Cerebrovascular and amyloid pathology in predementia stages: The relationship with neurodegeneration and cognitive decline

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Cerebrovascular and amyloid pathology in predementia stages : The relationship with neurodegeneration and cognitive decline. / Bos, Isabelle; Verhey, Frans R.; Ramakers, Inez H.G.B.; Jacobs, Heidi I.L.; Soininen, Hilkka; Freund-Levi, Yvonne; Hampel, Harald; Tsolaki, Magda; Wallin, Åsa K.; Van Buchem, Mark A.; Oleksik, Ania; Verbeek, Marcel M.; Olde Rikkert, Marcel; Van Der Flier, Wiesje M.; Scheltens, Philip; Aalten, Pauline; Visser, Pieter Jelle; Vos, Stephanie J.B.

In: Alzheimer's Research and Therapy, Vol. 9, No. 1, 101, 29.12.2017.

Research output: Contribution to journalArticle

Harvard

Bos, I, Verhey, FR, Ramakers, IHGB, Jacobs, HIL, Soininen, H, Freund-Levi, Y, Hampel, H, Tsolaki, M, Wallin, ÅK, Van Buchem, MA, Oleksik, A, Verbeek, MM, Olde Rikkert, M, Van Der Flier, WM, Scheltens, P, Aalten, P, Visser, PJ & Vos, SJB 2017, 'Cerebrovascular and amyloid pathology in predementia stages: The relationship with neurodegeneration and cognitive decline', Alzheimer's Research and Therapy, vol. 9, no. 1, 101. https://doi.org/10.1186/s13195-017-0328-9

APA

Bos, I., Verhey, F. R., Ramakers, I. H. G. B., Jacobs, H. I. L., Soininen, H., Freund-Levi, Y., ... Vos, S. J. B. (2017). Cerebrovascular and amyloid pathology in predementia stages: The relationship with neurodegeneration and cognitive decline. Alzheimer's Research and Therapy, 9(1), [101]. https://doi.org/10.1186/s13195-017-0328-9

CBE

Bos I, Verhey FR, Ramakers IHGB, Jacobs HIL, Soininen H, Freund-Levi Y, Hampel H, Tsolaki M, Wallin ÅK, Van Buchem MA, Oleksik A, Verbeek MM, Olde Rikkert M, Van Der Flier WM, Scheltens P, Aalten P, Visser PJ, Vos SJB. 2017. Cerebrovascular and amyloid pathology in predementia stages: The relationship with neurodegeneration and cognitive decline. Alzheimer's Research and Therapy. 9(1). https://doi.org/10.1186/s13195-017-0328-9

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Author

Bos, Isabelle ; Verhey, Frans R. ; Ramakers, Inez H.G.B. ; Jacobs, Heidi I.L. ; Soininen, Hilkka ; Freund-Levi, Yvonne ; Hampel, Harald ; Tsolaki, Magda ; Wallin, Åsa K. ; Van Buchem, Mark A. ; Oleksik, Ania ; Verbeek, Marcel M. ; Olde Rikkert, Marcel ; Van Der Flier, Wiesje M. ; Scheltens, Philip ; Aalten, Pauline ; Visser, Pieter Jelle ; Vos, Stephanie J.B. / Cerebrovascular and amyloid pathology in predementia stages : The relationship with neurodegeneration and cognitive decline. In: Alzheimer's Research and Therapy. 2017 ; Vol. 9, No. 1.

RIS

TY - JOUR

T1 - Cerebrovascular and amyloid pathology in predementia stages

T2 - Alzheimer's Research & Therapy

AU - Bos, Isabelle

AU - Verhey, Frans R.

AU - Ramakers, Inez H.G.B.

AU - Jacobs, Heidi I.L.

AU - Soininen, Hilkka

AU - Freund-Levi, Yvonne

AU - Hampel, Harald

AU - Tsolaki, Magda

AU - Wallin, Åsa K.

AU - Van Buchem, Mark A.

AU - Oleksik, Ania

AU - Verbeek, Marcel M.

AU - Olde Rikkert, Marcel

AU - Van Der Flier, Wiesje M.

AU - Scheltens, Philip

AU - Aalten, Pauline

AU - Visser, Pieter Jelle

AU - Vos, Stephanie J.B.

PY - 2017/12/29

Y1 - 2017/12/29

N2 - Background: Cerebrovascular disease (CVD) and amyloid-β (Aβ) often coexist, but their influence on neurodegeneration and cognition in predementia stages remains unclear. We investigated the association between CVD and Aβ on neurodegenerative markers and cognition in patients without dementia. Methods: We included 271 memory clinic patients with subjective or objective cognitive deficits but without dementia from the BioBank Alzheimer Center Limburg cohort (n = 99) and the LeARN (n = 50) and DESCRIPA (n = 122) multicenter studies. CSF Aβ1-42 and white matter hyperintensities (WMH) on magnetic resonance imaging (MRI) scans were used as measures of Aβ and CVD, respectively. Individuals were classified into four groups based on the presence (+) or absence (-) of Aβ and WMH. We investigated differences in phosphorylated tau, total tau (t-tau), and medial temporal lobe atrophy (MTA) between groups using general linear models. We examined cognitive decline and progression to dementia using linear mixed models and Cox proportional hazards models. All analyses were adjusted for study and demographics. Results: MTA and t-tau were elevated in the Aβ - WMH+, Aβ + WMH-, and Aβ + WMH+ groups. MTA was most severe in the Aβ + WMH+ group compared with the groups with a single pathology. Both WMH and Aβ were associated with cognitive decline, but having both pathologies simultaneously was not associated with faster decline. Conclusions: In the present study, we found an additive association of Aβ and CVD pathology with baseline MTA but not with cognitive decline. Because our findings may have implications for diagnosis and prognosis of memory clinic patients and for future scientific research, they should be validated in a larger sample with longer follow-up.

AB - Background: Cerebrovascular disease (CVD) and amyloid-β (Aβ) often coexist, but their influence on neurodegeneration and cognition in predementia stages remains unclear. We investigated the association between CVD and Aβ on neurodegenerative markers and cognition in patients without dementia. Methods: We included 271 memory clinic patients with subjective or objective cognitive deficits but without dementia from the BioBank Alzheimer Center Limburg cohort (n = 99) and the LeARN (n = 50) and DESCRIPA (n = 122) multicenter studies. CSF Aβ1-42 and white matter hyperintensities (WMH) on magnetic resonance imaging (MRI) scans were used as measures of Aβ and CVD, respectively. Individuals were classified into four groups based on the presence (+) or absence (-) of Aβ and WMH. We investigated differences in phosphorylated tau, total tau (t-tau), and medial temporal lobe atrophy (MTA) between groups using general linear models. We examined cognitive decline and progression to dementia using linear mixed models and Cox proportional hazards models. All analyses were adjusted for study and demographics. Results: MTA and t-tau were elevated in the Aβ - WMH+, Aβ + WMH-, and Aβ + WMH+ groups. MTA was most severe in the Aβ + WMH+ group compared with the groups with a single pathology. Both WMH and Aβ were associated with cognitive decline, but having both pathologies simultaneously was not associated with faster decline. Conclusions: In the present study, we found an additive association of Aβ and CVD pathology with baseline MTA but not with cognitive decline. Because our findings may have implications for diagnosis and prognosis of memory clinic patients and for future scientific research, they should be validated in a larger sample with longer follow-up.

KW - Alzheimer's disease

KW - Amyloid

KW - Cerebrospinal fluid

KW - Cerebrovascular disease

KW - Cognition

KW - Medial temporal lobe atrophy

KW - MRI

KW - Neurodegeneration

KW - Tau

UR - http://www.scopus.com/inward/record.url?scp=85039756986&partnerID=8YFLogxK

UR - https://doi.org/10.1186/s13195-018-0391-x

U2 - 10.1186/s13195-017-0328-9

DO - 10.1186/s13195-017-0328-9

M3 - Article

VL - 9

JO - Alzheimer's Research & Therapy

JF - Alzheimer's Research & Therapy

SN - 1758-9193

IS - 1

M1 - 101

ER -