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Amyloid cascade and tau pathology cerebrospinal fluid markers in mild cognitive impairment with regards to Alzheimer's disease cerebral metabolic signature.
J Alzheimers Dis 2013; 36(2):401-8JA

Abstract

BACKGROUND

Biomarker relationships in early stages of Alzheimer's disease (AD) are elusive. Cerebrospinal fluid (CSF) levels of amyloid-β 1-42 (Aβ42) and total tau (tTau) as well as 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) contribute to help unravel AD pathology. Furthermore, peptides related to amyloid-β protein precursor (AβPP) processing [e.g., soluble AβPPα and β (sAβPPα and sAβPPβ, respectively); sortilin-related receptor with A-type repeats (SORL1, also called LR11 or SORLA)] are factors crucially implicated in the formation of pathological hallmarks of AD.

OBJECTIVE

To unveil differences in CSF concentrations of Aβ42, sAβPPα, sAβPPβ, tTau, and SORL1 between patients with mild cognitive impairment (MCI) who were categorized according to expert interpretation of FDG scans.

METHODS

PET results were classified as suggesting high likelihood for AD (MCI-AD high), intermediate likelihood for AD (MCI-AD intermediate), or little likelihood for AD (MCI-AD unlikely). An AD dementia group was also included. Differences between the groups were tested by Kruskal- Wallis test, Mann-Whitney test, or χ2. Provided statistically significant differences were detected, multiple linear regression models were employed.

RESULTS

Aβ42 levels in patients with MCI-AD high (n = 15) were lower compared to MCI-AD intermediate (n = 18) and MCI-AD unlikely patients (n = 25) (p = 0.002), while they did not differ from patients with AD dementia (n = 17). The regression model revealed a significant impact of the metabolic pattern on Aβ42 concentrations. SORL1, tTau, sAβPPα, and sAβPPβ concentrations did not differ between the groups.

CONCLUSION

These findings point to linkages between plaque pathology and glucose cerebral hypometabolism.

Authors+Show Affiliations

Department of Psychiatry and Psychotherapy, Klinikum rechts der Isar der Technischen Universität München, Munich, Germany. panos.alexopoulos@lrz.tum.deNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

23609762

Citation

Alexopoulos, Panagiotis, et al. "Amyloid Cascade and Tau Pathology Cerebrospinal Fluid Markers in Mild Cognitive Impairment With Regards to Alzheimer's Disease Cerebral Metabolic Signature." Journal of Alzheimer's Disease : JAD, vol. 36, no. 2, 2013, pp. 401-8.
Alexopoulos P, Guo LH, Jiang M, et al. Amyloid cascade and tau pathology cerebrospinal fluid markers in mild cognitive impairment with regards to Alzheimer's disease cerebral metabolic signature. J Alzheimers Dis. 2013;36(2):401-8.
Alexopoulos, P., Guo, L. H., Jiang, M., Bujo, H., Grimmer, T., Förster, S., ... Perneczky, R. (2013). Amyloid cascade and tau pathology cerebrospinal fluid markers in mild cognitive impairment with regards to Alzheimer's disease cerebral metabolic signature. Journal of Alzheimer's Disease : JAD, 36(2), pp. 401-8. doi:10.3233/JAD-122329.
Alexopoulos P, et al. Amyloid Cascade and Tau Pathology Cerebrospinal Fluid Markers in Mild Cognitive Impairment With Regards to Alzheimer's Disease Cerebral Metabolic Signature. J Alzheimers Dis. 2013;36(2):401-8. PubMed PMID: 23609762.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Amyloid cascade and tau pathology cerebrospinal fluid markers in mild cognitive impairment with regards to Alzheimer's disease cerebral metabolic signature. AU - Alexopoulos,Panagiotis, AU - Guo,Liang-Hao, AU - Jiang,Meizi, AU - Bujo,Hideaki, AU - Grimmer,Timo, AU - Förster,Stefan, AU - Drzezga,Alexander, AU - Kurz,Alexander, AU - Perneczky,Robert, PY - 2013/4/24/entrez PY - 2013/4/24/pubmed PY - 2014/1/28/medline SP - 401 EP - 8 JF - Journal of Alzheimer's disease : JAD JO - J. Alzheimers Dis. VL - 36 IS - 2 N2 - BACKGROUND: Biomarker relationships in early stages of Alzheimer's disease (AD) are elusive. Cerebrospinal fluid (CSF) levels of amyloid-β 1-42 (Aβ42) and total tau (tTau) as well as 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) contribute to help unravel AD pathology. Furthermore, peptides related to amyloid-β protein precursor (AβPP) processing [e.g., soluble AβPPα and β (sAβPPα and sAβPPβ, respectively); sortilin-related receptor with A-type repeats (SORL1, also called LR11 or SORLA)] are factors crucially implicated in the formation of pathological hallmarks of AD. OBJECTIVE: To unveil differences in CSF concentrations of Aβ42, sAβPPα, sAβPPβ, tTau, and SORL1 between patients with mild cognitive impairment (MCI) who were categorized according to expert interpretation of FDG scans. METHODS: PET results were classified as suggesting high likelihood for AD (MCI-AD high), intermediate likelihood for AD (MCI-AD intermediate), or little likelihood for AD (MCI-AD unlikely). An AD dementia group was also included. Differences between the groups were tested by Kruskal- Wallis test, Mann-Whitney test, or χ2. Provided statistically significant differences were detected, multiple linear regression models were employed. RESULTS: Aβ42 levels in patients with MCI-AD high (n = 15) were lower compared to MCI-AD intermediate (n = 18) and MCI-AD unlikely patients (n = 25) (p = 0.002), while they did not differ from patients with AD dementia (n = 17). The regression model revealed a significant impact of the metabolic pattern on Aβ42 concentrations. SORL1, tTau, sAβPPα, and sAβPPβ concentrations did not differ between the groups. CONCLUSION: These findings point to linkages between plaque pathology and glucose cerebral hypometabolism. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/23609762/Amyloid_cascade_and_tau_pathology_cerebrospinal_fluid_markers_in_mild_cognitive_impairment_with_regards_to_Alzheimer's_disease_cerebral_metabolic_signature_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-122329 DB - PRIME DP - Unbound Medicine ER -