scholarly journals The Learning Ratio in Early-Onset Alzheimer’s Disease

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Taylor Diedrich ◽  
Dustin Hammers ◽  
Sára Nemes

Background: The Learning Ratio (LR) is a novel marker of learning capacity. Unlike traditional raw learning scores (RLS), LR controls for the number of words learned by participants after the first trial, thus avoiding a common confound with learning slope research. While investigation has been conducted on the relationship between LR and late-onset Alzheimer’s Disease, little to no information on LR in the context of early-onset Alzheimer’s Disease (EOAD) exists. The goal of this study was to establish criterion validity for the LR by showing that it outperforms the traditional RLS in EOAD. Methods: Rey Auditory Verbal Learning Test individual trial scores (Trials 1-5) were obtained from 314 participants (82 cognitively normal [CN], 168 EOAD, and 64 Early-Onset Non-Alzheimer’s Disease [EOnonAD]) enrolled in the Longitudinal Early-Onset Alzheimer’s Disease Study. RLS for each participant was calculated as follows: Highest Trial score (of Trials 2 through 5) – Trial One score. LR was calculated as follows: RLS / (Maximum trial score possible – Trial One score). In essence, LR is the proportion of available information learned after Trial 1. Results: When controlling for age, education, sex, and ethnicity, significant differences were observed between groups for both LR (p<0.001, η=0.485) and RLS (p<0.001, η=0.325). For both LR and RLS, CN participants performed better than EOnonAD participants, who performed better than EOAD participants. Upon direct comparison, the magnitude of the effect for LR was stronger than for RLS. Conclusion: Results support criterion validity for LR by establishing that LR values are consistently lower for more severe disease states to a greater extent than a traditional learning metric. Such a finding suggests that LR is useful for measuring learning for those with EOAD.

2019 ◽  
Vol 34 (7-8) ◽  
pp. 433-438 ◽  
Author(s):  
Sarah Baillon ◽  
Amy Gasper ◽  
Frances Wilson-Morkeh ◽  
Megan Pritchard ◽  
Amala Jesu ◽  
...  

Background: The study aimed to compare neuropsychiatric symptoms (NPS) in people with early-onset Alzheimer’s disease (EOAD) and late-onset AD (LOAD). Methods: Fifty-six participants with LOAD and 24 participants with EOAD having mild dementia were assessed for NPS for their frequency, severity, and caregiver distress as measured by Neuropsychiatry Inventory (NPI) along with assessments of cognition and functional dependence. Results: Participants with EOAD and LOAD were not significantly different for total NPI score ( P = .057). Early-onset Alzheimer disease had greater prevalence of all the NPS except apathy. Participants with EOAD were significantly worse on anxiety ( P = .03), irritability ( P = .01), and sleep ( P < .01) subscales and their carers significantly more distressed by their irritability ( P = .002) and sleeping patterns ( P = .005). Regression analysis showed that higher NPI score was associated with longer duration of illness in EOAD and higher functional dependence in LOAD. Conclusions: The NPS severity was similar between EOAD and LOAD although EOAD had higher symptom prevalence and carer distress.


2020 ◽  
Vol 88 (01) ◽  
pp. 4

Hohe Cholesterinwerte sind ein Risikofaktor für die Entwicklung der altersbedingten, späten Form der Alzheimer-Krankheit, der „Late-onset Alzheimer`s disease“ (LOAD). Doch wie die seltenere, frühe Form, die „Early-onset Alzheimer‘s disease“ (EOAD) mit Cholesterin zusammenhängt, war bisher unklar. In dieser Studie untersuchten die Forscher Assoziationen zwischen Cholesterinwerten und EOAD, sowie zugrunde liegende genetische Mechanismen.


2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Lea Tenenholz Grinberg ◽  
Cathrine Petersen ◽  
Amber L. Nolan ◽  
Elisa de Paula França Resende ◽  
Zachary A. Miller ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Perry G. Ridge ◽  
Mark T. W. Ebbert ◽  
John S. K. Kauwe

Alzheimer’s disease is the most common form of dementia and is the only top 10 cause of death in the United States that lacks disease-altering treatments. It is a complex disorder with environmental and genetic components. There are two major types of Alzheimer’s disease, early onset and the more common late onset. The genetics of early-onset Alzheimer’s disease are largely understood with variants in three different genes leading to disease. In contrast, while several common alleles associated with late-onset Alzheimer’s disease, including APOE, have been identified using association studies, the genetics of late-onset Alzheimer’s disease are not fully understood. Here we review the known genetics of early- and late-onset Alzheimer’s disease.


2017 ◽  
Vol 13 (7S_Part_22) ◽  
pp. P1083-P1083
Author(s):  
Young Noh ◽  
Han Kyu Na ◽  
Seongho Seo ◽  
Sang-Yoon Lee ◽  
Hye Jin Jeong ◽  
...  

Author(s):  
Ratnavalli Ellajosyula

The term ‘early onset Alzheimer’s disease’ (EOAD) is used when symptoms of Alzheimer’s disease (AD) occur in patients younger than 65 years. EOAD is an uncommon condition and data on epidemiology is limited. Prevalence rates range from 15 to 200 and incidence rates 2.4–22.6 per 100,000 population. Prevalence rates increase with age similar to that for late onset AD. The prevalence of autosomal dominant EOAD is 5.2 per 100,000. Half of these patients have an underlying mutation in amyloid precursor protein, presenilin 1 or 2 genes. Apolipoprotein E genotype is a risk factor for EOAD and homozygotes have an earlier age of onset. Methodological issues and geographical location make comparisons across epidemiological studies difficult. Further cross-national and cross-cultural studies with standardized methodology are necessary to understand the role of risk and protective factors, as well as to estimate the burden of the disease.


2021 ◽  
Vol 21 (2) ◽  
Author(s):  
Temitope Ayodele ◽  
Ekaterina Rogaeva ◽  
Jiji T. Kurup ◽  
Gary Beecham ◽  
Christiane Reitz

Abstract Purpose of Review Early-onset Alzheimer’s disease (EOAD), defined as Alzheimer’s disease (AD) occurring before age 65, is significantly less well studied than the late-onset form (LOAD) despite EOAD often presenting with a more aggressive disease progression. The aim of this review is to summarize the current understanding of the etiology of EOAD, their translation into clinical practice, and to suggest steps to be taken to move our understanding forward. Recent Findings EOAD cases make up 5–10% of AD cases but only 10–15% of these cases show known mutations in the APP, PSEN1, and PSEN2, which are linked to EOAD. New data suggests that these unexplained cases following a non-Mendelian pattern of inheritance is potentially caused by a mix of common and newly discovered rare variants. However, only a fraction of this genetic variation has been identified to date leaving the molecular mechanisms underlying this type of AD and their association with clinical, biomarker, and neuropathological changes unclear. Summary While great advancements have been made in characterizing EOAD, much work is needed to disentangle the molecular mechanisms underlying this type of AD and to identify putative targets for more precise disease screening, diagnosis, prevention, and treatment.


2021 ◽  
Author(s):  
Liana G. Apostolova ◽  
Paul Aisen ◽  
Ani Eloyan ◽  
Anne Fagan ◽  
Keith N. Fargo ◽  
...  

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