Long-term cognitive outcome of Alzheimer’s disease and dementia with Lewy bodies: dual disease is worse

Blanc, F.; Mahmoudi, Rachid; Jonveaux, Thérèse Rivasseau; Galmiche, Jean; Chopard, Gilles; Crétin, Benjamin; Demuynck, Catherine; Milch, Catherine; Philippi, Nathalie; Sellal, François; Michel, Jean-Marc; Tio, Grégory; Stackfleth, Mélanie; Vandel, Pierre; Magnin, Éloi; Novella, Jean‐Luc; Kaltenbach, Georges; Bénétos, Athanase; Sauleau, Erik

doi:10.1186/s13195-017-0272-8

Cited by 31 publications

(26 citation statements)

References 25 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Visual recognition memory, semantic fluency and ideomotor praxis are more severely impaired in DLB patients , who also show significantly lower scores on the tests of attention, executive function and constructional tasks . Episodic verbal memory is also worse in DLB than PDD, and the rate of cognitive decline is faster in DLB than PDD and AD . One study showed that the average annual decline in MMSE score in DLB is approximately two points in comparison with PDD (1.8) and AD (1.6) .…”

Section: Methodsmentioning

confidence: 99%

Review: Clinical, neuropathological and genetic features of Lewy body dementias

Hansen

Ling

Lashley

et al. 2019

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

2019) Neuropathology and Applied Neurobiology 45, 635-654 Clinical, neuropathological and genetic features of Lewy body dementias Lewy body dementias are the second most common neurodegenerative dementias after Alzheimer's disease and include dementia with Lewy bodies and Parkinson's disease dementia. They share similar clinical and neuropathological features but differ in the time of dementia and parkinsonism onset. Although Lewy bodies are their main pathological hallmark, several studies have shown the emerging importance of Alzheimer's disease pathology. Clinical amyloid-b imaging using Pittsburgh Compound B (PiB) supports neuropathological studies which found that amyloid-b pathology is more common in dementia with Lewy bodies than in Parkinson's disease dementia. Nevertheless, other co-occurring pathologies, such as cerebral amyloid angiopathy, TDP-43 pathology and synaptic pathology may also influence the development of neurodegeneration and dementia. Recent genetic studies demonstrated an important role of APOE genotype and other genes such as GBA and SNCA which seem to be involved in the pathophysiology of Lewy body dementias. The aim of this article is to review the main clinical, neuropathological and genetic aspects of dementia with Lewy bodies and Parkinson's disease dementia. This is particularly relevant as future management for these two conditions may differ.

show abstract

Section: Methodsmentioning

confidence: 99%

Review: Clinical, neuropathological and genetic features of Lewy body dementias

Hansen

Ling

Lashley

et al. 2019

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

show abstract

“…The pattern of initial cognitive dysfunction differs between DLB and PDD [ 60 ], with greater deficiencies of attention, executive function, and constructive abilities, as well as significantly lower ratings in episodic verbal memory tasks, in DLB [ 61 , 62 ]. Further, the rate of cognitive decline is reportedly faster in DLB than in PDD and AD [ 63 , 64 ] (Table 1 ).…”

Section: Introductionmentioning

confidence: 99%

Are dementia with Lewy bodies and Parkinson’s disease dementia the same disease?

Jellinger¹,

Korczyn

2018

BMC Med

264

216

View full text Add to dashboard Cite

BackgroundDementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), which share many clinical, neurochemical, and morphological features, have been incorporated into DSM-5 as two separate entities of major neurocognitive disorders with Lewy bodies. Despite clinical overlap, their diagnosis is based on an arbitrary distinction concerning the time of onset of motor and cognitive symptoms, namely as early cognitive impairment in DLB and later onset following that of motor symptoms in PDD. Their morphological hallmarks – cortical and subcortical α-synuclein/Lewy body plus β-amyloid and tau pathologies – are similar, but clinical differences at onset suggest some dissimilar profiles. Based on recent publications, including the fourth consensus report of the DLB Consortium, a critical overview is provided herein.DiscussionThe clinical constellations of DLB and PDD include cognitive impairment, parkinsonism, visual hallucinations, and fluctuating attention. Intravitam PET and postmortem studies have revealed a more pronounced cortical atrophy, elevated cortical and limbic Lewy body pathologies, higher Aβ and tau loads in cortex and striatum in DLB compared to PDD, and earlier cognitive defects in DLB. Conversely, multitracer PET studies have shown no differences in cortical and striatal cholinergic and dopaminergic deficits. Clinical management of both DLB and PDD includes cholinesterase inhibitors and other pharmacologic and non-drug strategies, yet with only mild symptomatic effects. Currently, no disease-modifying therapies are available.ConclusionDLB and PDD are important dementia syndromes that overlap in many clinical features, genetics, neuropathology, and management. They are currently considered as subtypes of an α-synuclein-associated disease spectrum (Lewy body diseases), from incidental Lewy body disease and non-demented Parkinson’s disease to PDD, DLB, and DLB with Alzheimer’s disease at the most severe end. Cognitive impairment in these disorders is induced not only by α-synuclein-related neurodegeneration but by multiple regional pathological scores. Both DLB and PDD show heterogeneous pathology and neurochemistry, suggesting that they share important common underlying molecular pathogenesis with Alzheimer’s disease and other proteinopathies. While we prefer to view DLB and PDD as extremes on a continuum, there remains a pressing need to more clearly differentiate these syndromes and to understand the synucleinopathy processes leading to either one.

show abstract

“…Recently, Blanc et al 6 reported the frequency of dementia patients as 1000 AD (86.3%), 131 DLB (11.3%) and 28 dual diseases (2.4%). The ratio of DLB vs AD is 1:7.6, and the frequency of dual disease among total DLB is 0.7%.…”

Section: Discussionmentioning

confidence: 99%

Prevalence and clinical features of dual diseases of Alzheimer's disease and dementia with Lewy bodies: A neuroimaging‐based study

Sakakibara

Tateno

Aiba

et al. 2019

Neurology & Clinical Neurosc

View full text Add to dashboard Cite

Background While dual diseases of Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are documented pathologically, few studies are available concerning the frequency of dual diseases. Aim We present our data of the frequency of AD, DLB and dual diseases based on neuroimaging, together with the frequency of Parkinson's disease (PD) without dementia. Methods This is a prospective cohort study (745 dementia and/or movement disorder referred patients; recruiting period, 3 years; prospectively follow‐up period, 2.0 ± 1.8 years; age 73.0 ± 6.3 years at the first visit; 360 men, 385 women; all underwent MRI scan). Patients met the published criteria at least once during a course of disease. We included both dopaminergic denervation in the striatum and noradrenergic denervation in the heart to the inclusion criteria of DLB and PD. Results Among them, total 476 patients met the criteria as follows: 232 AD (48.7%), 91 DLB (19.1%), 29 dual diseases (6.1%), and 124 PD (26.1%). Patients with dual diseases were initially diagnosed as AD in 18, PD in 8, DLB in two, and Lewy body disease in one. Conclusion In the cases presented, 6.1% of patients who visited dementia/movement disorder clinics showed duals diseases. It is therefore important to follow such patients, from the view point of disease progression and necessary care.

show abstract

Long-term cognitive outcome of Alzheimer’s disease and dementia with Lewy bodies: dual disease is worse

Cited by 31 publications

References 25 publications

Review: Clinical, neuropathological and genetic features of Lewy body dementias

Review: Clinical, neuropathological and genetic features of Lewy body dementias

Are dementia with Lewy bodies and Parkinson’s disease dementia the same disease?

Prevalence and clinical features of dual diseases of Alzheimer's disease and dementia with Lewy bodies: A neuroimaging‐based study

Contact Info

Product

Resources

About