Centerscope

Centerscope, formerly Scope, was published by the Boston University Medical Center "to communicate the concern of the Medical Center for the development and maintenance of improved health care in contemporary society.

What is in a tomato? Mapping the building blocks of food

When you bite into a tomato, what exactly are you eating? Join us for a tour of tomatoes, as we learn about the building blocks of food, known as biomolecules. Our tour explores the thousands of biomolecules in food, many of which play important roles in nutrition and health. An examination of tomatoes from various farms tells us that not all tomatoes have the same biomolecules. Lots of things affect the amounts and types of biomolecules in tomatoes, including their genetics, where and how they are grown, and even how they are stored and cooked. Our tour ends with a peek into a lab where scientists work on a global project to map all the biomolecules in foods. Welcome to an exciting frontier of science, where discoveries can lead to big improvements in the health of people and the planet

Patterns and implications of neurological examination findings in autosomal dominant Alzheimer disease

Introduction: As knowledge about neurological examination findings in autosomal dominant Alzheimer disease (ADAD) is incomplete, we aimed to determine the frequency and significance of neurological examination findings in ADAD. Methods: Frequencies of neurological examination findings were compared between symptomatic mutation carriers and non mutation carriers from the Dominantly Inherited Alzheimer Network (DIAN) to define AD neurological examination findings. AD neurological examination findings were analyzed regarding frequency, association with and predictive value regarding cognitive decline, and association with brain atrophy in symptomatic mutation carriers. Results: AD neurological examination findings included abnormal deep tendon reflexes, gait disturbance, pathological cranial nerve examination findings, tremor, abnormal finger to nose and heel to shin testing, and compromised motor strength. The frequency of AD neurological examination findings was 65.1 %. Cross-sectionally, mutation carriers with AD neurological examination findings showed a more than two-fold faster cognitive decline and had greater parieto-temporal atrophy, including hippocampal atrophy. Longitudinally, AD neurological examination findings predicted a significantly greater decline over time. Discussion: ADAD features a distinct pattern of neurological examination findings that is useful to estimate prognosis and may inform clinical care and therapeutic trial designs

Toward a digital One CGIAR: Strategic research on digital transformation in food, land, and water systems in a climate crisis

The global research consortium CGIAR is restructuring itself to build a more integrated global organization (“One CGIAR”) that fully leverages its strengths and refocuses its research strategy through 2030 in service of a renewed mission: End hunger—through science to transform food, land, and water systems in a climate crisis. The CGIAR Platform for Big Data in Agriculture led strategic research in support of this effort, looking into digital trends that have the potential to transform global agriculture in the coming years, the roles public-interest organizations should play in the digital agriculture landscape, and the capabilities CGIAR must have if it is to use data and digital technology to their full potential in the service of its mission

Clinical, pathophysiological and genetic features of motor symptoms in autosomal dominant Alzheimer's disease

Owing to an early and marked deposition of amyloid-beta in the basal ganglia, autosomal dominant Alzheimer's disease could distinctly involve motor symptoms. Therefore, we aimed to assess the prevalence and characteristics of motor signs in autosomal dominant Alzheimer's disease. Baseline Unified Parkinson Disease Rating Scale part three scores (UPDRS-III) from 433 participants of the Dominantly Inherited Alzheimer's Network observational study were analysed. Motor symptoms were scrutinized with respect to associations with mutation carrier status, mutation site within PSEN1, basal ganglia amyloid-beta as measured by Pittsburgh compound B PET, estimated years to symptom onset and Clinical Dementia Rating Scale-Sum of Boxes. Motor findings in mutation carriers were compared to patients with sporadic Alzheimer's disease using data of the National Alzheimer's Coordination Center. Mutation carriers showed motor findings at a higher frequency (28.4% versus 12.8%;P < 0.001) and severity (mean UPDRS-III scores 2.0 versus 0.4;P < 0.001) compared to non-carriers. Eleven of the 27 UPDRS-III items were statistically more frequently affected in mutation carriers after adjustment for multiple comparisons. Ten of these 11 items were subscale components of bradykinesia. In cognitively asymptomatic mutation carriers, dysdiadochokinesia was more frequent compared to non-carriers (right hand: 3.8% versus 0%;adjusted P = 0.023;left: 4.4% versus 0.6%;adjusted P = 0.031). In this cohort, the positive predictive value for mutation carrier status in cognitively asymptomatic participants (50% a priori risk) of dysdiadochokinesia was 100% for the right and 87.5% for the left side. Mutation carriers with motor findings more frequently were basal ganglia amyloid-beta positive (84% versus 63.3%;P = 0.006) and showed more basal ganglia amyloid-beta deposition (Pittsburgh compound B-standardized uptake value ratio 2.472 versus 1.928;P = 0.002) than those without. Frequency and severity of motor findings were greater in post-codon 200 PSEN1 mutations (36%;mean UPDRS-III score 3.03) compared to mutations pre-codon 200 PSEN1 (19.3%, P = 0.022;0.91, P = 0.013). In mutation carriers, motor symptom severity was significantly positively correlated with basal ganglia amyloid-beta deposition, Clinical Dementia Rating scores and estimated years to symptom onset. Mutation carriers with a Clinical Dementia Rating global score of 2 exhibited more pronounced motor symptoms than sporadic Alzheimer's disease patients with the same Clinical Dementia Rating global score (mean UPDRS-III scores 20.71 versus 5.96;P < 0.001). With a prevalence of approximately 30% and increasing severity with progression of dementia, motor symptoms are proven as a clinically relevant finding in autosomal dominant Alzheimer's disease, in particular in advanced dementia stages, that correlates with deposition of amyloid-beta in the basal ganglia. In a very small per cent of cognitively asymptomatic members of families with autosomal dominant Alzheimer's disease, dysdiadochokinesia may increase the chance of an individual's status as mutation carrier

Placental malaria is associated with attenuated CD4 T-cell responses to tuberculin PPD 12 months after BCG vaccination

BackgroundPlacental malaria (PM) is associated with prenatal malaise, but many PM+ infants are born without symptoms. As malaria has powerful immunomodulatory effects, we tested the hypothesis that PM predicts reduced T-cell responses to vaccine challenge. MethodsWe recruited healthy PM+ and PM- infants at birth. At six and 12 months, we stimulated PBMCs with tuberculin purified protein derivative (PPD) and compared expression of CD154, IL-2 and IFN? by CD4 T-cells to a negative control using flow cytometry. We measured the length, weight and head circumference at birth and 12 months.ResultsIL-2 and CD154 expression were low in both groups at both timepoints, without discernable differences. Expression of IFN? was similarly low at 6 months but by 12 months, the median response was higher in PM- than PM + infants (p = 0.026). The PM+ infants also had a lower weight (p = 0.032) and head circumference (p = 0.041) at 12 months, indicating lower growth rates. At birth, the size and weight of the PM+ and PM- infants were equivalent. By 12 months, the PM+ infants had a lower weight and head circumference than the PM- infants. ConclusionsPlacental malaria was associated with reduced immune responses 12 months after immune challenge in infants apparently healthy at birth. <br/