scholarly journals Is Female Gender a Risk Factor for Alzheimer's Disease?

1999 ◽  
Vol 11 (3) ◽  
pp. 219-222 ◽  
Author(s):  
Gregory Swanwick ◽  
Brian A. Lawlor

Despite a growing list of potential new risk factors for Alzheimer's disease (AD), one of the oldest remains controversial. Is female gender a risk factor for AD? It is likely that the greatest influence on the gender differential in crude prevalence rates is the increasing incidence of dementia with age (Paykel et al., 1994) combined with the greater longevity women (Moritz & Ostfeld, 1990). This must be distinguished from the hypothesis that there may also be a gender difference in the age-specific prevalence rates some dementias such as AD. In turn, this could be due to either a higher incidence dementia in women, or to longer survival times in women following diagnosis. What is the evidence for these hypotheses?

Author(s):  
Robert Stewart

Vascular disease is the most important environmental risk factor for dementia but this research area has been hampered by inadequate outcome definitions – in particular, a diagnostic system that attempts to separate overlapping and probably interacting pathologies. There is now substantial evidence that the well-recognised risk factors for cardiovascular disease and stroke are also risk factors for dementia, including Alzheimer’s disease. However, these risk factors frequently act over several decades, meaning that the chances of definitive randomised controlled trial evidence for risk-modifying interventions are slim. This should not obscure the wide opportunity for delaying or preventing dementia through risk factor control and uncontroversial healthy lifestyles. Care should also be taken that comorbid cerebrovascular disease is not considered as excluding a diagnosis of Alzheimer’s disease, particularly now that this determines treatment eligibility.


2016 ◽  
Vol 37 (1) ◽  
pp. 201-216 ◽  
Author(s):  
Eseosa T Ighodaro ◽  
Erin L Abner ◽  
David W Fardo ◽  
Ai-Ling Lin ◽  
Yuriko Katsumata ◽  
...  

Risk factors and cognitive sequelae of brain arteriolosclerosis pathology are not fully understood. To address this, we used multimodal data from the National Alzheimer's Coordinating Center and Alzheimer's Disease Neuroimaging Initiative data sets. Previous studies showed evidence of distinct neurodegenerative disease outcomes and clinical-pathological correlations in the “oldest-old” compared to younger cohorts. Therefore, using the National Alzheimer's Coordinating Center data set, we analyzed clinical and neuropathological data from two groups according to ages at death: < 80 years ( n = 1008) and ≥80 years ( n = 1382). In both age groups, severe brain arteriolosclerosis was associated with worse performances on global cognition tests. Hypertension (but not diabetes) was a brain arteriolosclerosis risk factor in the younger group. In the ≥ 80 years age at death group, an ABCC9 gene variant (rs704180), previously associated with aging-related hippocampal sclerosis, was also associated with brain arteriolosclerosis. A post-hoc arterial spin labeling neuroimaging experiment indicated that ABCC9 genotype is associated with cerebral blood flow impairment; in a convenience sample from Alzheimer's Disease Neuroimaging Initiative ( n = 15, homozygous individuals), non-risk genotype carriers showed higher global cerebral blood flow compared to risk genotype carriers. We conclude that brain arteriolosclerosis is associated with altered cognitive status and a novel vascular genetic risk factor.


Author(s):  
K.J. Anstey ◽  
R. Peters

The evidence for specific risk factors for Alzheimer’s disease, vascular dementia and all cause dementia is increasing rapidly in quantity and quality. This has enabled the compilation of risk assessment tools for Alzheimer’s disease (1), and their validation (2). It has also supported the promulgation of public health messaging about dementia risk reduction or dementia prevention. In general these developments are strong advances in the field of dementia prevention. However, the oversimplification of the findings and possible over-or mis-interpretation of their meaning, poses risks to accurate and effective knowledge translation in this field. Lack of balance in the interpretation of evidence on risk factors for dementia may lead to trials of interventions for dementia prevention that are ineffective. This will waste resources and create pessimism about dementia prevention research. Two potential problems that may occur when translating evidence from observational research into prescriptions for prevention are identified here. The first is the generalisation of specific findings about risk factors either to multiple types of dementia or to multiple populations, when the evidence is in fact relevant to specific populations or outcomes. The second is the inference that reversal of a risk factor will lead to prevention, without knowledge of the threshold at which a factor becomes a ‘risk’, or evidence that reversal of the risk factor also reverses neuropathological processes instigated or caused by the risk factor.


1994 ◽  
Vol 6 (2) ◽  
pp. 209-223 ◽  
Author(s):  
Amy B. Graves ◽  
Eric B. Larson ◽  
Lon R. White ◽  
Evelyn L. Teng ◽  
Akira Homma

Estimates of the prevalence rates for dementia vary significantly among countries. Such variation may be explained, at least in part, by methodologic differences in studies. The disparities in prevalence rates of dementia subtypes, particularly Alzheimer's disease and multi-infarct dementia, are especially apparent in studies conducted in Eastern and Western countries. In Japan and China, the prevalence of multi-infarct dementia exceeds that of Alzheimer's disease, whereas in the West, Alzheimer's disease predominates in the vast majority of studies. Clearly, cross-cultural studies of incidence using standard methods are needed to investigate whether a true difference in risk exists, and which risk factors differentially contribute to this variation. Migrant studies of genetically homogeneous populations offer a unique opportunity to answer these questions. This article explores the value of migrant studies, their application to etiologic questions of dementia and its subtypes, and recommendations concerning how to conduct such studies.


2008 ◽  
Vol 20 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Moon Ho Park ◽  
Sangmee Ahn Jo ◽  
Inho Jo ◽  
Eunkyung Kim ◽  
Eun Kyung Woo ◽  
...  

Objective:Although there are rapidly growing concerns about the high rates of cognitive dysfunction in Korea, the knowledge of risk factors for Alzheimer’s disease (AD) among the general public in Korea remains to be elucidated.Methods:A total of 2767 randomly selected subjects from the Ansan Geriatric Study were questioned on their knowledge of putative risk factors for AD. Their answers were compared with their sociodemographic data and other variables.Results:The most common stated risk factor was being older (59.6%), followed by head trauma (33.6%) and cerebrovascular disease (30.4%). However, a substandard education, which is a known risk factor, was considered significant by only 9.5% of the subjects. Predictors for a worse knowledge of the risk factors for AD were being older, a lower level of education, lower economic status and the attitude that dementia is not curable.Conclusion:This study revealed that misunderstanding about AD is more prevalent in older subjects and those with a lower level of education, and so public health education on the basic concepts of AD should be targeted at this population.


2021 ◽  
Author(s):  
João Pedro Ferrari-Souza ◽  
Wagner S. Brum ◽  
Lucas A. Hauschild ◽  
Lucas U. Da Ros ◽  
Pâmela C. L. Ferreira ◽  
...  

Understanding whether vascular risk factors synergistically potentiate Alzheimer's disease progression is important in the context of emerging treatments for preclinical Alzheimer's disease. The existence of a synergistic relationship could suggest that the combination of therapies targeting Alzheimer's disease pathophysiology and vascular risk factors might potentiate treatment outcomes. In the present retrospective cohort study, we tested whether vascular risk factor burden interacts with Alzheimer's disease pathophysiology to accelerate neurodegeneration and cognitive decline in cognitively unimpaired subjects. We evaluated 503 cognitively unimpaired participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. Baseline vascular risk factor burden was calculated considering the history of cardiovascular disease, hypertension, diabetes mellitus, hyperlipidemia, stroke or transient ischemic attack, smoking, atrial fibrillation, and left ventricular hypertrophy. Alzheimer's disease pathophysiology was evaluated using cerebrospinal fluid (CSF) amyloid-β1-42 (Aβ1-42) reflecting brain amyloidosis (A) and tau phosphorylated at threonine 181 (p-tau181) reflecting brain tau pathology (T). Individuals were dichotomized as having an elevated vascular risk factor burden (V+ if having two or more vascular risk factors) and as presenting preclinical Alzheimer's disease [(AT)+ if having abnormal CSF p-tau181 and Aβ1-42 levels]. Neurodegeneration was assessed with plasma neurofilament light (NfL) and global cognition with the modified version of the Preclinical Alzheimer's Cognitive Composite. Linear mixed-effects models revealed that an elevated vascular risk factor burden synergistically interacted with Alzheimer's disease pathophysiology to drive longitudinal increases in plasma NfL levels (β = 5.08, P = 0.016) and cognitive decline (β = -0.43, P = 0.020). Additionally, we observed that vascular risk factor burden was not associated with CSF Aβ1-42 or p-tau181 changes over time. Survival analysis demonstrated that individuals with preclinical Alzheimer's disease and elevated vascular risk factor burden [(AT)+V+] had a significantly greater risk of clinical progression to cognitive impairment (adjusted Hazard Ratio = 3.5, P < 0.001). Our results support the notion that vascular risk factor burden and Alzheimer's disease pathophysiology are independent processes; however, they synergistically lead to neurodegeneration and cognitive decline. These findings can help in providing the blueprints for the combination of vascular risk factor management and Alzheimer's disease pathophysiology treatment in preclinical stages. Moreover, we observed plasma NfL as a robust marker of disease progression that may be used to track therapeutic response in future trials.


1995 ◽  
Vol 167 (6) ◽  
pp. 732-738 ◽  
Author(s):  
Lawrence J. Whalley ◽  
Brenda M. Thomas ◽  
John M. Starr

Background and MethodWe related geographical variation of ‘probable’ presenile Alzheimer's disease (AD PSD) to exposures to possible risk factors for AD PSD and vascular dementia (VaD) and to geographical differences in survival times after presentation with AD PSD.ResultsWe found that an ecological measure of socio-economic deprivation was related to VaD but not to AD PSD. Among men with AD PSD and VaD, specific occupations conveyed no altered risk but having fathers who were coal miners was associated with AD PSD and VaD in offspring. Increased paternal age was associated with AD PSD but only in men. These factors acted independently of one another and did not distinguish between geographical areas of high and low incidence.ConclusionsThe length of survival after presentation with AD PSD distinguished between these areas, and when migration between these areas was taken into account, a plausible multifactorial model of the harmful effects of environment emerged, which acted independently of risk factors acting earlier in life.


2019 ◽  
Vol 9 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Hege Rasmussen Eid ◽  
Tor Atle Rosness ◽  
Ole Bosnes ◽  
Øyvind Salvesen ◽  
Marlen Knutli ◽  
...  

Background: Few studies have assessed smoking and obesity together as risk factors for frontotemporal dementia (FTD) and Alzheimer’s disease (AD). Objective: To study smoking and obesity as risk factors for FTD and AD. Methods: Ninety patients with FTD and 654 patients with AD were compared with 116 cognitively healthy elderly individuals in a longitudinal design with 15–31 years between measurements of risk factors before the dementia diagnosis. Results: There were no associations between smoking and FTD (p = 0.218; odds ratio [OR]: 0.990; 95% confidence interval [CI]: 0.975–1.006). There were significant associations between obesity and FTD (p = 0.049; OR: 2.629; 95% CI: 1.003–6.894). There were significant associations between both smoking (p = 0.014; OR: 0.987; 95% CI: 0.977–0.997) and obesity (p = 0.015; OR: 2.679; 95% CI: 1.211–5.928) and AD. Conclusion: Our findings suggest that obesity is a shared risk factor for FTD and AD, while smoking plays various roles as a risk factor for FTD and AD.


Author(s):  
Robert Stewart

Vascular disease is the most important environmental risk factor for dementia but this research area has been hampered by inadequate outcome definitions—in particular, a diagnostic system that attempts to separate overlapping and probably interacting pathologies. There is now substantial evidence that the well-recognized risk factors for cardiovascular disease and stroke are also risk factors for dementia, including Alzheimer’s disease. However, these risk factors frequently act over several decades, meaning that the chances of definitive randomized controlled trial evidence for risk-modifying interventions are slim. This should not obscure the wide opportunity for delaying or preventing dementia through risk factor control and uncontroversial healthy lifestyles. Care should also be taken that comorbid cerebrovascular disease is not considered as excluding a diagnosis of Alzheimer’s disease, particularly now that this determines treatment eligibility.


1998 ◽  
Vol 32 (5) ◽  
pp. 698-706 ◽  
Author(s):  
Kathleen Hall ◽  
Frederick W. Unverzagt ◽  
Hugh C. Hendrie ◽  
Oye Gureje ◽  
Sujuan Gao ◽  
...  

Objective: To determine the association between demographic, lifestyle and medical history factors to Alzheimer's disease (AD), we studied samples of two community dwelling populations with significantly different prevalence rates of AD in Indianapolis, USA (6.24%) and Ibadan, Nigeria (1.4%). Methods: The samples were drawn from African—American community dwelling residents 65 years of age and over in Indianapolis, and Yoruba community-dwelling residents 65 years of age and over in Ibadan. A two-stage epidemiological design was used in which diagnosis of AD was by National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association criteria. Results: In Indianapolis, age (odds ratio [OR] = 1.16; 95% confidence interval [Cl] = 1.11-1.21), family history of dementia (OR = 5.40; 95% Cl = 1.99-14.62), low education (0-6 years, OR = 3.49; 95% Cl = 1.06-11.48) and rural residence (OR = 2.49; 95% CI = 1.05-5.88) were associated with a higher risk of AD. In Ibadan, age (OR = 1.15; 95% Cl = 1.12-1.18) and female gender (OR = 13.9; 95% Cl = 3.85-50.28) were associated with a higher risk of AD. Conclusions: The remarkably similar odds ratios between age and AD between sites suggest that biological processes associated with ageing are essential elements in the development of AD but that genetic and environmental risk factors may alter age-specific rates. In our longitudinal study, we intend to investigate in more depth the interaction between these ageing, genetic and environmental factors.


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