Objective: The incidence of cases of older onset anorexia nervosa (AN) has increased in recent years. However, the literature on late-onset AN has been inconclusive. The goal of this study was to compare late-onset with early-onset cases of AN.
Methods: Cases of AN presenting to an eating disorders treatment service were identified and the associated medical records were studied retrospectively.
Results: Of the 577 cases of AN that were studied, 7.1% were late-onset. Unlike the early-onset cases of AN, the late-onset cases reported less teasing and more relationship problems as a trigger for the illness. They were also less likely to join the eating disorders treatment program. Otherwise, the late-onset AN cases were largely similar to the early-onset cases.
Conclusions: Although differences exist between early-onset and late-onset cases of AN, these are few. Until stronger evidence emerges over time, there currently seems to be minimal justification to accord late-onset AN a unique position in psychiatric nosology.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1097/PRA.0000000000000296 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most prevalent type of senile dementia affecting more than 6 million Americans in 2023. Most of these AD cases are sporadic or late-onset AD with unclear etiology. Recent clinical trials on antibody drug clearing Ab plagues in brain show modest benefits of slowing down cognitive decline.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Michigan Alzheimer's Disease Research Center, Ann Arbor, MI, USA.
Background: Non-coding RNA species, such as microRNA (miRNA), regulate multiple biological and pathological processes by binding to target mRNAs and facilitating alteration of translation levels via complexes such as RNA-induced silencing complex (RISC). Disrupting this process could contribute to AD pathogenesis by fostering aggregation of hyperphosphorylated microtubule-associated protein tau and amyloid-β (Aβ) peptides, and neuroinflammation. Understanding how these pathological changes are regulated remains our research focus.
View Article and Find Full Text PDFBackground: Autosomal dominant Alzheimer's Disease (ADAD) represents around 0.5% of all AD cases, and is caused by mutations in PSEN1, PSEN2 and APP genes. Gene expression studies can be useful for unravelling the physiopathology of AD and identifying potential biomarkers.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Stanford University, Stanford, CA, USA.
Background: APOE*4 is the strongest genetic risk for late-onset Alzheimer's disease (AD), but other genetic loci may counter its detrimental effect, providing therapeutic avenues. Expanding beyond non-Hispanic White subjects, we sought to additionally leverage genetic data from non-Hispanic and Hispanic subjects of admixed African ancestry to perform trans-ancestry APOE*4-stratified GWAS, anticipating that allele frequency differences across populations would boost power for gene discovery.
Method: Participants were ages 60+, of European (EU; ≥75%) or admixed African (AFR; ≥25%) ancestry, and diagnosed as cases or controls.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Background: Late onset dementia due to Alzheimer's disease (AD) has a sex-biased incidence with females comprising nearly two thirds of all cases. Females have a more rapid progression in cognitive decline and higher levels of known AD biomarker pathology compared to men. Genetic sequence variation does not account for the sex-biased incidence of AD, directing attention to the emerging role of epigenetics in AD.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!