Cognitive decline similar in LBD and AD

This is an interesting study of 58 DLB (Dementia with Lewy Bodies) subjects and 100 AD (Alzheimer’s Disease) subjects, followed over a one-year period at 40 European centers. All patients had mild-moderate dementia. The diagnosis required a 123I-FP-CIT (dopamine transporter) SPECT. (There was no autopsy confirmation of the diagnoses.)

The authors state that DLB is associated with “earlier institutionalisation and a higher level of carer distress than are seen in Alzheimer’s disease.”

The authors believe prognosis info is important information for caregivers:

“Awareness of the rate of cognitive decline and also of non-cognitive symptoms can help carers and patients to adjust and plan appropriate lifestyle changes and to make arrangements for the future. This frequently involves making difficult decisions regarding treatment of psychiatric and motor symptoms and utilisation of limited resources available for patients with dementia.”

The authors want to investigate why the prognosis in DLB is worse than in AD. They thought perhaps it was due to a faster cognitive decline in DLB as compared to AD. In fact, they found that there were no significant differences when comparing the rates of decline of cognitive and neuropsychiatric symptoms in DLB and AD. One of the key messages of the article is: “the worse prognosis of DLB is likely to be mediated by neuropsychiatric or other symptoms and not only by cognitive decline.”

I’ve copied the abstract below.



BMJ Open. 2012 Feb 8.

Comparison of cognitive decline between dementia with Lewy bodies and Alzheimer’s disease: a cohort study.

Walker Z, McKeith I, Rodda J, Qassem T, Tatsch K, Booij J, Darcourt J, O’Brien J.
Research Department of Mental Health Sciences, University College London, Bloomsbury Campus, London, UK.


Dementia with Lewy bodies (DLB) accounts for 10%-15% of dementia cases at autopsy and has distinct clinical features associated with earlier institutionalisation and a higher level of carer distress than are seen in Alzheimer’s disease (AD). At present, there is on-going debate as to whether DLB is associated with a more rapid cognitive decline than AD. An understanding of the rate of decline of cognitive and non-cognitive symptoms in DLB may help patients and carers to plan for the future.

In this cohort study, the authors compared 100 AD and 58 DLB subjects at baseline and at 12-month follow-up on cognitive and neuropsychiatric measures.

Patients were recruited from 40 European centres.

Subjects with mild-moderate dementia. Diagnosis of DLB or AD required agreement between consensus panel clinical diagnosis and visual rating of 123I-FP-CIT (dopamine transporter) single photon emission computed tomography neuroimaging.

The Cambridge Cognitive Examination including Mini-Mental State Examination and Neuropsychiatric Inventory (NPI).

The AD and DLB groups did not differ at baseline in terms of age, gender, Clinical Dementia Rating score and use of cholinesterase inhibitors or memantine. NPI and NPI carer distress scores were statistically significantly higher for DLB subjects at baseline and at follow-up, and there were no differences between AD and DLB in cognitive scores at baseline or at follow-up. There was no significant difference in rate of progression of any of the variables analysed.

DLB subjects had more neuropsychiatric features at baseline and at follow-up than AD, but the authors did not find any statistically significant difference in rate of progression between the mild-moderate AD and DLB groups on cognitive or neuropsychiatric measures over a 12-month follow-up period.

PubMed ID#: 22318660 (

Treatment Options for PSP, CBD, and FTD (Review)

This medical journal article is a review of what we know about treatment of PSP (progressive supranuclear palsy), CBD (corticobasal degeneration), and FTD (frontotemporal dementia). Some general statements are made about “diet and lifestyle,” then several medications are discussed including anti-depressants (SSRIs in particular), dementia medications, antipsychotics, and levodopa. Finally, “emerging therapies” are briefly described.

I’ve copied the abstract below.

For me, the one new piece of information is that Abilify and Seroquel are the two most commonly prescribed antipsychotics “in parkinsonian disorders.” It would be interesting to know how frequently they are prescribed in PSP and CBD. Certainly most of the prescriptions are for Parkinson’s Disease and Parkinson’s Disease Dementia (Lewy Body Dementia). Though we have a few local support group members with PSP and CBD taking these medications, the majority do not.



Current Treatment Options in Neurology. 2012 Feb 4. [Epub ahead of print]

Treatment Options for Tauopathies.

Karakaya T, Fußer F, Prvulovic D, Hampel H.
Department of Psychiatry, J.W. Goethe-University, Frankfurt, Germany.

OPINION STATEMENT: To date, there are no approved and established pharmacologic treatment options for tauopathies, a very heterogenous group of neuropsychiatric diseases often leading to dementia and clinically diagnosed as atypical Parkinson syndromes.

Among these so-called Parkinson plus syndromes are progressive supranuclear palsy (PSP), also referred to as Steele-Richardson-Olszewski syndrome; frontotemporal dementia (FTD); and corticobasal degeneration (CBD).

Available treatment strategies are based mainly on small clinical trials, miscellaneous case reports, or small case-controlled studies. The results of these studies and conclusions about the efficacy of the medication used are often contradictory.

Approved therapeutic agents for Alzheimer´s dementia, such as acetylcholinesterase inhibitors and memantine, have been used off-label to treat cognitive and behavioral symptoms in tauopathies, but the outcome has not been consistent.

Therapeutic agents for the symptomatic treatment of Parkinson’s disease (levodopa or dopamine agonists) are used for motor symptoms in tauopathies.

For behavioral or psychopathological symptoms, treatment with antidepressants-especially selective serotonin reuptake inhibitors-could be helpful.

Antipsychotics are often not well tolerated because of their adverse effects, which are pronounced in tauopathies; these drugs should be given very carefully because of an increased risk of cerebrovascular events.

In addition to pharmacologic options, physical, occupational, or speech therapy can be applied to improve functional abilities.

Each pharmacologic or nonpharmacologic intervention should be fitted to the specific symptoms of the individual patient, and decisions about the type and duration of treatment should be based on its efficacy for the individual and the patient’s tolerance.

Currently, no effective treatment is available that targets the cause of these diseases. Current research focuses on targeting tau protein pathology, including pathologic aggregation or phosphorylation; these approaches seem to be very promising.

PubMed ID: #22307450 (see for this abstract only)

Dopamine Transporter Loss Differs in MSA, PSP and PD

With a special PET scan that focuses on dopamine transport, these Korean researchers concluded that PSP (progressive supranuclear palsy) patients showed “more prominent and earlier dopamine transporter loss” in the anterior caudate, a region of the brain, and that MSA (multiple system atrophy) patients showed “more prominent and earlier dopamine transporter loss” in the ventral putamen, another region of the brain, when compared to Parkinson’s Disease.

None of the diagnoses are autopsy-confirmed, which is what is needed for the medical community to embrace this sort of PET scan.

I’ve copied the abstract below.



Journal of Nuclear Medicine. 2012 Feb 9. [Epub ahead of print]

Subregional Patterns of Preferential Striatal Dopamine Transporter Loss Differ in Parkinson Disease, Progressive Supranuclear Palsy, and Multiple-System Atrophy.

Oh M, Kim JS, Kim JY, Shin KH, Park SH, Kim HO, Moon DH, Oh SJ, Chung SJ, Lee CS.
Department of Nuclear Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.

Parkinson disease (PD), progressive supranuclear palsy (PSP), and multiple-system atrophy (MSA) are known to affect dopaminergic neurons of the brain stem and striatum with different preferential involvement. Here we investigated differences in striatal subregional dopamine transporter loss in PD, PSP, and MSA and assessed the diagnostic value of (18)F-fluorinated-N-3-fluoropropyl-2-beta-carboxymethoxy-3-beta-(4-iodophenyl)nortropane ((18)F-FP-CIT) PET in differentiating PSP and MSA from PD.

Forty-nine patients with PD, 19 patients with PSP, 24 patients with MSA, and 21 healthy people (healthy controls) were examined with (18)F-FP-CIT PET.

The PET images were spatially normalized and analyzed with 12 striatal subregional volume-of-interest (VOI) templates (bilateral ventral striatum [VS], anterior caudate [AC], posterior caudate, anterior putamen, posterior putamen [PP], and ventral putamen [VP]) and 1 occipital VOI template. The nondisplaceable binding potential (BP(ND)) and intersubregional ratio (ISR; defined as the ratio of the BP(ND) of one striatal subregion to that of another striatal subregion) of subregional VOIs were calculated.

The BP(ND) of all VOIs in the PD, MSA, and PSP groups were significantly lower than those in the healthy controls (P < 0.05). The BP(ND) of AC and the AC/VS ISR in the PSP group were significantly lower than those in the PD group. The BP(ND) of VP was significantly lower, but the PP/VP ISR was significantly higher in the MSA group than in the PD group. At the cutoff value for the AC/VS ISR (<0.7), the sensitivity and specificity for differentiating PSP from PD were 94% and 92%, respectively. At the cutoff value for the PP/VP ISR (>0.65), the sensitivity and specificity for differentiating MSA from PD were 90% and 45%, respectively.

The diagnostic accuracy of visual analysis was similar to that of quantitative analysis for differentiating PSP from PD but was significantly higher for differentiating MSA from PD.

Compared with PD, PSP and MSA showed more prominent and earlier dopamine transporter loss in the AC and VP, respectively. These findings could be useful for suggesting PSP or MSA in parkinsonian cases without characteristic atypical features.

PubMed ID#: 22323779 (see for this abstract only)

“Little-known brain disease rips apart lives” (FTD)

This is a terrific article in today’s Los Angeles Times ( about a family challenged by FTD (frontotemporal dementia), which used to be called Pick’s Disease.  In the local Brain Support Network group, we’ve had two people with a clinical diagnosis of PSP who were diagnosed with FTD (Pick’s Disease) upon brain autopsy.  Also, one person in our BSN support group was clinically diagnosed with DLB but ended up with a different type of frontotemporal dementia on brain autopsy.  So….it’s probably good for those dealing with dementia to know about FTD as it can look like the disorders in our group.

I do wish we could get some wonderful articles written about the disorders in our group in the SF Chronicle or SJ Mercury News!



Little-known brain disease rips apart lives of victim, loved ones

By Thomas Curwen
Los Angeles Times
February 10, 2012

When Stu Bryant began acting rude and impulsive, his family was baffled. Then they learned he had frontotemporal disease, which strips away self-restraint and the ability to decipher social situations. More than a year after the diagnosis, Maureen Bryant had grown accustomed to making excuses for her husband. When Stu stood behind a tattooed woman in line at Panda Express, and said loudly, “Wow, that’s a lot of tattoos,” Moe stepped between him and the woman and apologized.

When he repeatedly wandered into the house that was being built down the street — despite the “No Trespassing” sign and the fence — she explained to the owner that he was just curious. Possibly the most embarrassing episode occurred when they were coming home from dinner, and she dashed into a mini-mart at a marina in Oxnard to buy milk.

Here’s a link to the full article:,0,5574998.story

Scientific American article on bexarotene

This article in Scientific American is about the scramble within the Alzheimer’s community to find some treatment for AD. The latest treatment to be considered is a skin cancer drug called Bexarotene.

Here’s a link to the full article:

Alzheimer’s Disease Symptoms Reversed in Mice
A cancer drug given to mice eliminates brain-damaging proteins, leading to improved cognition within days, but will it work in humans?
Scientific American
By Gary Stix
Thursday, February 9, 2012