Dementia in Parkinson disease

Lieberman, Abraham; Dziatolowski, Marie; Kupersmith, Mark J.; Serby, Michael; Goodgold, Albert; Korein, Julius; Goldstein, Menek

doi:10.1002/ana.410060409

Cited by 297 publications

(81 citation statements)

References 29 publications

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“…The estimate of the frequency of dementia is a very controversial issue [8,38], Our results, and those of others [6], indicate that the great majority of the nondemented patients show no generalized cognitive changes over time. In the group of parkinsonian patients without mental deterioration, dementia was manifested in 21.4% of the cases over the 7-year observation period, a period of time that seems long enough to reveal the onset of cognitive deficits.…”

Section: Discussionsupporting

confidence: 55%

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

Piccirilli

D’Alessandro²,

Finali³

et al. 1994

Dement Geriatr Cogn Disord

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In order to evaluate possible progression in the severity of their cognitive impairment, 34 parkinsonians with intellectual impairment were followed longitudinally for 7 years. Each patient was matched for age, sex, severity and duration of illness, and pharmacological treatment, with a parkinsonian patient without cognitive impairment. Results suggest that cognitive deficits are not static but rather there is a progression in the severity. Furthermore, patients suffering from severe dementia are more likely to die during the follow-up period. The prognosis of Parkinson''s disease seems to be changed substantially by the occurrence of dementia. The natural history of parkinsonian dementia does not seem to differ from the history of other forms of dementia with a progressively disabling course leading to a complete loss of autonomy.

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Section: Discussionsupporting

confidence: 55%

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

Piccirilli

D’Alessandro²,

Finali³

et al. 1994

Dement Geriatr Cogn Disord

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“…PD is a neurodegenerative disorder characterized by disturbances in motor function [11] and a loss of dopa mine neurons in the pars compacta of the substantia nigra [12,13], Furthermore, some PD patients develop demen tia, and it is now widely accepted that the incidence of cognitive disorders is higher in PD patients than it is in control populations [14,15], Although demented PD patients can show the characteristic pathology of the Alz heimer type [16,17], ischemic lesions [17,18] and/or sev eral neurotransmitter changes [7,10,19] have also been reported in these patients.…”

Section: Introductionmentioning

confidence: 99%

Calbindin D-28k and Monoamine Oxidase A Immunoreactive Neurons in the Nucleus Basalis of Meynert in Senile Dementia of the Alzheimer Type and Parkinson's Disease

Chan‐Palay¹,

Höchli²,

Savaskan³

et al. 1993

Dement Geriatr Cogn Disord

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In this study, calbindin D-28k (CaBP), monoamine oxidase A (MAO A) and nerve growth factor receptor (NGFr) immunoreactivities were investigated in the nucleus basalis of Meynert (NbM) in patients with senile dementia of the Alzheimer type (SDAT), with Parkinson''s disease (PD) with or without dementia, and in controls. Immunocytochemistry using specific antibodies in differing serial sections was employed, and cell counts and NbM nuclear volume measurements were made. Most of the large multipolar NbM neurons showed CaBP immunoreactivity in the cytoplasm of their somata, dendrites and axons. In adjacent, NGFr-reacted sections, the large NbM neurons were also found to be intensely immunoreactive for NGFr on their cellular surfaces. In addition, a subpopulation of large NbM neurons and glial cells were found to be immunoreactive for MAO A. The number of CaBP-immunoreactive (CaBP-i) neurons was decreased by an average of 55% in the 6 SDAT patients, 70% in the 2 nondemented PD patients and 40% in the 1 demented PD patient. The volume calculated for the compact part of the NbM formed by the CaBP-i neuronal somata decreased by an average of 47% in SDAT. On the other hand, measurements in the volume of NGFr-i neurons (including the dendritic arborization) showed an average decrease of 25% in SDAT patients compared to controls. Although all SDAT and PD patients showed a decrease of CaBP-i neurons in the NbM, a loss of MAO-A-i NbM neurons was found only in those patients with dementia. Therefore, the relative proportions of MAO-A-i to CaBP-i neurons were increased in the nondemented PD patients (14.2 and 19.6%) when compared with those in the demented PD patient (2.2%) and with the SDAT patients (0.3-5.6%). These data indicate that a balanced presence of MAO-A-i cholinergic, large NbM neurons may be necessary for the proper maintenance of cognitive function. Functionally this may be translated to mean that dementing changes may cause a decrease from the normal amount of MAO A enzyme activity. This suggests that therapeutic strategies based upon correction of MAO-A activities by MAO-A inhibitors may be important to ameliorating some of the loss in cholinergic function in dementias of SDAT and PD.

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“…For example, Lou Gehrig's disease (ALS), Parkinson's disease and Alzheimer's disease are frequently viewed as totally unrelated and completely distinct from each other, even though there are extremely clear cases that prove the opposite: ALS-parkinsonism dementia complex (ALS-PDC) of Guam and the Western Pacific often combines the features of all, albeit with the ALS phenotype usually preceding the loss of neurons in other CNS fields [1]. Parkinson's disease and ALS frequently feature aspects of Alzheimer's like dementia [2][3][4][5]; fronto-temporal dementia can have motor neuron loss, etc., as part of the long-term spectrum of disease expression [6]. The risk of ALS is significantly increased in people who suffer from asthma, celiac disease, early diabetes, multiple sclerosis, myasthenia gravis, hypothyroidism, Sjögren'ssyndrome, systemic lupus erythematosus (SLE) and ulcerative colitis [7].…”

Section: Introductionmentioning

confidence: 99%

Aluminum?s Role in CNS-immune System Interactions leading to Neurological Disorders

CA¹

2013

Immunome Res

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Multisystem interactions are well established in neurological disorders, in spite of conventional views that only the central nervous system (CNS) is impacted. We review evidence for mutual interactions between the immune and nervous systems and show how these seem to be implicated in the origin and progression of nervous system disorders. Well-established immune system triggers leading to autoimmune reactions are considered. Of these, aluminum, a known neurotoxicant, may be of particular importance. We have demonstrated elsewhere that aluminum has the potential to induce damage at a range of levels in the CNS leading to neuronal death, circuit malfunction and ultimately, system failure. Aluminum is widely used as an adjuvant in various vaccine formulations and has been implicated in a multisystem disorder termed "autoimmune/inflammatory syndrome induced by adjuvants" (ASIA). The implications of aluminum-induced ASIA in some disorders of the CNS are considered. We propose a unified theory capturing a progression from a local response to a systemic response initiated by disruption of water-based interfaces of exposed cells.

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Dementia in Parkinson disease

Cited by 297 publications

References 29 publications

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

Neuropsychological Follow-Up of Parkinsonian Patients with and without Cognitive Impairment

Calbindin D-28k and Monoamine Oxidase A Immunoreactive Neurons in the Nucleus Basalis of Meynert in Senile Dementia of the Alzheimer Type and Parkinson's Disease

Aluminum?s Role in CNS-immune System Interactions leading to Neurological Disorders

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