PERFORM Publications

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Title		Authors	PubMed ID
1	Longitudinal relationships among cerebrospinal fluid biomarkers, cerebral blood flow, and grey matter volume in individuals with a familial history of Alzheimer s disease	Sanami S; Intzandt B; Huck J; Villeneuve S; Iturria-Medina Y; Gauthier CJ; Prevent-Ad Research Group None;	40347524 CONCORDIA
2	Sleep spindles and slow oscillations predict cognition and biomarkers of neurodegeneration in mild to moderate Alzheimer's disease	Páez A; Gillman SO; Dogaheh SB; Carnes A; Dakterzada F; Barbé F; Dang-Vu TT; Ripoll GP;	39878233 CONCORDIA
3	The MyLo CRISPR-Cas9 Toolkit: A Markerless Yeast Localization and Overexpression CRISPR-Cas9 Toolkit	Bean BDM; Whiteway M; Martin VJJ;	35708612 BIOLOGY
4	Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex	Olajide OJ; Chapman CA;	34144329 PSYCHOLOGY
5	Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.	Olajide OJ, Suvanto ME, Chapman CA	33495355 PSYCHOLOGY
6	Topographical distribution of Aβ predicts progression to dementia in Aβ positive mild cognitive impairment	Pascoal TA, Therriault J, Mathotaarachchi S, Kang MS, Shin M, Benedet AL, Chamoun M, Tissot C, Lussier F, Mohaddes S, Soucy JP, Massarweh G, Gauthier S, Rosa-Neto P,	32582834 PERFORM
7	Flavanone glycosides inhibit β-site amyloid precursor protein cleaving enzyme 1 and cholinesterase and reduce Aβ aggregation in the amyloidogenic pathway.	Ali MY, Jannat S, Edraki N, Das S, Chang WK, Kim HC, Park SK, Chang MS	31194956 BIOLOGY
8	Amyloid and tau signatures of brain metabolic decline in preclinical Alzheimer's disease.	Pascoal TA, Mathotaarachchi S, Shin M, Park AY, Mohades S, Benedet AL, Kang MS, Massarweh G, Soucy JP, Gauthier S, Rosa-Neto P, Alzheimer’s Disease Neuroimaging Initiative	29396637 PERFORM

Title:	Amyloid and tau signatures of brain metabolic decline in preclinical Alzheimer's disease.
Authors:	Pascoal TA, Mathotaarachchi S, Shin M, Park AY, Mohades S, Benedet AL, Kang MS, Massarweh G, Soucy JP, Gauthier S, Rosa-Neto P, Alzheimer’s Disease Neuroimaging Initiative
Link:	https://www.ncbi.nlm.nih.gov/pubmed/29396637?dopt=Abstract
DOI:	10.1007/s00259-018-3933-3
Publication:	European journal of nuclear medicine and molecular imaging
Keywords:	Amyloid-PET; Phosphorylated tau; Preclinical Alzheimer'; s disease; [18F]FDG PET;
PMID:	29396637	Category:	Eur J Nucl Med Mol Imaging	Date Added:	2019-04-15
Dept Affiliation:	PERFORM 1 Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Douglas Hospital, McGill University, 6875 La Salle Blvd - FBC room 3149, Montreal, QC, H4H 1R3, Canada. 2 Statistical Laboratory, University of Cambridge, Cambridge, UK. 3 Montreal Neurological Institute, Montreal, Canada. 4 PERFORM Centre, Concordia University, Montreal, Canada. 5 Alzheimer's Disease Research Unit, The McGill University Research Centre for Studies in Aging, Douglas Hospital, McGill University, Montreal, Canada. 6 Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Douglas Hospital, McGill University, 6875 La Salle Blvd - FBC room 3149, Montreal, QC, H4H 1R3, Canada. pedro.rosa@mcgill.ca. 7 Montreal Neurological Institute, Montreal, Canada. pedro.rosa@mcgill.ca. 8 Alzheimer's Disease Research Unit, The McGill University Research Centre for Studies in Aging, Douglas Hospital, McGill University, Montreal, Canada. pedro.rosa@mcgill.ca. 9 Department of Neurology and Neurosurgery, McGill University, Montreal, Canada. pedro.rosa@mcgill.ca.

Description:

Amyloid and tau signatures of brain metabolic decline in preclinical Alzheimer's disease.

Eur J Nucl Med Mol Imaging. 2018 06;45(6):1021-1030

Authors: Pascoal TA, Mathotaarachchi S, Shin M, Park AY, Mohades S, Benedet AL, Kang MS, Massarweh G, Soucy JP, Gauthier S, Rosa-Neto P, Alzheimer’s Disease Neuroimaging Initiative

Abstract

PURPOSE: We aimed to determine the amyloid (Aß) and tau biomarker levels associated with imminent Alzheimer's disease (AD) - related metabolic decline in cognitively normal individuals.

METHODS: A threshold analysis was performed in 120 cognitively normal elderly individuals by modelling 2-year declines in brain glucose metabolism measured with [18F]fluorodeoxyglucose ([18F]FDG) as a function of [18F]florbetapir Aß positron emission tomography (PET) and cerebrospinal fluid phosphorylated tau biomarker thresholds. Additionally, using a novel voxel-wise analytical framework, we determined the sample sizes needed to test an estimated 25% drugeffect with 80% of power on changes in FDG uptake over 2 years at every brain voxel.

RESULTS: The combination of [18F]florbetapir standardized uptake value ratios and phosphorylated-tau levels more than one standard deviation higher than their respective thresholds for biomarker abnormality was the best predictor of metabolic decline in individuals with preclinical AD. We also found that a clinical trial using these thresholds would require as few as 100 individuals to test a 25% drug effect on AD-related metabolic decline over 2 years.

CONCLUSIONS: These results highlight the new concept that combined Aß and tau thresholds can predict imminent neurodegeneration as an alternative framework with a high statistical power for testing the effect of disease-modifying therapies on [18F]FDG uptake decline over a typical 2-year clinical trial period in individuals with preclinical AD.

PMID: 29396637 [PubMed - indexed for MEDLINE]

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