‘Lewy body disease’: clinico-pathological correlations in 18 consecutive cases of Parkinson's disease with and without dementia

Vos, Rob A. I. de; Jansen, E. N. H.; Stam, Frans C.; Ravid, Rivka; Swaab, Dick F.

doi:10.1016/0303-8467(94)00060-j

Cited by 69 publications

(44 citation statements)

References 32 publications

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“…Two of the 5 cases had a clinical history of cognitive impairment which developed late in the disease process and was thought to be related to the 306 Dementia 1996;7:304-313 (table 2). Patients with latc-onset PD all showed the severe brainstem pathology of PD in addition to significant numbers of diffuse cortical plaques and rare cortical Lcwy bodies, both of which are normally associated with age [17,28,29], Gender has previously been found to be a significant variable in the study of brain volume [19J. In the present study patients were primarily male and there were insufficient female patients to investi gate gender effects.…”

Section: Aterials and M Ethodsmentioning

confidence: 70%

Regional Brain Atrophy in Idiopathic Parkinson's Disease and Diffuse Lewy Body Disease

Double

Halliday²,

Mcritchie³

et al. 1996

Dement Geriatr Cogn Disord

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This study measured brain atrophy in patients with idiopathic Parkinson''s disease and diffuse Lewy body disease, all of whom had equivalent loss of midbrain dopaminergic neurons and absence of Alzheimer''s disease. Characteristic patterns of volume loss were found throughout the brain, depending on the age of onset and clinical signs. An equivalent loss of medial temporal lobe structures occurred in all parkinsonian patients. This atrophy was similar in magnitude to that seen in Alzheimer''s disease and is likely to be the anatomical substrate for the memory deficits found in each of these patient groups. Frontal lobe atrophy was a feature of both late-onset Parkinson''s disease (mild atrophy) and diffuse Lewy body disease (significant atrophy) groups, with all cases analyzed having dementia. Atrophy of frontal lobes correlated with the duration of motor symptoms in these patients and may suggest an association between dopaminergic deafferentation, frontal atrophy and dementia.

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Section: Aterials and M Ethodsmentioning

confidence: 70%

Regional Brain Atrophy in Idiopathic Parkinson's Disease and Diffuse Lewy Body Disease

Double

Halliday²,

Mcritchie³

et al. 1996

Dement Geriatr Cogn Disord

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“…Sometimes it is difficult to distinguish a specific pattern in the cognitive or behavioral symptoms of dementia that would differentiate DLBD from AD [49]. It may be possible that, although DLBD and AD are distinct clinicopathological entities, the biochemical mechanism of dementia in these diseases might be similar.…”

Section: Discussionmentioning

confidence: 99%

Oxidation of Cytosolic Proteins and Expression of Creatine Kinase BB in Frontal Lobe in Different Neurodegenerative Disorders

Aksenova¹,

Aksenov²,

Payne

et al. 1999

Dement Geriatr Cogn Disord

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The presence of the biomarkers of oxidative damage, protein carbonyl formation and the inactivation of oxidatively sensitive brain creatine kinase (CK BB, cytosolic isoform), were studied in frontal lobe autopsy specimens obtained from patients with different age-related neurodegenerative diseases: Alzheimer’s disease (AD), Pick’s disease (PkD), diffuse Lewy body disease (DLBD), Parkinson’s disease (PD), and age-matched control subjects. The CK activity was significantly reduced in the frontal lobe of AD, PkD and DLBD subjects, and CK BB-specific mRNA was significantly reduced in AD and DLBD. Protein carbonyl content was significantly increased in AD, PkD and DLBD. The results of this study confirm that the presence of biomarkers of oxidative damage is related to the presence of histopathological markers of neurodegeneration. Our data suggest that oxidative damage contributes to the development of the symptoms of frontal dysfunction in AD, PkD and DLBD. The development of frontal dysfunction in idiopathic PD might be secondary to oxidative damage and neuronal loss primarily located in the nigrostriatal system. The results of CK BB expression analysis demonstrate that the loss of the isoenzyme in different neurodegenerative diseases is likely the consequence of its posttranslational modification, possibly oxidative damage. Changes in CK BB expression may be an early indicator of oxidative stress in neurons.

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“…Pathologically, PD is characterized by neuronal cell loss and Lewy bodies in the surviving neurones of the substantia nigra (Hughes et al, 1993). In addition, Lewy bodies are found in the cortex of nearly all PD patients (Hughes et al, 1993;de Vos et al, 1995), particularly in PD patients with dementia (Matilla et al, 1998;Hurtig et al, 2000). Accordingly, DLB and PD share common clinical and neuropathologic features.…”

Section: Introductionmentioning

confidence: 95%

A comparative study of psychiatric symptoms in dementia with Lewy bodies and Parkinson's disease with and without dementia

Aarsland¹,

Ballard

Larsen³

et al. 2001

Int J Geriat Psychiatry

296

196

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‘Lewy body disease’: clinico-pathological correlations in 18 consecutive cases of Parkinson's disease with and without dementia

Cited by 69 publications

References 32 publications

Regional Brain Atrophy in Idiopathic Parkinson's Disease and Diffuse Lewy Body Disease

Regional Brain Atrophy in Idiopathic Parkinson's Disease and Diffuse Lewy Body Disease

Oxidation of Cytosolic Proteins and Expression of Creatine Kinase BB in Frontal Lobe in Different Neurodegenerative Disorders

A comparative study of psychiatric symptoms in dementia with Lewy bodies and Parkinson's disease with and without dementia

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