scholarly journals The Influence of Psychosocial and Cognitive Factors on Perceived Threat of Alzheimer’s Disease

2017 ◽  
Vol 32 (5) ◽  
pp. 289-299 ◽  
Author(s):  
Jenny E. Ostergren ◽  
Steven G. Heeringa ◽  
Carlos F. Mendes de Leon ◽  
Cathleen M Connell ◽  
J. Scott Roberts

This study explored psychosocial and cognitive predictors of perceived threat of Alzheimer’s disease (AD). Respondents were 1641 adults (mean age: 64.4; 54% female; 82% white) who completed a module in the Health and Retirement Study, a nationally representative survey of adults aged ≥50. Findings show that perceived threat was significantly higher for those aged 50 to 64 ( P < .001) and 65 to 74 ( P < .05) than for those ≥75. Respondents with a family history of AD had significantly greater perceived threat ( P < .001) than those with no experience. Stronger endorsement of the beliefs that stress ( P < .01) or genetics ( P < .01) are important AD risk factors was significantly associated with greater perceived threat, as was having more depressive symptoms ( P < .01), poorer self-rated memory ( P < .01), and lower cognitive function ( P < .01). Personal experience moderated the relationship between perceived threat and 2 variables: age and self-rated memory. Understanding perceived AD threat may inform practice and policies centered on early and accurate diagnosis.

2018 ◽  
Vol 31 (04) ◽  
pp. 571-577 ◽  
Author(s):  
Margaret Miller ◽  
Dennis Orwat ◽  
Gelareh Rahimi ◽  
Jacobo Mintzer

ABSTRACTIntroduction:The relationship between Alzheimer’s Disease (AD) and alcohol addiction is poorly characterized. Arrests for driving under the influence (DUI) can serve as a proxy for alcohol addiction. Therefore, the potential association between DUI and AD could be helpful in understanding the relationship between alcohol abuse and AD.Materials and methods:A retrospective, population-based cohort study using state health and law enforcement data was performed. The study cross-referenced 141,281 South Carolina Alzheimer’s Disease Registry cases with state law enforcement data.Results:Of the 2,882 registry cases (1.4%) found to have a history of at least one DUI arrest, cases were predominantly White (58.7%) and male (77.4%). Results showed a correlation coefficient of 0.7 (p &lt; 0.0001) between the age of first DUI arrest and the age of AD diagnosis. A dose-response relationship between the number of DUIs and age of AD onset was found to exist, where those with a history of DUI arrest were diagnosed an average of 9.1 years earlier, with a further 1.8 years earlier age at diagnosis in those with two or more arrests for DUI. A history of DUI arrest was also found to be negatively associated with survival after diagnosis, with a 10% decreased life expectancy in those with a DUI arrest history.Conclusions:Driving under the influence, a potential indicator of alcohol addiction, is associated with an earlier onset of AD registry diagnosis and shortened survival after diagnosis. This study contributes to the growing body of evidence suggesting that some cases of AD are alcohol related and, possibly, postponable or preventable.


2000 ◽  
Vol 12 (S1) ◽  
pp. 63-66 ◽  
Author(s):  
David W. Gilley

Alzheimer's disease (AD) is associated with a substantial reduction in life expectancy, and mortality has long been evaluated as part of the natural history of this progressive disease. Survival time also plays an important role in projecting the future public health costs of AD. There is now considerable evidence linking mortality in AD with the severity of cognitive impairment and the level of disability in common activities of daily living (Bowen et al., 1996; Jagger et al., 1995; Moritz et al., 1997); established predictors of mortality in AD are listed in Table 1. However, the relationship between mortality and other disease characteristics has received less attention.


1997 ◽  
Vol 10 (4) ◽  
pp. 105-108 ◽  
Author(s):  
G. Macchi ◽  
C. Brahe ◽  
M. Pomponi

Three points of interest lie in considering how Alzheimer, and more significantly Perusini, struggled to throw light on the cause of this devastating disease. There is a stimulating possibility that Perusini believed presenile forms of Alzheimer’s disease described the same disease as senile forms. If so this would anticipate current opinion, and reveal Perusini to dissent from Kraepelin. In addition, Perusini may have understood the pathological relationship between neuritic plaques and vascular changes, once more foreseeing the modern view of Alzheimer’s disease. Finally, Perusini and Alzheimer disagreed with Jung's view concerning the relationship between neuropathology and clinical psychiatry. This point highlights the major change occurring at that time from classical neurology to the psychoanalytic era. In his last work (1911) Alzheimer quoted his Italian disciple many times, even speaking of ‘Perusini's cases’ (Perusinischen Fälle). This article is an attempt to change the eponym of Alzheimer’s disease into the Alzheimer-Perusini disease. This is a brief history of a master and his disciple, whose scientific lives were, by events, divided.


1995 ◽  
Vol 7 (3) ◽  
pp. 367-376 ◽  
Author(s):  
Susan McPherson ◽  
Asenath La Rue ◽  
Allan Fitz ◽  
Steven Matsuyama ◽  
Lissy F. Jarvik

This study examined the relationship between subjective memory complaints and performance on tests of memory by relatives of patients with probable Alzheimer's disease (AD) and by older adults without a family history of dementia. Relatives of AD patients did not differ significantly from controls either in level of complaint or in performance on neuropsychological tests. However, among relatives of patients with early-onset AD, significant correlations were found between performance on memory tests and self-rated changes in everyday memory. These findings raise the possibility that relatives who have entered the age range in which their parents or siblings developed dementia symptoms are monitoring their memory performance more diligently than relatives of patients whose illness began at much later ages or persons who have no close relatives with AD.


2008 ◽  
Vol 39 (4) ◽  
pp. 665-673 ◽  
Author(s):  
N. Archer ◽  
R. G. Brown ◽  
S. Reeves ◽  
H. Nicholas ◽  
H. Boothby ◽  
...  

BackgroundThere may be important public health implications of increasing our knowledge of factors associated with age of dementia onset. The pre-morbid personality domain of Neuroticism constituted an interesting and theoretically plausible, yet uninvestigated, candidate for such an association. We aimed to examine whether midlife Neuroticism was associated with earlier age of onset of Alzheimer's disease (AD).MethodThis was a case–comparison study of 213 patients with probable AD. Detailed clinical information was collected for all patients including age of onset of dementia symptoms. One or two knowledgeable informants rated each patient's midlife personality retrospectively using the Neuroticism, Extraversion, Openness Five-Factor Inventory (NEO-FFI) questionnaire. The relationship between midlife Neuroticism and age of dementia onset was evaluated using both correlational analysis and backward linear regression analysis.ResultsMidlife Neuroticism predicted younger age of dementia onset in females but not in males. The association found in females was independent of pre-morbid history of affective disorder.ConclusionsThis finding and its potential mechanism warrant further investigation.


2020 ◽  
Vol 17 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Dan Wang ◽  
Zhifu Fei ◽  
Song Luo ◽  
Hai Wang

Objectives: Alzheimer's disease (AD), also known as senile dementia, is a common neurodegenerative disease characterized by progressive cognitive impairment and personality changes. Numerous evidences have suggested that microRNAs (miRNAs) are involved in the pathogenesis and development of AD. However, the exact role of miR-335-5p in the progression of AD is still not clearly clarified. Methods: The protein and mRNA levels were measured by western blot and RNA extraction and quantitative real-time PCR (qRT-PCR), respectively. The relationship between miR-335-5p and c-jun-N-terminal kinase 3 (JNK3) was confirmed by dual-luciferase reporter assay. SH-SY5Y cells were transfected with APP mutant gene to establish the in vitro AD cell model. Flow cytometry and western blot were performed to evaluate cell apoptosis. The APP/PS1 transgenic mice were used as an in vivo AD model. Morris water maze test was performed to assess the effect of miR- 335-5p on the cognitive deficits in APP/PS1 transgenic mice. Results: The JNK3 mRNA expression and protein levels of JNK3 and β-Amyloid (Aβ) were significantly up-regulated, and the mRNA expression of miR-335-5p was down-regulated in the brain tissues of AD patients. The expression levels of miR-335-5p and JNK3 were significantly inversely correlated. Further, the dual Luciferase assay verified the relationship between miR-335- 5p and JNK3. Overexpression of miR-335-5p significantly decreased the protein levels of JNK3 and Aβ and inhibited apoptosis in SH-SY5Y/APPswe cells, whereas the inhibition of miR-335-5p obtained the opposite results. Moreover, the overexpression of miR-335-5p remarkably improved the cognitive abilities of APP/PS1 mice. Conclusion: The results revealed that the increased JNK3 expression, negatively regulated by miR-335-5p, may be a potential mechanism that contributes to Aβ accumulation and AD progression, indicating a novel approach for AD treatment.


2018 ◽  
Vol 15 (5) ◽  
pp. 429-442 ◽  
Author(s):  
Nishant Verma ◽  
S. Natasha Beretvas ◽  
Belen Pascual ◽  
Joseph C. Masdeu ◽  
Mia K. Markey ◽  
...  

Background: Combining optimized cognitive (Alzheimer's Disease Assessment Scale- Cognitive subscale, ADAS-Cog) and atrophy markers of Alzheimer's disease for tracking progression in clinical trials may provide greater sensitivity than currently used methods, which have yielded negative results in multiple recent trials. Furthermore, it is critical to clarify the relationship among the subcomponents yielded by cognitive and imaging testing, to address the symptomatic and anatomical variability of Alzheimer's disease. Method: Using latent variable analysis, we thoroughly investigated the relationship between cognitive impairment, as assessed on the ADAS-Cog, and cerebral atrophy. A biomarker was developed for Alzheimer's clinical trials that combines cognitive and atrophy markers. Results: Atrophy within specific brain regions was found to be closely related with impairment in cognitive domains of memory, language, and praxis. The proposed biomarker showed significantly better sensitivity in tracking progression of cognitive impairment than the ADAS-Cog in simulated trials and a real world problem. The biomarker also improved the selection of MCI patients (78.8±4.9% specificity at 80% sensitivity) that will evolve to Alzheimer's disease for clinical trials. Conclusion: The proposed biomarker provides a boost to the efficacy of clinical trials focused in the mild cognitive impairment (MCI) stage by significantly improving the sensitivity to detect treatment effects and improving the selection of MCI patients that will evolve to Alzheimer’s disease.


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