longitudinal course
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2021 ◽  
pp. 1-15
Author(s):  
Sally Day ◽  
Stefanie Roberts ◽  
Nathalie H. Launder ◽  
Anita M.Y. Goh ◽  
Brian Draper ◽  
...  

Background: Understanding how the age of dementia symptom onset affects the longitudinal course of dementia can assist with prognosis and care planning. Objective: To synthesize evidence regarding the relationship of age of symptom onset with the longitudinal course of sporadic Alzheimer’s disease (AD), vascular dementia (VaD), and frontotemporal dementia (FTD). Methods: We searched Medline, CINAHL, Embase, PsycINFO, PubMed, and Scopus for longitudinal studies that examined the impact of sporadic AD, VaD, or FTD symptom onset age on measures of cognition, function, or behavioral symptoms. Studies that examined age at diagnosis only were excluded. Quantitative meta-analysis was conducted where studies reported sufficient data for pooling. Results: Thirty studies met all inclusion criteria (people with AD (n = 26), FTD (n = 4)) though no studies examined VaD. Earlier onset of AD was associated with more rapid annual cognitive decline (estimate = –0.07; 95% CI –0.14 to 0.00; p = 0.045). Most studies that stratified their sample reported that younger AD onset (usually <  65 years) was associated with more rapid cognitive decline. Other evidence was inconclusive. Conclusion: Younger people with AD appear to have a poorer prognosis in terms of faster cognitive decline than older people with AD. More research is required to determine the impact of symptom onset age in VaD and FTD, and on functional decline in all dementias.


2021 ◽  
Author(s):  
Tobey J. Betthauser ◽  
Murat Bilgel ◽  
Rebecca L. Koscik ◽  
Bruno M. Jedynak ◽  
Yang An ◽  
...  

AbstractAlzheimer’s disease biomarkers are becoming increasingly important for characterizing the longitudinal course of disease, predicting the timing of clinical and cognitive symptoms, and for recruitment and treatment monitoring in clinical trials. In this work, we develop and evaluate three methods for modeling the longitudinal course of amyloid accumulation in three cohorts using amyloid PET imaging. We then use these novel approaches to investigate factors that influence the timing of amyloid onset and the timing from amyloid onset to impairment onset in the Alzheimer’s disease continuum.Data were acquired from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), the Baltimore Longitudinal Study of Aging (BLSA) and the Wisconsin Registry for Alzheimer’s Prevention (WRAP). Amyloid PET was used to assess global amyloid burden. Three methods were evaluated for modeling amyloid accumulation using 10-fold cross-validation and hold-out validation where applicable. Estimated amyloid onset age was compared across all three modeling methods and cohorts. Cox regression and accelerated failure time models were used to investigate whether sex, apolipoprotein E genotype and e4 carriage were associated with amyloid onset age in all cohorts. Cox regression was used to investigate whether apolipoprotein E (e4 carriage and e3e3, e3e4, e4e4 genotypes), sex or age of amyloid onset were associated with the time from amyloid onset to impairment onset (global Clinical Dementia Rating ≥1) in a subset of 595 ADNI participants that were not impaired prior to amyloid onset.Model prediction and estimated amyloid onset age were similar across all three amyloid modeling methods. Sex and apolipoprotein E-e4 carriage were not associated with PET-measured amyloid accumulation rates. Apolipoprotein E genotype and e4 carriage, but not sex, were associated with amyloid onset age such that e4 carriers became amyloid positive at an earlier age compared to non-carriers, and greater e4 dosage was associated with an earlier amyloid onset age. In the ADNI, e4 carriage, being female and a later amyloid onset age were all associated with a shorter time from amyloid onset to impairment onset. The risk of impairment onset due to age of amyloid onset was nonlinear and accelerated for amyloid onset age >65. These findings demonstrate the feasibility of modeling longitudinal amyloid accumulation to enable individualized estimates of amyloid onset age from amyloid PET imaging. These estimates provide a more direct way to investigate the role of amyloid and other factors that influence the timing of clinical impairment in Alzheimer’s disease.


PAIN Reports ◽  
2021 ◽  
Vol 6 (4) ◽  
pp. e976
Author(s):  
K. Mikayla Flowers ◽  
Meghan Beck ◽  
Carin Colebaugh ◽  
Simon Haroutounian ◽  
Robert R. Edwards ◽  
...  

2021 ◽  
Vol 51 ◽  
pp. e107-e108
Author(s):  
Amedeo Primerano ◽  
Katherine Gordon-Smith ◽  
Lisa Jones ◽  
Valentina Escott-Price ◽  
Nick Craddock ◽  
...  

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Rugina I Neuman ◽  
Willy Visser ◽  
Jan H Danser

Low soluble Fms-like tyrosine kinase (sFlt-1) has been reported in women with suspected or confirmed preeclampsia (PE) coincidentally using proton pump inhibitors (PPIs), suggesting a role for these agents as potential treatment for PE. Here, we examined whether administration of omeprazole to women with PE could acutely reduce their circulating levels of sFlt-1 or enhance their placental growth factor (PlGF) concentrations. We performed a randomized controlled trial in which women (≥ 18 years) with confirmed preeclampsia and a gestational age between 20 +0 and 34 +6 weeks were allocated to receive 40mg omeprazole once daily or no omeprazole. Blood was collected at baseline and days 1,2,4,8 followed by twice-weekly until delivery. Primary outcome was specified as the difference in sFlt-1 or PlGF 4 days after omeprazole initiation compared to the non-omeprazole group. Secondary outcomes were defined as between-group differences in longitudinal course of sFlt-1 and PlGF and pregnancy outcomes. Between Dec 2018 and June 2021, 50 women with PE were randomized, of which 40 women remained pregnant after 4 days. Mean maternal age was 30 years, and median gestational age was 31 weeks. Baseline sFlt-1 levels did not differ between non-omeprazole (n=20) and omeprazole group (n=20) (10743 vs. 7110pg/mL, p=0.11), neither did the levels of PlGF (p=0.14). After 4 days, sFlt-1 levels remained similar in women receiving omeprazole compared to women not receiving omeprazole (8364 vs. 13017pg/mL, p=0.14), and the same was true for PlGF (90 vs. 55pg/mL, p=0.14). Using linear mixed models, no difference in longitudinal course of sFlt-1 or PlGF could be attributed to the treatment group, when adjusted for baseline values and GA at enrollment (p=0.47). Women receiving omeprazole had a similar length of pregnancy compared with those not receiving this drug (median 15 vs. 14 days, p=0.70). Except for a higher neonatal intubation rate in the non-omeprazole group (31% vs 4%, p=0.02) there were no differences in maternal/perinatal complications between the two groups. Our findings suggest that daily administration of 40mg in women with PE do not alter their circulating levels of sFlt-1 and PlGF, arguing against a role for this drug as a potential treatment for this syndrome.


Author(s):  
Nicholas A. Livingston ◽  
Stacey L. Farmer ◽  
Colin T. Mahoney ◽  
Brian P. Marx ◽  
Terence M. Keane

Author(s):  
Marco Spangaro ◽  
Francesca Martini ◽  
Margherita Bechi ◽  
Mariachiara Buonocore ◽  
Giulia Agostoni ◽  
...  

Author(s):  
Eric Taylor

This chapter covers the profiles of difficulties in relating, to other people and the world, that are included in the international schemes of classification as spectra of autism, schizophrenia, and psychosis. In autism, there is a marked reduction in, or oddity of, social communication, and an increase of repetitive and stereotyped behaviours. In psychoses, including schizophrenia and catatonia, there is disordered testing of reality (resulting in hallucinations, delusions, and disorganized speech), and deficits in volition (involving apathy, social isolation, and lack of initiative). These are described as they present in children and young people, together with their prevalence and the coexistent problems of emotion and behaviour that occur frequently. The longitudinal course is considered up to the transition into adult life. Potential causes and pathophysiology are considered in so far as they apply specifically to these disorders.


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