Journal of Neural Transmission

, Volume 125, Issue 4, pp 615–650 | Cite as

Dementia with Lewy bodies and Parkinson’s disease-dementia: current concepts and controversies

  • Kurt A. JellingerEmail author
High Impact Review in Neuroscience, Neurology or Psychiatry - Review Article


Dementia with Lewy bodies (DLB) and Parkinson’s disease-dementia (PDD), although sharing many clinical, neurochemical and morphological features, according to DSM-5, are two entities of major neurocognitive disorders with Lewy bodies of unknown etiology. Despite considerable clinical overlap, their diagnosis is based on an arbitrary distinction between the time of onset of motor and cognitive symptoms: dementia often preceding parkinsonism in DLB and onset of cognitive impairment after onset of motor symptoms in PDD. Both are characterized morphologically by widespread cortical and subcortical α-synuclein/Lewy body plus β-amyloid and tau pathologies. Based on recent publications, including the fourth consensus report of the DLB Consortium, a critical overview is given. The clinical features of DLB and PDD include cognitive impairment, parkinsonism, visual hallucinations, and fluctuating attention. Intravitam PET and post-mortem studies revealed more pronounced cortical atrophy, elevated cortical and limbic Lewy pathologies (with APOE ε4), apart from higher prevalence of Alzheimer pathology in DLB than PDD. These changes may account for earlier onset and greater severity of cognitive defects in DLB, while multitracer PET studies showed no differences in cholinergic and dopaminergic deficits. DLB and PDD sharing genetic, neurochemical, and morphologic factors are likely to represent two subtypes of an α-synuclein-associated disease spectrum (Lewy body diseases), beginning with incidental Lewy body disease—PD-nondemented—PDD—DLB (no parkinsonism)—DLB with Alzheimer’s disease (DLB-AD) at the most severe end, although DLB does not begin with PD/PDD and does not always progress to DLB-AD, while others consider them as the same disease. Both DLB and PDD show heterogeneous pathology and neurochemistry, suggesting that they share important common underlying molecular pathogenesis with AD and other proteinopathies. Cognitive impairment is not only induced by α-synuclein-caused neurodegeneration but by multiple regional pathological scores. Recent animal models and human post-mortem studies have provided important insights into the pathophysiology of DLB/PDD showing some differences, e.g., different spreading patterns of α-synuclein pathology, but the basic pathogenic mechanisms leading to the heterogeneity between both disorders deserve further elucidation. In view of the controversies about the nosology and pathogenesis of both syndromes, there remains a pressing need to differentiate them more clearly and to understand the processes leading these synucleinopathies to cause one disorder or the other. Clinical management of both disorders includes cholinesterase inhibitors, other pharmacologic and nonpharmacologic strategies, but these have only a mild symptomatic effect. Currently, no disease-modifying therapies are available.


Dementia with Lewy bodies Parkinson’s disease-dementia Clinical features Diagnostic criteria Neuropathology Diagnostic tests Biomarker Controversy Management 





Alzheimer’s disease

Amyloid β


Cerebral amyloid angiopathy


Cholinesterase inhibitor




Dopamine transporter


Dementia with Lewy bodies


DLB with Alzheimer’s disease


Functional connectivity




Genome-wide association studies


5-Hydroxyindole acetic acid


Homovanillic acid


Incidental Lewy body disease


Lewy bodies


Lewy body disease


Lewy body pathology


Microtubule-associated protein tau




Magnetic resonance spectroscopy


Medial temporal lobe




National Alzheimer’s Coordinating Center


Neurofibrillary tangle


Parkinson’s disease nondemented


Parkinson’s disease


Parkinson’s disease-dementia


Positron emission tomography


Presenilin 1


Phosphorylated tau


REM sleep behavior disorder


Substantia nigra


Substantia nigra pars compacta


α-Synuclein gene


Single-photon emission computed tomography


Tyrosine hydroxylase


Total tau


Mitochondrial transcription factor A


Voxel-based morphometric


Ventral tegmental area


White matter hyperintensity



The author would like to thank Mr. E. Mitter-Ferstl, Ph.D., for secretarial and graphical work.

Compliance with ethical standards

Conflict of interest

The author declares that he has no conflict of interest.


The study was partially funded by the Society for the Promotion of Research in Experimental Neurology, Vienna, Austria.


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© Springer-Verlag GmbH Austria, part of Springer Nature 2017

Authors and Affiliations

  1. 1.Institute of Clinical NeurobiologyViennaAustria

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