Relevance of plasma biomarkers to pathologies in Alzheimer’s disease, Parkinson’s disease and frontotemporal dementia
Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the...
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Published in | Scientific reports Vol. 12; no. 1; pp. 17919 - 9 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
26.10.2022
Nature Publishing Group Nature Portfolio |
Subjects | |
Online Access | Get full text |
ISSN | 2045-2322 2045-2322 |
DOI | 10.1038/s41598-022-22647-6 |
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Abstract | Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1–40 (Aβ
1–40
), Aβ
1–42
, T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice. |
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AbstractList | Abstract Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1–40 (Aβ1–40), Aβ1–42, T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice. Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1–40 (Aβ 1–40 ), Aβ 1–42 , T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice. Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer's disease (AD). Parkinson's disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1-40 (Aβ1-40), Aβ1-42, T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice.Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer's disease (AD). Parkinson's disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1-40 (Aβ1-40), Aβ1-42, T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice. Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1–40 (Aβ1–40), Aβ1–42, T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice. Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer's disease (AD). Parkinson's disease (PD) results from the accumulation of α-synuclein. TAR DNA-binding protein (TDP-43) and total tau protein (T-Tau) play roles in FTD pathology. All of the pathological evidence was found in the biopsy. However, it is impossible to perform stein examinations in clinical practice. Assays of biomarkers in plasma would be convenient. It would be better to investigate the combinations of various biomarkers in AD, PD and FTD. Ninety-one subjects without neurodegenerative diseases, 76 patients with amnesic mild cognitive impairment (aMCI) or AD dementia, combined as AD family, were enrolled. One hundred and nine PD patients with normal cognition (PD-NC) or dementia (PDD), combined as PD family, were enrolled. Twenty-five FTD patients were enrolled for assays of plasma amyloid β 1-40 (Aβ ), Aβ , T-Tau, α-synuclein and TDP-43 using immunomagnetic reduction (IMR). The results show that Aβs and T-Tau are major domains in AD family. α-synuclein is highly dominant in PD family. FTD is closely associated with TDP-43 and T-Tau. The dominant plasma biomarkers in AD family, PD family and FTD are consistent with pathology. This implies that plasma biomarkers are promising for precise and differential assessments of AD, PD and FTD in clinical practice. |
ArticleNumber | 17919 |
Author | Chiu, Pai-Yi Lu, Cheng-Hsien Chiu, Ming-Jang Yang, Shieh-Yueh Yang, Fu-Chi Lin, Wei-Che |
Author_xml | – sequence: 1 givenname: Pai-Yi surname: Chiu fullname: Chiu, Pai-Yi organization: Department of Neurology, Show Chwan Memorial Hospital, MR-Guided Focus Ultrasound Center, Chang Bin Shaw Chwan Memorial Hospital – sequence: 2 givenname: Fu-Chi surname: Yang fullname: Yang, Fu-Chi organization: Department of Neurology, Tri-Service General Hospital, National Defense Medical Center – sequence: 3 givenname: Ming-Jang surname: Chiu fullname: Chiu, Ming-Jang organization: Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Graduate Institute of Brain and Mind Sciences, College of Medicine, National Taiwan University, Department of Psychology, National Taiwan University, Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University – sequence: 4 givenname: Wei-Che surname: Lin fullname: Lin, Wei-Che organization: Department of Diagnostic Radiology, Kaohsiung Chang Gung Memorial Hospital, College of Medicine, Chang Gung University – sequence: 5 givenname: Cheng-Hsien surname: Lu fullname: Lu, Cheng-Hsien organization: Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, College of Medicine, Chang Gung University – sequence: 6 givenname: Shieh-Yueh surname: Yang fullname: Yang, Shieh-Yueh email: syyang@magqu.com organization: MagQu Co., Ltd |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36289355$$D View this record in MEDLINE/PubMed |
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Snippet | Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of α-synuclein.... Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer's disease (AD). Parkinson's disease (PD) results from the accumulation of α-synuclein.... Abstract Amyloid plaques and tau tangles are pathological hallmarks of Alzheimer’s disease (AD). Parkinson’s disease (PD) results from the accumulation of... |
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SubjectTerms | 631/378 631/45 631/61 alpha-Synuclein Alzheimer Disease - diagnosis Alzheimer's disease Amyloid Amyloid beta-Peptides Biomarkers Biopsy Clinical medicine Cognitive ability Dementia Dementia disorders DNA-binding protein DNA-Binding Proteins Frontotemporal dementia Frontotemporal Dementia - diagnosis Humanities and Social Sciences Humans Movement disorders multidisciplinary Neurodegenerative diseases Parkinson Disease - diagnosis Parkinson's disease Pathology Patients Peptide Fragments Plasma Science Science (multidisciplinary) Senile plaques Synuclein Tau protein tau Proteins |
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Title | Relevance of plasma biomarkers to pathologies in Alzheimer’s disease, Parkinson’s disease and frontotemporal dementia |
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