Mortality Risk after Diagnosis of Early-Onset Alzheimer’s Disease versus Late-Onset Alzheimer’s Disease: A Propensity Score Matching Analysis

2017 ◽  
Vol 56 (4) ◽  
pp. 1341-1348 ◽  
Author(s):  
Ki Jung Chang ◽  
Chang Hyung Hong ◽  
Kang Soo Lee ◽  
Dae Ryong Kang ◽  
Jeong Dong Lee ◽  
...  
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 ◽  
...  

2020 ◽  
Vol 78 (2) ◽  
pp. 699-709
Author(s):  
Ling Gao ◽  
Jin Wang ◽  
Yu Jiang ◽  
Shan Wei ◽  
Suhang Shang ◽  
...  

Background: Transport proteins, soluble LRP1 (sLRP1) and soluble RAGE (sRAGE), play a pivotal role in the peripheral clearance of plasma amyloid-β (Aβ). However, their relationship is seldom discussed, especially in Alzheimer’s disease (AD). Objective: To explore whether their relationship in patients with AD varied from those in cognitively normal (CN) controls. Methods: We initially recruited 70 patients with AD and 725 CN controls, then applied propensity score matching (PSM) analysis to balance the differences between two groups. Plasma levels of sLRP1, sRAGE, and Aβ were measured using commercial ELISA kits and log transformed when skewed distributed. The relationship between sLRP1/sRAGE and plasma Aβ were analyzed using Pearson’s correlation analysis followed by multiple linear regression separately in the original population and matched participants. Results: After PSM, 70 patients with AD and 140 matched controls were included for further analysis. Log sLRP1 was positively correlated with plasma Aβ40 in matched CN controls (r = 0.222, p = 0.008) but not in patients with AD (r = 0.137, p = 0.260). After multivariable adjustment, Log sLRP1 remained significantly associated with plasma Aβ40 in the CN group (β= 7.347, p = 0.014) but not in the AD group (β= 10.409, p = 0.105). In contrast, Log sLRP1 was not correlated with plasma Aβ42 in patients with AD or CN controls, and Log sRAGE was consistently not associated with plasma Aβ40 or Aβ42 in either group. Conclusion: The significant correlation between sLRP1 and plasma Aβ40 present in CN controls was not found in patients with AD, suggesting that their relationship was different in AD. However, the specific mechanisms and its influence on cerebral amyloid burden require further validation.


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.


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