Clinical and pathological features affecting cardiac sympathetic denervation in autopsy-confirmed dementia with Lewy bodies.
Alzheimer’s disease
autonomic nervous system
dementia with Lewy bodies
Journal
European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
22
01
2020
accepted:
09
03
2020
pubmed:
3
4
2020
medline:
29
6
2021
entrez:
3
4
2020
Statut:
ppublish
Résumé
The aim was to clarify the features affecting cardiac sympathetic denervation in autopsy-confirmed dementia with Lewy bodies (DLB) patients. Fifty-four autopsy-confirmed DLB patients were enrolled. Tissue samples of the left ventricular anterior wall were immunostained with anti-tyrosine hydroxylase antibody to identify catecholaminergic nerve axons. Immunostained areas were quantified as residual cardiac sympathetic nerve (CSN) axons and the relationship between the degree of residual CSN axons and clinical and neuropathological features was examined. Virtually all patients showed small amounts of residual CSN axons (0.87%, range 0.02%-9.98%), with 50 patients (92.6%) showing <2.0% of residual axons. The patients who showed psychological symptoms within the first year of the disease had significantly more residual CSN axons than the remaining patients did (1.50% vs. 0.40%, P < 0.01). Patients with a short disease duration and neocortical-type Lewy body pathology tended to have more preserved CSN axons, although this difference was not statistically significant. Fifty-three patients (98.1%) who had neurofibrillary tangles in the brain and strong concomitant Alzheimer's disease pathology also had statistically significantly more preserved CSN axons. The patient with the most preserved CSN axons showed different characteristics from the results, except for the first symptom. Psychological symptoms within the first year of the disease, a short disease duration, neocortical-type Lewy body pathology and strong concomitant Alzheimer's disease pathology may be related to mild CSN degeneration in DLB patients. Thus, DLB patients with broad Lewy body pathology in the brain in the early stages may show mild CSN degeneration.
Sections du résumé
BACKGROUND AND PURPOSE
The aim was to clarify the features affecting cardiac sympathetic denervation in autopsy-confirmed dementia with Lewy bodies (DLB) patients.
METHODS
Fifty-four autopsy-confirmed DLB patients were enrolled. Tissue samples of the left ventricular anterior wall were immunostained with anti-tyrosine hydroxylase antibody to identify catecholaminergic nerve axons. Immunostained areas were quantified as residual cardiac sympathetic nerve (CSN) axons and the relationship between the degree of residual CSN axons and clinical and neuropathological features was examined.
RESULTS
Virtually all patients showed small amounts of residual CSN axons (0.87%, range 0.02%-9.98%), with 50 patients (92.6%) showing <2.0% of residual axons. The patients who showed psychological symptoms within the first year of the disease had significantly more residual CSN axons than the remaining patients did (1.50% vs. 0.40%, P < 0.01). Patients with a short disease duration and neocortical-type Lewy body pathology tended to have more preserved CSN axons, although this difference was not statistically significant. Fifty-three patients (98.1%) who had neurofibrillary tangles in the brain and strong concomitant Alzheimer's disease pathology also had statistically significantly more preserved CSN axons. The patient with the most preserved CSN axons showed different characteristics from the results, except for the first symptom.
CONCLUSION
Psychological symptoms within the first year of the disease, a short disease duration, neocortical-type Lewy body pathology and strong concomitant Alzheimer's disease pathology may be related to mild CSN degeneration in DLB patients. Thus, DLB patients with broad Lewy body pathology in the brain in the early stages may show mild CSN degeneration.
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1155-1163Subventions
Organisme : Japan Agency for Medical Research and Development (AMED)
ID : JP18dm0107105
Pays : International
Organisme : Japan Agency for Medical Research and Development (AMED)
ID : JP16kk0205009
Pays : International
Organisme : Grants-in-Aid from the Research Committee of CNS Degenerative Diseases
Pays : International
Organisme : Research on Policy Planning and Evaluation for Rare and Intractable Diseases, Health, Labour and Welfare Sciences Research Grants; the Ministry of Health, Labour and Welfare, Japan (MY)
Pays : International
Organisme : JSPS KAKENHI
ID : 18H02533
Pays : International
Organisme : The Collaborative Research Project of the Brain Research Institute, Niigata University (KA)
Pays : International
Organisme : Strategic Research Program for Brain Sciences from AMED (KA)
Pays : International
Informations de copyright
© 2020 European Academy of Neurology.
Références
Walker Z, Possin KL, Boeve BF, Aarsland D. Lewy body dementias. Lancet 2015; 386: 1683-1697.
Uchihara T, Giasson BI. Propagation of alpha-synuclein pathology: hypotheses, discoveries, and yet unresolved questions from experimental and human brain studies. Acta Neuropathol 2016; 131: 49-73.
McKeith I, Boeve B, Dickson D, et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report of the DLB consortium. Neurolo gy 2017; 89: 88-100.
Orimo S, Ozawa E, Nakade S, Sugimoto T, Mizusawa H. 123I-metaiodobenzylguanidine myocardial scintigraphy in Parkinson’s disease. J Neurol Neurosurg Psychiatry 1999; 67: 189-194.
Takahashi M, Ikemura M, Oka T, et al. Quantitative correlation between cardiac MIBG uptake and remaining axons in the cardiac sympathetic nerve in Lewy body disease. J Neurol Neurosurg Psychiatry 2015; 86: 939-944.
Komatsu J, Samuraki M, Nakajima K, et al. I-MIBG myocardial scintigraphy for the diagnosis of DLB: a multicentre 3-year follow-up study. J Neurol Neurosurg Psychiatry 2018; 89: 1167-1173.
Tsujikawa K, Hasegawa Y, Yokoi S, et al. Chronological changes of 123I-MIBG myocardial scintigraphy and clinical features of Parkinson’s disease. J Neurol Neurosurg Psychiatry 2015; 86: 945-951.
McKeith IG, Dickson DW, Lowe J, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB consortium. Neurology 2005; 65: 1863-1872.
Braak H, Braak E. Neuropathological staging of Alzheimer-related changes. Acta Neuropathol 1991; 82: 239-259.
Delli Pizzi S, Franciotti R, Taylor JP, et al. Thalamic involvement in fluctuating cognition in dementia with Lewy bodies: magnetic resonance evidences. Cereb Cortex 2015; 25: 3682-3689.
Firbank MJ, Lloyd J, O’Brien JT. The relationship between hallucinations and FDG-PET in dementia with Lewy bodies. Brain Imaging Behav 2016; 10: 636-639.
Goldstein DS, Holmes C, Li ST, Bruce S, Metman LV, Cannon RO. Cardiac sympathetic denervation in Parkinson disease. Ann Intern Med 2000; 133: 338-347.
Orimo S, Takahashi A, Uchihara T, et al. Degeneration of cardiac sympathetic nerve begins in the early disease process of Parkinson’s disease. Brain Pathol 2007; 17: 24-30.
Guo JL, Covell DJ, Daniels JP, et al. Distinct α-synuclein strains differentially promote tau inclusions in neurons. Cell 2013; 154: 103.
Roberts HL, Schneider BL, Brown DR. α-Synuclein increases β-amyloid secretion by promoting β-/γ-secretase processing of APP. PLoS ONE 2017; 12: 1-22.
Kosaka K. Diffuse Lewy body disease in Japan. J Neurol 1990; 237: 197-204.
McKeith IG. Dementia with Lewy bodies and Parkinson’s disease with dementia: where two worlds collide. Practical Neurology 2007; 7: 374-382.
Hansen D, Ling H, Lashley T, Holton JL, Warner TT. Review: clinical, neuropathological and genetic features of Lewy body dementias. Neuropath Appl Neuro 2019; 45: 635-654.
Braak H, Del Tredici K. Spreading of tau pathology in sporadic Alzheimer’s disease along cortico-cortical top-down connections. Cereb Cortex 2018; 28: 3372-3384.