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Limbic neuropathology in idiopathic Parkinson's disease with concomitant dementia.
Folia Neuropathol. 2004; 42(3):141-50.FN

Abstract

To study pathological background of dementia in idiopathic Parkinson's disease (PD), 41 autopsy brains (31 cases with and 10 cases without dementia) were investigated. The severity of degenerative changes was evaluated in selected limbic regions (trans- and entorhinal cortex, hippocampus, and amygdala). The densities of Lewy bodies (LBs), Lewy neurites (LNs), neurofibrillary tangles (NFTs), and amyloid neuritic plaques (NPs) were determined on immunohistochemically stained sections using antibodies against alpha-synuclein, tau-protein, and amyloid-beta. Precisely defined modern criteria for selecting study cohort (Newcastle, CERAD and Braak et al.) ensured homogeneity of the study sample and reliability of the results. Comparisons between the cases of Parkinson's disease with dementia (PDD) and those without (PD-only) revealed that the former were characterised by significantly higher densities of LBs and LNs in transentorhinal and entorhinal cortices as well as in the CA2-3 region of the hippocampus and cortical complex of amygdala. In the PDD sub-set we found statistically significant correlation of LBs with LNs counts in CA2-3 region of hippocampus as well as of LBs counts in transentorhinal cortex with LNs counts in CA2-3 hippocampal region. The relationship was also observed between LBs counts in CA2-3 region of the hippocampus and LNs counts in cortical complex of amygdala. Our studies suggest that dementia in PD may be associated with the presence of degenerative changes of PD-type in leading limbic structures, without co-existent Alzheimer's disease (AD). They also imply that LBs and LNs may appear to be morphological hallmarks of the pathological process associated with dementia in PD. LBs and LNs distribution pattern and correlations of LBs with LNs counts in limbic regions observed in our study suggest the cumulative patomechanism of changes dependent on transsynaptic alpha-syn pathology and indicate the spread of the pathological process via axonal transport. The coexistence of the small number of changes of AD-type may exacerbate cognitive deficits in PDD.

Authors+Show Affiliations

Department of Neuropathology, Institute of Psychiatry and Neurology, Warszawa, Poland. bertrand@ipin.edu.plNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15535032

Citation

Bertrand, Ewa, et al. "Limbic Neuropathology in Idiopathic Parkinson's Disease With Concomitant Dementia." Folia Neuropathologica, vol. 42, no. 3, 2004, pp. 141-50.
Bertrand E, Lechowicz W, Szpak GM, et al. Limbic neuropathology in idiopathic Parkinson's disease with concomitant dementia. Folia Neuropathol. 2004;42(3):141-50.
Bertrand, E., Lechowicz, W., Szpak, G. M., Lewandowska, E., Dymecki, J., & Wierzba-Bobrowicz, T. (2004). Limbic neuropathology in idiopathic Parkinson's disease with concomitant dementia. Folia Neuropathologica, 42(3), 141-50.
Bertrand E, et al. Limbic Neuropathology in Idiopathic Parkinson's Disease With Concomitant Dementia. Folia Neuropathol. 2004;42(3):141-50. PubMed PMID: 15535032.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Limbic neuropathology in idiopathic Parkinson's disease with concomitant dementia. AU - Bertrand,Ewa, AU - Lechowicz,Waldemar, AU - Szpak,Grazyna M, AU - Lewandowska,Eliza, AU - Dymecki,Jerzy, AU - Wierzba-Bobrowicz,Teresa, PY - 2004/11/13/pubmed PY - 2004/12/23/medline PY - 2004/11/13/entrez SP - 141 EP - 50 JF - Folia neuropathologica JO - Folia Neuropathol VL - 42 IS - 3 N2 - To study pathological background of dementia in idiopathic Parkinson's disease (PD), 41 autopsy brains (31 cases with and 10 cases without dementia) were investigated. The severity of degenerative changes was evaluated in selected limbic regions (trans- and entorhinal cortex, hippocampus, and amygdala). The densities of Lewy bodies (LBs), Lewy neurites (LNs), neurofibrillary tangles (NFTs), and amyloid neuritic plaques (NPs) were determined on immunohistochemically stained sections using antibodies against alpha-synuclein, tau-protein, and amyloid-beta. Precisely defined modern criteria for selecting study cohort (Newcastle, CERAD and Braak et al.) ensured homogeneity of the study sample and reliability of the results. Comparisons between the cases of Parkinson's disease with dementia (PDD) and those without (PD-only) revealed that the former were characterised by significantly higher densities of LBs and LNs in transentorhinal and entorhinal cortices as well as in the CA2-3 region of the hippocampus and cortical complex of amygdala. In the PDD sub-set we found statistically significant correlation of LBs with LNs counts in CA2-3 region of hippocampus as well as of LBs counts in transentorhinal cortex with LNs counts in CA2-3 hippocampal region. The relationship was also observed between LBs counts in CA2-3 region of the hippocampus and LNs counts in cortical complex of amygdala. Our studies suggest that dementia in PD may be associated with the presence of degenerative changes of PD-type in leading limbic structures, without co-existent Alzheimer's disease (AD). They also imply that LBs and LNs may appear to be morphological hallmarks of the pathological process associated with dementia in PD. LBs and LNs distribution pattern and correlations of LBs with LNs counts in limbic regions observed in our study suggest the cumulative patomechanism of changes dependent on transsynaptic alpha-syn pathology and indicate the spread of the pathological process via axonal transport. The coexistence of the small number of changes of AD-type may exacerbate cognitive deficits in PDD. SN - 1641-4640 UR - https://www.unboundmedicine.com/medline/citation/15535032/Limbic_neuropathology_in_idiopathic_Parkinson's_disease_with_concomitant_dementia_ DB - PRIME DP - Unbound Medicine ER -