Amyloid Pattern Similarity Score (AMPSS): A reference region free measure of amyloid PET deposition in Alzheimer’s disease

Background: Amyloid PET allows for the assessment of amyloid β status in the brain, distinguishing true Alzheimer’s disease from Alzheimer’s disease-mimicking conditions. Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. However, a limited number of studies had been conducted this subpopulation in terms of clinical progression. Objective: We investigated the risk factors that could affect the progression to dementia in patients with amyloid-negative amnestic mild cognitive impairment (MCI). Methods: This study was a single-institutional, retrospective cohort study of patients over the age of 50 with amyloidnegative amnestic MCI who visited the memory clinic of Asan Medical Center with a follow-up period of more than 36 months. All participants underwent brain magnetic resonance imaging (MRI), detailed neuropsychological testing, and fluorine-18[F18]-florbetaben amyloid PET. Results: During the follow-up period, 39 of 107 patients progressed to dementia from amnestic MCI. In comparison with the stationary group, the progressed group had a more severe impairment in verbal and visual episodic memory function and hippocampal atrophy, which showed an Alzheimer’s disease-like pattern despite the lack of evidence for significant Alzheimer’s disease pathology. Voxel-based morphometric MRI analysis revealed that the progressed group had a reduced gray matter volume in the bilateral cerebellar cortices, right temporal cortex, and bilateral insular cortices. Conclusion: Considering the lack of evidence of amyloid pathology, clinical progression of these subpopulation may be caused by other neuropathologies such as TDP-43, abnormal tau or alpha synuclein that lead to neurodegeneration independent of amyloid-driven pathway. Further prospective studies incorporating biomarkers of Alzheimer’s diseasemimicking dementia are warranted.

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P4-307: THE ADDED VALUE OF QUANTITATIVE AMYLOID PET IN DETERMINING ALZHEIMER'S DISEASE (AD) DEMENTIA RISK: THE AMYPAD PROGNOSTIC AND NATURAL HISTORY STUDY

Alzheimer s & Dementia ◽

10.1016/j.jalz.2019.06.3977 ◽

2019 ◽

Vol 15 ◽

pp. P1408-P1409

Author(s):

Isadora Lopes Alves ◽

Laura Doull ◽

Fiona Gunn ◽

Gill Farrar ◽

Frederik Barkhof ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Natural History ◽

Added Value ◽

Amyloid Pet ◽

Natural History Study ◽

Dementia Risk

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Interactions between sleep disturbances and Alzheimer’s disease on brain function: a preliminary study combining the static and dynamic functional MRI

Scientific Reports ◽

10.1038/s41598-019-55452-9 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 2

Author(s):

Kaicheng Li ◽

Xiao Luo ◽

Qingze Zeng ◽

Yerfan Jiaerken ◽

Shuyue Wang ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Risk Factor ◽

Sleep Disturbance ◽

Brain Function ◽

Sleep Disturbances ◽

Brain Activity ◽

Vascular Risk Factor ◽

Underlying Mechanism ◽

Amyloid Pet

AbstractThough sleep disturbance constitutes the risk factor for Alzheimer’s disease (AD), the underlying mechanism is still unclear. This study aims to explore the interaction between sleep disturbances and AD on brain function. We included 192 normal controls, 111 mild cognitive impairment (MCI), and 30 AD patients, with either poor or normal sleep (PS, NS, respectively). To explore the strength and stability of brain activity, we used static amplitude of low-frequency fluctuation (sALFF) and dynamic ALFF (dALFF) variance. Further, we examined white matter hyperintensities (WMH) and amyloid PET deposition, representing the vascular risk factor and AD-related hallmark, respectively. We observed that sleep disturbance significantly interacted with disease severity, exposing distinct effects on sALFF and dALFF variance. Interestingly, PS groups showed the dALFF variance trajectory of initially increased, then decreased and finally increased along the AD spectrum, while showing the opposite trajectory of sALFF. Further correlation analysis showed that the WMH burden correlates with dALFF variance in PS groups. Conclusively, our study suggested that sleep disturbance interacts with AD severity, expressing as effects of compensatory in MCI and de-compensatory in AD, respectively. Further, vascular impairment might act as important pathogenesis underlying the interaction effect between sleep and AD.

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Influence of scan duration on the accuracy of β-amyloid PET with florbetaben in patients with Alzheimer’s disease and healthy volunteers

European Journal of Nuclear Medicine and Molecular Imaging ◽

10.1007/s00259-012-2268-8 ◽

2012 ◽

Vol 40 (2) ◽

pp. 238-244 ◽

Cited By ~ 17

Author(s):

Solveig Tiepolt ◽

Henryk Barthel ◽

Daniel Butzke ◽

Swen Hesse ◽

Marianne Patt ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Healthy Volunteers ◽

Amyloid Pet ◽

Β Amyloid

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A Systematic Review and Aggregated Analysis on the Impact of Amyloid PET Brain Imaging on the Diagnosis, Diagnostic Confidence, and Management of Patients being Evaluated for Alzheimer’s Disease

Journal of Alzheimer s Disease ◽

10.3233/jad-171093 ◽

2018 ◽

Vol 63 (2) ◽

pp. 783-796 ◽

Cited By ~ 20

Author(s):

Enrico R. Fantoni ◽

Anastasia Chalkidou ◽

John T. O’ Brien ◽

Gill Farrar ◽

Alexander Hammers

Keyword(s):

Systematic Review ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Brain Imaging ◽

Amyloid Pet ◽

Diagnostic Confidence ◽

The Impact

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Soluble P-tau217 reflects amyloid and tau pathology and mediates the association of amyloid with tau

10.21203/rs.3.rs-101153/v2 ◽

2021 ◽

Author(s):

Niklas Mattsson-Carlgren ◽

Shorena Janelidze ◽

Randall Bateman ◽

Ruben Smith ◽

Erik Stomrud ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Medial Temporal Lobe ◽

Amyloid Plaques ◽

Amyloid Plaque ◽

Amyloid Pet ◽

Tau Pathology ◽

Β Amyloid ◽

Tau Pet ◽

Disease Stages

Abstract Alzheimer’s disease is characterized by β-amyloid plaques and tau tangles. Plasma levels of phospho-tau217 (P-tau217) accurately differentiate Alzheimer’s disease dementia from other dementias, but it is unclear to what degree this reflects β-amyloid plaque accumulation, tau tangle accumulation, or both. In a cohort with post-mortem neuropathological data (N=88), both plaque and tangle density contributed independently to higher P-tau217. Several findings were replicated in a cohort with PET imaging (“BioFINDER-2”, N=426), where β-amyloid and tau PET were independently associated to P-tau217. P-tau217 correlated with β-amyloid PET (but not tau PET) in early disease stages, and with both β-amyloid and (more strongly) tau PET in late disease stages. Finally, P-tau217 mediated the association between β-amyloid and tau in both cohorts, especially for tau outside of the medial temporal lobe. These findings support the hypothesis that plasma P-tau217 is increased by both β-amyloid plaques and tau tangles and is congruent with the hypothesis that P-tau is involved in β-amyloid-dependent formation of neocortical tau tangles.

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Semi-quantification and grading of amyloid PET: A project of the European Alzheimer's Disease Consortium (EADC)

NeuroImage Clinical ◽

10.1016/j.nicl.2019.101846 ◽

2019 ◽

Vol 23 ◽

pp. 101846 ◽

Cited By ~ 5

Author(s):

A. Chincarini ◽

E. Peira ◽

S. Morbelli ◽

M. Pardini ◽

M. Bauckneht ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Amyloid Pet

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The Impact of Amyloid-Beta Positivity with 18F-Florbetaben PET on Neuropsychological Aspects in Parkinson’s Disease Dementia

Metabolites ◽

10.3390/metabo10100380 ◽

2020 ◽

Vol 10 (10) ◽

pp. 380

Author(s):

Seunghee Na ◽

Hyeonseok Jeong ◽

Jong-Sik Park ◽

Yong-An Chung ◽

In-Uk Song

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Amyloid Beta ◽

Neuropsychiatric Symptoms ◽

Amyloid Pet ◽

Motor Symptoms ◽

Parkinson’S Disease Dementia ◽

The Impact

The neuropathology of Parkinson’s disease dementia (PDD) is heterogenous, and the impacts of each pathophysiology and their synergistic effects are not fully understood. The aim of this study was to evaluate the frequency and impacts of co-existence with Alzheimer’s disease in patients with PDD by using 18F-florbetaben PET imaging. A total of 23 patients with PDD participated in the study. All participants underwent 18F-florbetaben PET and completed a standardized neuropsychological battery and assessment of motor symptoms. The results of cognitive tests, neuropsychiatric symptoms, and motor symptoms were analyzed between the positive and negative 18F-florbetaben PET groups. Four patients (17.4%) showed significant amyloid burden. Patients with amyloid-beta showed poorer performance in executive function and more severe neuropsychiatric symptoms than those without amyloid-beta. Motor symptoms assessed by UPDRS part III and the modified H&Y Scale were not different between the two groups. The amyloid PET scan of a patient with PDD can effectively reflect a co-existing Alzheimer’s disease pathology. Amyloid PET scans might be able to help physicians of PDD patients showing rapid progression or severe cognitive/behavioral features.

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