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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

Abstract

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.

Keywords

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

Abbreviations

αSyn

α-Synuclein

AD

Alzheimer’s disease

Amyloid β

CAA

Cerebral amyloid angiopathy

ChEI

Cholinesterase inhibitor

Cr

Creatinine

DAT

Dopamine transporter

DLB

Dementia with Lewy bodies

DLB-AD

DLB with Alzheimer’s disease

FC

Functional connectivity

GBA

Glucocerebrosidase

GWAS

Genome-wide association studies

5-HIAA

5-Hydroxyindole acetic acid

HVA

Homovanillic acid

iLBD

Incidental Lewy body disease

LB

Lewy bodies

LBD

Lewy body disease

LBP

Lewy body pathology

MAPT

Microtubule-associated protein tau

MIBG

123I-Metaiodobenzylguanidine

MRS

Magnetic resonance spectroscopy

MTL

Medial temporal lobe

NAA

N-Acetylaspartate

NACC

National Alzheimer’s Coordinating Center

NFT

Neurofibrillary tangle

PD/ND

Parkinson’s disease nondemented

PD

Parkinson’s disease

PDD

Parkinson’s disease-dementia

PET

Positron emission tomography

PSEN1

Presenilin 1

p-tau

Phosphorylated tau

RBD

REM sleep behavior disorder

SN

Substantia nigra

SNc

Substantia nigra pars compacta

SNCA

α-Synuclein gene

SPECT

Single-photon emission computed tomography

TH

Tyrosine hydroxylase

t-tau

Total tau

TFAM

Mitochondrial transcription factor A

VBM

Voxel-based morphometric

VTA

Ventral tegmental area

WMH

White matter hyperintensity

Notes

Acknowledgements

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.

Funding

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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