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BackgroundHere, we address a pivotal factor in Alzheimer’s prevention—identifying those at risk early, when dementia can still be avoided. Recent research highlights an accelerated forgetting phenotype as a risk factor for Alzheimer’s disease. We hypothesized that delayed recall over 4 weeks would predict cognitive decline over 1 year better than 30-min delayed recall, the current gold standard for detecting episodic memory problems which could be an early clinical manifestation of incipient Alzheimer’s disease. We also expected hippocampal subfield volumes to improve predictive accuracy.MethodsForty-six cognitively healthy older people (mean age 70.7 ± 7.97, 21/46 female), recruited from databases such as Join Dementia Research, or a local database of volunteers, performed 3 memory tasks on which delayed recall was tested after 30 min and 4 weeks, as well as Addenbrooke’s Cognitive Examination III (ACE-III) and CANTAB Paired Associates Learning. Medial temporal lobe subregion volumes were automatically measured using high-resolution 3T MRI. The ACE-III was repeated after 12 months to assess the change in cognitive ability. We used univariate linear regressions and ROC curves to assess the ability of tests of delayed recall to predict cognitive decline on ACE-III over the 12 months.ResultsFifteen of the 46 participants declined over the year (≥ 3 points lost on ACE-III). Four-week verbal memory predicted cognitive decline in healthy older people better than clinical gold standard memory tests and hippocampal MRI. The best single-test predictor of cognitive decline was the 4-week delayed recall on the world list (R2 = .123, p = .018, β = .418). Combined with hippocampal subfield volumetry, 4-week verbal recall identifies those at risk of cognitive decline with 93% sensitivity and 86% specificity (AUC = .918, p ConclusionsWe show that a test of accelerated long-term forgetting over 4 weeks can predict cognitive decline in healthy older people where traditional tests of delayed recall cannot. Accelerated long-term forgetting is a sensitive, easy-to-test predictor of cognitive decline in healthy older people. Used alone or with hippocampal MRI, accelerated forgetting probes functionally relevant Alzheimer’s-related change. Accelerated forgetting will identify early-stage impairment, helping to target more invasive and expensive molecular biomarker testing.

Additional file 1. Supplementary tables.

Supplemental material, Supplementary_Materials_3 for A Comparison of T2 Relaxation-Based MRI Stroke Timing Methods in Hyperacute Ischemic Stroke Patients: A Pilot Study by Bryony L McGarry, Robin A Damion, Isabel Chew, Michael J Knight, George WJ Harston, Davide Carone, Peter Jezzard, Amith Sitaram, Keith W Muir, Philip Clatworthy and Risto A Kauppinen in Journal of Central Nervous System Disease

Background and Purpose: Incomplete hippocampal inversion (IHI) is an atypical anatomical pattern presented by the hippocampus. It is associated with several neuropathological conditions and is thought to be a factor of susceptibility to hippocampal sclerosis and loss of volume. The volume loss of hippocampus is an inevitable consequence of aging, and when accelerated it is commonly considered an imaging biomarker of Alzheimer’s disease dementia. Methods: We have studied the relationship between IHI and hippocampal subfield volumes in a cohort of 60 healthy participants of 49 to 87 years of age. The presence and severity of IHI and hippocampal subfield volumes were quantified from T2 MR images acquired at 3T. Results: It was found that IHI presented in 23.3% of participants. Right unilateral IHI was rare (2 cases, 3.3%) in comparison to left unilateral IHI (9 cases, 15%), with 3 (5%) of participants showing bilateral IHI. No significant relationships between the whole hippocampal volumes and IHI was observed. Instead, significant relationships between the volumes of the left and right Cornu Ammonis subfield-1 (CA1) and IHI scores were evident. Conclusions: The rates of IHI prevalence in the current cohort are similar to those previously reported in healthy cohorts. The IHI severity is related to hippocampal subfield volumes, most notably the CA1, which is a novel finding with potential implications in research on aging and dementia.

BACKGROUND AND PURPOSE: Preterm birth is associated with worse neurodevelopmental outcome, but brain maturation in preterm infants is poorly characterized with standard methods. We evaluated white matter (WM) of infant brains at term-equivalent age, as a function of gestational age at birth, using multimodal magnetic resonance imaging (MRI). METHODS: Infants born very preterm (

Background: Objective timing of stroke in emergency departments is expected to improve patient stratification. Magnetic resonance imaging (MRI) relaxations times, T2 and T1ρ, in abnormal diffusion delineated ischaemic tissue were used as proxies of stroke time in a rat model. Methods: Both ‘non-ischaemic reference’-dependent and -independent estimators were generated. Apparent diffusion coefficient (ADC), T2 and T1ρ, were sequentially quantified for up to 6 hours of stroke in rats (n=8) at 4.7T. The ischaemic lesion was identified as a contiguous collection of voxels with low ADC. T2 and T1ρ in the ischaemic lesion and in the contralateral non-ischaemic brain tissue were determined. Differences in mean MRI relaxation times between ischaemic and non-ischaemic volumes were used to create reference-dependent estimator. For the reference-independent procedure, only the parameters associated with log-logistic fits to the T2 and T1ρ distributions within the ADC-delineated lesions were used for the onset time estimation. Result: The reference-independent estimators from T2 and T1ρ data provided stroke onset time with precisions of ±32 and ±27 minutes, respectively. The reference-dependent estimators yielded respective precisions of ±47 and ±54 minutes. Conclusions: A ‘non-ischaemic anatomical reference’-independent estimator for stroke onset time from relaxometric MRI data is shown to yield greater timing precision than previously obtained through reference-dependent procedures., published version, peerReviewed

Magnetic resonance imaging (MRI) provides an excellent means of studying tissue microstructure noninvasively since the microscopic tissue environment is imprinted on the MRI signal even at macroscopic voxel level. Mesoscopic variations in magnetic field, created by microstructure, influence the transverse relaxation time (T2) in an orientation-dependent fashion (T2 is anisotropic). However, predicting the effects of microstructure upon MRI observables is challenging and requires theoretical insight. We provide a formalism for calculating the effects upon T2 of tissue microstructure, using a model of cylindrical magnetic field perturbers. In a cohort of clinically healthy adults, we show that the angular information in spin-echo T2 is consistent with this model. We show that T2 in brain white matter of nondemented volunteers follows a U-shaped trajectory with age, passing its minimum at an age of ∼30 but that this depends on the particular white matter tract. The anisotropy of T2 also interacts with age and declines with increasing age. Late-myelinating white matter is more susceptible to age-related change than early-myelinating white matter, consistent with the retrogenesis hypothesis. T2 mapping may therefore be incorporated into microstructural imaging.