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Could hyperlipidemia be a risk factor for corticobasal syndrome? — a pilot study
, 1, 2, 2, 3, 1, 4, 1
Affiliations- Department of Neurology, Medical University of Warsaw, Kondratowicza 8, 03/242 Warsaw, Poland
- Department of Neurology and Center of Clinical Neuroscience, First Faculty of Medicine, Charles University, General University Hospital in Prague, Czech Republic
- Diagnostic Ultrasound Lab, Department of Pediatric Radiology, Medical Faculty, Medical University of Warsaw, Poland
- Department of Internal Medicine and Endocrinology, Medical University of Warsaw,, Warsaw, Poland
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Abstract
Introduction. Corticobasal syndrome (CBS) is a specific clinical manifestation shared by multiple pathologies. The exact mechanism of this phenomenon remains unclear. Differential diagnosis of CBS in everyday clinical practice is challenging, as this syndrome can overlap with other entities, especially progressive supranuclear palsy Richardson-Steele phenotype (PSP-RS). Several papers have suggested a possible role of vascular pathology as a linking factor in the pathogenesis of CBS based on different neuropathologies. This paper analyses differences in the occurrence of the most common vascular risk factors such as hypertension and lipid profile with respect to dietary habits among patients who fulfill the diagnostic criteria for probable/possible CBS and PSP-RS.
Material and methods. Seventy (70) patients in total were included in the study. Exclusion criteria comprised hydrocephalus, stroke in the past, the presence of marked vascular changes in white matter defined as the presence of vascular change ≥ 1 mm in 3T MRI, medical history of hyperlipidemia or the use of drugs that could impact upon lipid metabolism before the initiation of the neurodegenerative disease, and neoplastic focuses in the central nervous system. Patients with diabetes, or with BMI exceeding 18–25, or who were smokers, or who were affected by chronic stress were also excluded. Data was analysed statistically using the Shapiro-Wilk test, the U Mann-Whitney test for group comparison, and a Bonferroni correction to control the false discovery rate (FDR).
Results. Our obtained results indicated a statistically significantly higher level of total cholesterol in the CBS group (p = 0.0039) without a correlation with dietary habits.
Conclusions and clinical implications. The results obtained in our study may suggest a possible role of vascular pathology in CBS development. This issue requires further research.
Abstract
Introduction. Corticobasal syndrome (CBS) is a specific clinical manifestation shared by multiple pathologies. The exact mechanism of this phenomenon remains unclear. Differential diagnosis of CBS in everyday clinical practice is challenging, as this syndrome can overlap with other entities, especially progressive supranuclear palsy Richardson-Steele phenotype (PSP-RS). Several papers have suggested a possible role of vascular pathology as a linking factor in the pathogenesis of CBS based on different neuropathologies. This paper analyses differences in the occurrence of the most common vascular risk factors such as hypertension and lipid profile with respect to dietary habits among patients who fulfill the diagnostic criteria for probable/possible CBS and PSP-RS.
Material and methods. Seventy (70) patients in total were included in the study. Exclusion criteria comprised hydrocephalus, stroke in the past, the presence of marked vascular changes in white matter defined as the presence of vascular change ≥ 1 mm in 3T MRI, medical history of hyperlipidemia or the use of drugs that could impact upon lipid metabolism before the initiation of the neurodegenerative disease, and neoplastic focuses in the central nervous system. Patients with diabetes, or with BMI exceeding 18–25, or who were smokers, or who were affected by chronic stress were also excluded. Data was analysed statistically using the Shapiro-Wilk test, the U Mann-Whitney test for group comparison, and a Bonferroni correction to control the false discovery rate (FDR).
Results. Our obtained results indicated a statistically significantly higher level of total cholesterol in the CBS group (p = 0.0039) without a correlation with dietary habits.
Conclusions and clinical implications. The results obtained in our study may suggest a possible role of vascular pathology in CBS development. This issue requires further research.
Keywords
corticobasal syndrome, hyperlipidemia, neurodegeneration, risk factor, CBS phenotype
About this articleTitle
Could hyperlipidemia be a risk factor for corticobasal syndrome? — a pilot study
Journal
Neurologia i Neurochirurgia Polska
Issue
Article type
Research Paper
Pages
177-182
Published online
2022-12-15
Page views
2159
Article views/downloads
528
DOI
Pubmed
Bibliographic record
Neurol Neurochir Pol 2023;57(2):177-182.
Keywords
corticobasal syndrome
hyperlipidemia
neurodegeneration
risk factor
CBS phenotype
Authors
Natalia Madetko-Alster
Piotr Alster
Tereza Bartošová
Jiří Klempíř
Bartosz Migda
Dominika Przewodowska
Anna Migda
Andrzej Friedman
References (32)- Armstrong MJ, Litvan I, Lang AE, et al. Criteria for the diagnosis of corticobasal degeneration. Neurology. 2013; 80(5): 496–503.
- Höglinger GU, Respondek G, Stamelou M, et al. Movement Disorder Society-endorsed PSP Study Group. Clinical diagnosis of progressive supranuclear palsy: The movement disorder society criteria. Mov Disord. 2017; 32(6): 853–864.
- Wadia PM, Lang AE. The many faces of corticobasal degeneration. Parkinsonism Relat Disord. 2007; 13 Suppl 3: S336–S340.
- Ali F, Josephs KA. Corticobasal degeneration: key emerging issues. J Neurol. 2018; 265(2): 439–445.
- Dunalska A, Pikul J, Schok K, et al. The significance of vascular pathogenesis in the examination of corticobasal syndrome. Front Aging Neurosci. 2021; 13: 668614.
- Respondek G, Grimm MJ, Piot I, et al. Movement Disorder Society-Endorsed Progressive Supranuclear Palsy Study Group. Validation of the movement disorder society criteria for the diagnosis of 4-repeat tauopathies. Mov Disord. 2020; 35(1): 171–176.
- Respondek G, Grimm MJ, Piot I, et al. Validation of the movement disorder society criteria for the diagnosis of 4-repeat tauopathies. Mov Disord. 2020; 35(1): 171–176.
- Grijalva RM, Pham NT, Huang Q, et al. Brainstem biomarkers of clinical variant and pathology in progressive supranuclear palsy. Mov Disord. 2022; 37(4): 702–712.
- Kasanuki K, Josephs KA, Ferman TJ, et al. Diffuse Lewy body disease manifesting as corticobasal syndrome: A rare form of Lewy body disease. [Erratum in: Neurology. 2018 Nov 20;91(21):986. PMID: 29898972; PMCID: PMC6059030]. Neurology. 2018; 91(3): e268–e279.
- Koga S, Roemer SF, Kasanuki K, et al. Cerebrovascular pathology presenting as corticobasal syndrome: An autopsy case series of "vascular CBS". Parkinsonism Relat Disord. 2019; 68: 79–84.
- Dugger BN, Malek-Ahmadi M, Monsell SE, et al. A cross-sectional analysis of late-life cardiovascular factors and their relation to clinically defined neurodegenerative diseases. Alzheimer Dis Assoc Disord. 2016; 30(3): 223–229.
- Winikates J, Jankovic J. Vascular progressive supranuclear palsy. J Neural Transm Suppl. 1994: 189–201.
- Tranchant C. [Other causes of parkinsonism]. Presse Med. 2017; 46(2 Pt 1): 210–217.
- Takase KI, Matsumoto S, Nishi H, et al. A case of superior sagittal sinus intracranial dural arteriovenous fistula mimicking corticobasal syndrome. J Neurol Sci. 2017; 376: 91–92.
- Kreisler A, Mastain B, Tison F, et al. [Multi-infarct disorder presenting as corticobasal degeneration (DCB): vascular pseudo-corticobasal degeneration?]. Rev Neurol (Paris). 2007; 163(12): 1191–1199.
- Ghika J, Bogousslavsky J. Presymptomatic hypertension is a major feature in the diagnosis of progressive supranuclear palsy. Arch Neurol. 1997; 54(9): 1104–1108.
- Kim YD, Kim JS, Lee ES, et al. Progressive "vascular" corticobasal syndrome due to bilateral ischemic hemispheric lesions. Intern Med. 2009; 48(18): 1699–1702.
- Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020; 396(10248): 413–446.
- Nation DA, Sweeney MD, Montagne A, et al. Blood-brain barrier breakdown is an early biomarker of human cognitive dysfunction. Nat Med. 2019; 25(2): 270–276.
- Van Gool B, Storck SE, Reekmans SM, et al. LRP1 has a predominant role in production over clearance of aβ in a mouse model of Alzheimer's disease. Mol Neurobiol. 2019; 56(10): 7234–7245.
- Zhao Y, Gong CX. From chronic cerebral hypoperfusion to Alzheimer-like brain pathology and neurodegeneration. Cell Mol Neurobiol. 2015; 35(1): 101–110.
- Liu X, Yamashita T, Shang J, et al. Twendee x ameliorates phosphorylated tau, α-Synuclein and neurovascular dysfunction in alzheimer's disease transgenic mice with chronic cerebral hypoperfusion. J Stroke Cerebrovasc Dis. 2019; 28(10): 104310.
- Alster P, Madetko N, Friedman A. Neutrophil-to-lymphocyte ratio (NLR) at boundaries of progressive supranuclear palsy syndrome (PSPS) and corticobasal syndrome (CBS). Neurol Neurochir Pol. 2021; 55(1): 97–101.
- Du XL, Song L, Schulz PE, et al. Associations between vascular diseases and alzheimer's disease or related dementias in a large cohort of men and women with colorectal cancer. J Alzheimers Dis. 2022; 90(1): 211–231.
- Kim SiE, Kim HJ, Jang H, et al. Interaction between Alzheimer's disease and cerebral small vessel disease: a review focused on neuroimaging markers. Int J Mol Sci. 2022; 23(18).
- Zaciragic A, Dervisevic A, Valjevac A, et al. Difference in the standard and novel lipid profile parameters between patients with Alzheimer’s disease and vascular dementia stratified by the degree of cognitive impairment. Mater Sociomed. 2022; 34(2): 100–106.
- Mundal LJ, Igland J, Svendsen K, et al. Association of familial hypercholesterolemia and statin use with risk of dementia in norway. JAMA Netw Open. 2022; 5(4): e227715.
- Iwagami M, Qizilbash N, Gregson J, et al. Blood cholesterol and risk of dementia in more than 1·8 million people over two decades: a retrospective cohort study. Lancet Healthy Longev. 2021; 2(8): e498–e506.
- Trumbore CN, Raghunandan A. An Alzheimer's disease mechanism based on early pathology, anatomy, vascular-induced flow, and migration of maximum flow stress energy location with increasing vascular disease. J Alzheimers Dis. 2022; 90(1): 33–59.
- Sahathevan R, Linden T, Villemagne VL, et al. Positron emission tomographic imaging in stroke: cross-sectional and follow-up assessment of amyloid in ischemic stroke. Stroke. 2016; 47(1): 113–119.
- Michels L, Warnock G, Buck A, et al. Arterial spin labeling imaging reveals widespread and Aβ-independent reductions in cerebral blood flow in elderly apolipoprotein epsilon-4 carriers. J Cereb Blood Flow Metab. 2016; 36(3): 581–595.
- Samborska-Ćwik J, Szlufik S, Migda B, et al. Carbohydrate metabolism and lipid profile in patients with Parkinson's disease with subthalamic deep brain stimulation. Neurol Neurochir Pol. 2022; 56(5): 441–450.
