ASHA PROFIND FOR DEMENTIA PLUS
ASHA PROFIND FOR DEMENTIA FREE

We tested the hypothesis that increased age is associated with deficits in olfactory-based memories of social and non-social stimuli.įactorial repeated measures ANOVA, with trials, biological sex, and age as factors, were performed to investigate group differences in learning performance.

All statistical tests were two-tailed and a significance level of p 365, n=6). Total time (in seconds) in open and closed arms was evaluated, and the results were expressed as mean and standard deviation.

ASHA PROFIND FOR DEMENTIA PLUS

The elevated plus maze test was performed on APP/PS1 (n = 7) and wild type (WT, n = 7) mice at 8 and 10 months of age. Thus, the aim of this study was evaluate the anxiety-related behavior of a double transgenic mouse model for Alzheimer's Disease, the APP/PS1, which overexpress the amyloid precursor protein (APP) and the presenilin-1 (PS1) protein. Despite its relevance, the pathophysiological mechanisms of the disease are still not well understood and the use of animal models may help to understand the neurodegenerative and neurocognitive changes that occur in AD. Email: disease (AD) is the largest cause of dementia in the world, characterized by behavioral changes, cognitive impairment and progressive loss of memory. Universidade Federal de Minas Gerais, Belo Horizonte, BrazilĬorrespondence Gabriela Lopes Martins, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. In the presence of a suitable reference region, the B/I method can be applied to calculate DVR using a static scan and without blood data.Įvaluation of anxiety-related behavior in an Alzheimer's disease mice model Further investigation is needed to understand arterial-venous -AV45 concentration differences to replace arterial by venous samples. The WM-DVR B/I showed +6.2☑.3 and the pons-DVR B/I showed +6.9☑.2% difference compared to the full-kinetic DVR 2TCM.Ģ0-min static B/I-PET with an arterial sample is sufficient to reproduce the full-kinetic V T,2TCM. In contrast, WM-DVR B/I and pons-DVR B/I were positively correlated to V T,B/I (Fig.2). When using tissue reference, CB-DVR B/I underestimated V T,B/I patterns due to the presence of cerebellar Aβ (Fig.2). Fp (9☒%) did not differ between arterial and venous blood. Tracer concentrations remained 32☑0% lower in venous compared to arterial plasma. At 55min post-injection, the arterial parent fraction stabilized at 31☒% and V T,B/I corresponded well to the full-kinetic V T,2TCM and V T,Logan (average cortical difference: 2.9☐.8 and 3.3☐.7%, respectively) (Fig.1).

ASHA PROFIND FOR DEMENTIA FREE

The plasma free fraction (Fp) was determined in both arterial and venous blood.īolus-plus-constant-infusion PET demonstrated true equilibrium with low rate of -AV45 concentration change (e.g., C parietal 2.0☑.4%, C CB: 3.1☓.4%, and C plasma: 5.6☓.5% change/20min). Last, DVR was calculated using cerebellar grey (CB-DVR), subcortical white matter (WM-DVR), or pons (pons-DVR) as the reference. Additionally, V T using bolus-plus-constant-infusion was determined as the equilibriumratio (55-75min) of tracer concentration in tissue to the average of 3 metabolite-corrected arterial or venous plasma samples (C tissue/C plasma=V T,B/I).

90-min continuous sampling, 10 arterial, and 6 venous samples were taken to determine individual metabolite-corrected plasma inputs and calculation of the ‘gold standard’, full-kinetic V T,2TCM and graphical V T,Logan. Here, we suggest an alternative tissue-to-plasma ratio method based on bolus-plus-constant-infusion (B/I) PET.įive PSEN1-carriers (MMSE 26.4☓) underwent 90-min -AV45-PET with continuous intravenous tracer infusion. In addition, both SUVR and DVR require selection of a reference region, which may suffer from Aβ (e.g. For more accurate Aβ quantification, the distribution volume ratio (DVR) can be applied, but requires a long dynamic scan. However, the method is prone to bias from variation in plasma clearance and cerebral blood flow. Email: standardized uptake value ratio (SUVR) has been widely applied in anti-Aβ trials of Alzheimer’s disease. A clinically applicable proxy for gold standard quantification of amyloid-beta in Alzheimer’s disease: Bolus plus constant infusion 18F-AV45 PET Poster Presentation (Posters will be Released on November 9 and Displayed Through the Duration of the Virtual Event)ġMolecular Imaging Center Antwerp, University of Antwerp, Antwerp, BelgiumĢTranslational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montréal, QC, CanadaģUniversity Hospital of Antwerp, Antwerp, BelgiumĤMontreal Neurological Institute, Montréal, QC, CanadaĬorrespondence Julie Ottoy, Molecular Imaging Center Antwerp, University of Antwerp, Antwerp, Belgium.

Asha profind for dementia