provides the opportunity for physicians to discontinue certain medications, identify which ones may be problematic, and start them on more appropriate medication regimes.


My dad has DLB and Alzheimer’s. The most distressing thing so far as a caregiver is some doctors’ lack of knowledge about DLB and that DLB is different from other types of dementia when prescribing medication. Is this just my sense?

It can take many years from the time a new disease is defined and for awareness of that disease to make its way through the entire medical profession. The diagnostic criteria for DLB was first published in 1996, and while most neurologists, psychiatrists and geriatricians are becoming more familiar with it, awareness of the disease, its symptoms and treatment issues is still low among generalists and other specialties.

My wife sees a head of a clinical department at an Ivy League medical school for an eye condition. When I told him about her dementia with Lewy bodies, he asked: “What’s that?” Where can I point the doctors so they can catch up on DLB?

The Lewy Body Dementia Association has just launched physician resources on their website. Physicians, nurses and other health care professionals will now find easy-to-read tables and figures on LBD diagnosis and treatment options along with family- and patient-centered publications that can be downloaded or ordered at no cost at

I am very much in agreement with the frustrations associated with diagnosis educating physicians! My husband was initially diagnosed with AD, which we treated for six years. Doing more reading, I discovered that he had all the symptoms of DLB. His REM sleep disorder goes back at least 30 years. He also has had no sense of smell for that many years. The Mayo clinic saw him in Scottsdale and agreed with the probable diagnosis of DLB. A well-regarded senior care physician made the statement that "while the universities may be trying to discern one type of dementia from another, they virtually all come down to Alzheimer's." Is that true?

The underlying brain pathology and symptoms are different among the many types of dementia, and there are important differences in treatment as well. People with Lewy body dementias need an early differential diagnosis to provide them with optimum care and to avoid unnecessary exposure to certain medications (like traditional antipsychotic medications, i.e. haloperidol) that may cause severe and sometimes irreversible side effects.

Many patients with LBD also have Alzheimer disease pathology at autopsy however, clinical, cognitive and behavioral features are distinct and research has shown differences in meaningful outcomes such as loss of functional abilities, nursing home placement and death.

How do I tactfully suggest that we have DLB, not Parkinson's and Alzheimer’s?

If your physician is not familiar with Lewy body dementias, providing them with publications from the Lewy Body Dementia Association can provide them with the information they need to make an accurate diagnosis. You can request a physician packet be mailed to your doctor by emailing LBDA


What is the best way for caregivers to deal with DLB?

This is a complicated disorder with an often unpredictable course. So there are a number of things that will help. First and foremost, become educated about the disease and be prepared to educate those around you (including some medical professionals). Second, find the support you need for everyday caregiving and locate resources in your community BEFORE you need them. And last, but not least, connect with other LBD families for understanding and support. The Lewy Body Dementia Association's website,, is a great place to start.

What is the best way to get DLB patients involved in activities to help stimulate them if they do not want to do them?

It is difficult to get people to do things they do not want to do, regardless of whether they have dementia. There can be many reasons for not wanting to participate; one of the more common ones is fear of the unknown. Slowly introducing a new activity in the comfort of a familiar surrounding may reduce anxiety.

Apathy (or lack of interest and motivation) is a common symptom of LBD, as is depression. Talk with your loved one's physician about whether or not there are symptoms of depression or apathy as the patient may benefit from an antidepressant medication.

Which websites are the most reputable for the latest DLB medical information?

The Lewy Body Dementia Association has a wealth of information on LBD for both families and physicians. Visit Related dementia and movement disorder organizations can also be found on LBDA’s website by clicking here.

Is there a "beginner's book" for the caretaker and the family? We need to read up on what to expect, what we can do. Thanks!

The Lewy Body Dementia Association lists a number of books on LBD and related dementias on their website, which you can find by clicking here.


Is DLB hereditary?

Because DLB is biologically related to Parkinson's disease, from a genetics point of view, what holds true for Parkinson's will hold true for DLB. So, yes, a small proportion of families with DLB will have a genetic connection, but the vast majority of cases are considered 'sporadic,' meaning no genetic causes have been identified.


My husband is 66. He was diagnosed with Alzheimer’s seven years ago. Four years ago after extensive testing, he was diagnosed with DLB with parkinsonian symptoms. He is on memantine (Namenda), carbidopa (Stelevo), selegiline (Zelapar) and the rivastigmine (Exelon) patch. He no longer drives and is having more trouble putting together sentences, dialing a phone, using the remote control, etc. He does mow the grass but misses a lot of it. He is now having much more trouble with grandchildren’s names, etc. Do you think research is getting any closer to reversing his problems?

At this time, we don't know what causes LBD. We do know that naturally occurring proteins misfold in the brains of people with LBD but to date we do not know fully comprehend the steps that cause the proteins to misfold. Until we understand the underlying disease mechanism, we are unable to halt the progression of the disease or reverse it.

Is LBD being aggressively investigated the way that AD is starting to be? Is your research funded by the Alzheimer's funders? Should there be a movement to distinguish LBD on a fundraising level or is that counterproductive due to the disease overlap?

Research into LBD is gaining attention from both the Alzheimer's and Parkinson's disease research communities, as it represents a link between these neurodegenerative diseases. Thus, research into one of these diseases often contributes to the understanding of the others. However, LBD research funding still lags behind, despite having approximately the same patient population as Parkinson's disease.

For more information on how to contribute to LBD research, visit LBDA's website.

When my loved one passes away, should I consider allowing an autopsy to aid in research to LBD?

A brain autopsy is the only definitive way to diagnose Lewy body dementia, but an autopsy alone does not benefit LBD research. Participating in a research study that includes an autopsy is one of the best ways to contribute to the growing body of LBD knowledge.

What research agency do I contact if I am willing to participate in a study about early biomarkers of DLB? provides regularly updated information about federally and privately supported clinical research in human volunteers. gives you information about a trial's purpose, who may participate, locations, and phone numbers for more details.

Edited by Dr. James Galvin, member of LBDA's Scientific Advisory Council

Fri Aug 28, 2009 9:19 pm

Joined: Sun Oct 21, 2007 4:18 pm
Posts: 835
Location: Acton, MA
Robin, Thank you for posting the Q&A from the webinar. I was disappointed that they didn't answer many at that time. Most of the questions you have answered over the many months that I've been reading. Thanks again.


Sun Aug 30, 2009 2:05 am
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