Pathologic Correlates of Dementia in Parkinson's Disease

Chui, Helena C.; Mortimer, James A.; Slager, Ursula T.; Zarow, Chris; Bondareff, William; Webster, David D.

doi:10.1001/archneur.1986.00520100013007

Cited by 133 publications

(36 citation statements)

References 32 publications

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“…In contrast, our patients had PD of the late onset type and most of them showed various degrees of mental impairment, four having dementia. PD of late onset with dementia as a frequent manifestation is probably a vari ant of classic PD and a degenerative disorder related to SDAT [5,7,21]. This may also explain the similarly decreased SLI levels in this study.…”

Section: Discussionsupporting

confidence: 55%

“…In a later study, however, a marked increase of SPLI in CSF was described, sug gesting that a compensatory increase in SP-ergic neu ronal activity might occur when dopaminergic transmis sion is failing [21], We studied CSF SPLI and SLI in a small group of senile patients with parkinsonism and report our findings because of the clinical interest of evaluating the CSF neuropeptide status and the possible pathophysiological significance of changes. Late onset PD appears to have pathological relationships with SDAT [5,7,22] and for comparative purposes we include results of CSF SPLI and SLI measurements in patients with SDAT, published in detail elsewhere [8].…”

Section: Introductionmentioning

confidence: 99%

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Immunoreactive Substance P and Somatostatin in the Cerebrospinal Fluid of Senile Parkinsonian Patients

et al. 1989

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The concentration of substance-P-like immunoreactivity (SPLI) and somatostatin-like immunoreactivity (SLI) in the lumbar spinal fluid of senile parkinsonian patients (mean age 77.6 ± 6.7 years) and senile control patients (mean age 83.5 ± 5.6 years) were determined by specific radioimmunoassays. Mean SPLI and SLI levels in the control group were 8.1 ± 2.0 (SD) and 32.5 ± 12.0 fmol/ml, respectively. The mean SPLI levels were not significantly different in the groups. The mean SLI level was significantly lower in the group of patients with Parkinson’s disease (19.8 ± 9.0 fmol/ml). A comparison with results in patients with senile dementia of Alzheimer type (SDAT) shows that, in addition to clinical and pathological correlations, Parkinson’s disease of late onset may share a deficit in somatostatinergic neuromodulation with SDAT.

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Section: Discussionsupporting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Immunoreactive Substance P and Somatostatin in the Cerebrospinal Fluid of Senile Parkinsonian Patients

et al. 1989

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“…3 deficits in the two groups, might reflect the well established involvement of septo-hippocampal systems in Alzheimer's patients; 4 while Alzheimer-type changes in the septo-hippocampal system are reported to occur in demented parkinsonian patients, 10 they are not always evident. 9 The observed milder impairments in Parkinson's patients may alternatively implicate dorsolateral striatal-frontal connections, which have tentatively been linked to spatial memory. 37 Both communalities and differences in these two dementia groups might also be related to characteristic neurotransmitter abnormalities.…”

Section: Discussionmentioning

confidence: 99%

“…4 ' [42][43][44][45] Deficits in this system, which has been associated with learning and memory, 46 " 48 could thus be a necessary but not sufficient condition for dementing symptoms. Compromises in cholinergic function, one of the central neurotransmitter deficits in Alzheimer's disease, 4 9 -5 0 have also been observed in Parkinson's disease, 9 but do not appear to be a consistent feature. 4 While the complexities of transmitter involvement in the primary degenerative dementias make conclusions difficult, 51 a more catecholamine based dementia in Parkinson's disease, compared to a more acetylcholine related dementia in Alzheimer disease, might account for some of the neurobehavioral differences observed here.…”

Section: Discussionmentioning

confidence: 99%

Selective Deficits in Alzheimer and Parkinsonian Dementia: Visuospatial Function

Litvan

Williams

Fedio

et al. 1990

Can. j. neurol. sci.

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Deficits in visuospatial cognition are frequently cited as an important component of the cognitive changes accompanying Parkinson's disease. To characterize possible differences between Parkinson's (PD) and Alzheimer's (AD) dementia, patients from both groups, matched for overall dementia severity, age and education, were contrasted neuropsychologically. Visuospatial tasks dissociated from memory, were significantly compromised in both patient groups. Differential impairment was evident on visuospatial abstraction and reasoning (Object Assembly), which was most deficient in PD. Visuospatial cognition associated with memory, classified both patient groups as impaired compared to controls, but AD patients demonstrated substantially lower performance levels than those with PD. Parkinsonian dementia thus appears to have some distinct features compared to Alzheimer's disease, which may indicate differences in underlying pathogenic mechanisms. RESUME: Deficits selectifs dans la demence de la maladie d'Alzheimer et de la maladie de Parkinson: fonction visuospatiale Des deficits dans la cognition visuospatiale sont souvent cites comme etant une composante importante des changements cognitifs accompagnant la maladie de Parkinson. Afin de caracteriser les differences possibles entre la demence de la maladie de Parkinson (MP) et celle de la maladie d'Alzheimer (MA), des patients de chacun de ces deux groupes, apparies pour la severite globale de la demence, l'age et le niveau d'education, ont ete compares au point de vue neuropsychologique. Les taches visuospatiales dissociees de la memoire etaient significativement compromises dans les deux groupes de patients. Une atteinte differentielle etait evidente au niveau de 1'abstraction visuospatiale et du raisonnement (assemblage d'objets), cette atteinte etant plus marquee dans la MP. La cognition visuospatiale associee a la mSmoire classifiait les deux groupes de patients comme atteints lorsqu'ils etaient compares aux controles, mais les patients avec MA avaient des niveaux de performance plus bas que ceux des patients avec MP. La demence parkinsonienne semble done posseder des caracteristiques distinctes comparativement a celles de la maladie d'Alzheimer, ce qui peut indiquer des differences sous-jacentes aux mecanisms pathogeniques.

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“…Due to the specificity of our antibody and to the fact that Tau 64 and 69 have a molecular weight higher than normal Tau, normal Tau proteins did not interfere with our detection 1171. Furthermore, we observed that the triplet is sta- [39][40][41]. Many reasons may explain these conflicting results: First, the methods used for detecting the Alzheimer changes and the criteria permitting the diagnosis of coexisting Alzheimer's disease 141, 423 ought to be considered.…”

Section: Discussionmentioning

confidence: 95%

Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins

Vermersch

Delacourte

Javoy‐Agid

et al. 1993

Annals of Neurology

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In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti-paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55, 64, and 69, which are known to be specific and reliable biochemical markers of Alzheimer-type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer-type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.

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Pathologic Correlates of Dementia in Parkinson's Disease

Cited by 133 publications

References 32 publications

Immunoreactive Substance P and Somatostatin in the Cerebrospinal Fluid of Senile Parkinsonian Patients

Immunoreactive Substance P and Somatostatin in the Cerebrospinal Fluid of Senile Parkinsonian Patients

Selective Deficits in Alzheimer and Parkinsonian Dementia: Visuospatial Function

Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins

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