Added value of amyloid PET in individualized risk predictions for MCI patients

Maurik, Ingrid S. van; Kall, Laura M. van Der; Wilde, Arno de; Bouwman, Femke H.; Scheltens, Philip; Berckel, Bart N.M. van; Berkhof, Johannes; Flier, Wiesje M. van der

doi:10.1016/j.dadm.2019.04.011

Cited by 13 publications

(21 citation statements)

References 54 publications

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“…Biomarker tests of Alzheimer's disease (AD) pathology can provide critical insights into the etiology of cognitive decline, 1‐3 and sharing such information with patients and families affected by mild cognitive impairment (MCI) could lessen their sense of ambiguity regarding the syndrome.…”

Section: Introductionmentioning

confidence: 99%

A randomized controlled trial of amyloid positron emission tomography results disclosure in mild cognitive impairment

Lingler

Sereika

Butters

et al. 2020

Alzheimer's & Dementia

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Introduction: Recent studies suggest that Alzheimer's disease (AD) biomarker disclosure has no discernable psychological impact on cognitively healthy persons. Far less is known about how such results affect symptomatic individuals and their caregivers. Methods: Randomized controlled trial of 82 mild cognitive impairment (MCI) patient and caregiver dyads (total n = 164) to determine the effect of receiving amyloid positron emission tomography results on understanding of, and perceived efficacy to cope with, MCI over 52 weeks of follow-up. Results: Gains in the primary outcomes were not consistently observed. Amyloid negative patients reported greater perceived ambiguity regarding MCI at follow-up, while moderate and sustained emotional distress was observed in patients, and to a lesser extent, caregivers, of those who were amyloid positive. There was no corresponding increase in depressive symptoms. Discussion: These findings point to the possibility that both MCI patients and caregivers may need emotional support after the disclosure of amyloid scan results.

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Section: Introductionmentioning

confidence: 99%

A randomized controlled trial of amyloid positron emission tomography results disclosure in mild cognitive impairment

Lingler

Sereika

Butters

et al. 2020

Alzheimer's & Dementia

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“…The risk factors are additive, and there are several indications of mechanistic interactions [11,12]. Recent studies support the use of amyloid positron emission tomography (PET) in patients with uncertain diagnosis in a memory clinic setting [13][14][15], but such studies are missing in the post-stroke population. Biomarkers of cortical amyloid deposition include cerebrospinal fluid (CSF) Amyloid-β peptide (Aβ 42 ) levels and amyloid-binding PET tracers.…”

Section: Introductionmentioning

confidence: 99%

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

et al. 2020

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Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18 F-Flut) positron emission tomography (PET), is common in seven-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18 F-Flut-PET uptake after 7 years correlates with amyloid-β peptide (Aβ 42) levels in cerebrospinal fluid (CSF) at 1 year, and with measures of neurodegeneration and cognition at 7 years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one-and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At 7 years, patients were offered 18 F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18 F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ 42 levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from 1 year. Thirteen out of 26 patients were diagnosed with CI 7 years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ 42 levels at 1 year, MTA grade, GCA scale, MMSE score or TMT-A at 7 years did not correlate with 18 F-Flut-PET SUVr in this cohort. Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore, amyloid pathology may not be a key mediator of neurodegeneration 7 years post-stroke.

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“…The risk factors are additive, and there are several indications of mechanistic interactions (11,12). Recent studies support the use of amyloid positron emission tomography (PET) in patients with uncertain diagnosis in a memory clinic setting (13)(14)(15), but studies are missing in the post-stroke population. Biomarkers of cortical amyloid deposition include cerebrospinal fluid (CSF) Amyloid-β peptide (Aβ₄₂) levels and amyloid-binding PET tracers.…”

Section: Introductionmentioning

confidence: 99%

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

Hagberg

Ihle‐Hansen²,

Fure

et al. 2020

Preprint

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Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in seven-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore, amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.Trial registration: Clinicaltrials.gov (NCT00506818). July 23, 2007. Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

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Added value of amyloid PET in individualized risk predictions for MCI patients

Cited by 13 publications

References 54 publications

A randomized controlled trial of amyloid positron emission tomography results disclosure in mild cognitive impairment

A randomized controlled trial of amyloid positron emission tomography results disclosure in mild cognitive impairment

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

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