Survival in Early Onset Dementia: Effects of Urbanization and Socio-Economic Deprivation

Presenile Dementia or Early Onset Dementia (EOD) is a public health problem, it differs from Senile Dementia, and encloses a significant number of cases; nevertheless, it is still poorly understood and underdiagnosed. This study aims to review the prevalence and etiology of EOD, comparing EOD with Senile Dementia, as well as to show the main causes of EOD and their prevalence in population and non-population based studies. The computer-supported search used the following databases: Pubmed/Medline, ISI Web of Knowledge and Scielo. The search terms were alcohol-associated dementia, Alzheimer’s disease, dementia, Creutzfeldt-jakob disease, dementia with lewy bodies, early onset dementia, frontotemporal lobar degeneration, Huntington’s disease, mixed dementia, neurodegenerative disorders, Parkinson’s disease dementia, presenile dementia, traumatic brain injury, vascular dementia. Only papers published in English and conducted from 1985 up to 2012 were preferentially reviewed. Neurodegenerative diseases are the most common etiologies seen in EOD. Among the general population, the prevalence of EOD was found to range between 0 to 700 per 100.000 habitants in groups of 25-64 years old, with an increasing incidence with age. The progression of EOD was found to range between 8.3 to 22.8 new cases per 100.000 in those aged under 65 years. Alzheimer's disease (AD) is the major etiology, followed by Vascular Dementia (VaD) and Frontotemporal Lobar Degeneration (FTLD). A larger number of epidemiological studies to elucidate how environmental issues contribute to EOD are necessary, thus, we can collaborate in the planning and prevention of services toward dementia patients.

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“…Thomas et al . [70] estimated a survival average for EOAD and VaD of 8.57 years and 6.1 years, respectively.…”

Section: Survival In Early-onset Dementiamentioning

confidence: 99%

Epidemiology of early-onset dementia: a review of the literature

Vieira

Caixeta

Machado³

et al. 2013

CPEMH

270

166

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“…In a younger cohort, lower childhood IQ was associated with higher blood pressure [24] ; the fact that this effect was not seen in this older cohort may be due to differential survival. Early-onset dementia is also associated with poorer survival in Scotland [41] , but the incidence of early-onset dementia is so low [42] that it is exceedingly unlikely to have any effect in this study. Nevertheless, to a lesser degree, if pre-morbid intelligence is an important contributor to cognitive reserve [28] , a surviving cohort would be expected to be relatively resistant to any adverse effects of raised blood pressure.…”

Section: Discussionmentioning

confidence: 61%

Blood Pressure and Cognition in the Aberdeen 1936 Birth Cohort

Starr¹,

Deary

Fox³

et al. 2007

Gerontology

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Background: The relationship between blood pressure and cognition in old age remains unclear. Some data indicate that elevated blood pressure causes cognitive deficits whilst others show that lower early life mental ability predicts high blood pressure in adulthood. Longitudinal studies in which mental ability earlier in life is known are needed to clarify the relationship. Objective: To measure the effect of blood pressure on cognition in late adulthood after adjusting for early life mental ability. Methods: The sample comprised survivors of the 1947 Scottish Mental Survey who had validated IQ scores at age 11. Six cognitive tests – Mini-Mental State Examination, Raven’s Progressive Matrices, Rey Auditory Verbal Learning Test, Uses of Common Objects Test, Digit Symbol Test and Block Design – were administered at ages 64, 66 and 68 years. Sitting and standing blood pressure was also measured at each wave of follow-up. Mixed general linear models were constructed with each cognitive test treated as a repeated measure of an underlying cognitive trait and with wave of testing also set as a repeated measure. Mental ability at age 11 was entered as a covariate. Results: 504 participants were tested at wave 1 with 368 returning at wave 2 and 300 at wave 3. Age 11 mental ability did not predict any of the blood pressure measures. There were several significant associations between blood pressure variables and cognitive test scores in univariate models. After adjusting for significant effects of wave of testing, type of cognitive test, the interaction between these, age 11 mental ability, age, gender and occupation in a multivariate model, the main effect of BP trait was no longer significant (p = 0.44) nor its effect over time (p = 0.26), though there was a significant interaction between blood pressure trait (BP) and test type with a distinctly negative effect of BP on Auditory Verbal Learning Test (p = 0.007, –0.13 points per mm Hg higher, 95% CI –0.22 to –0.033). Conclusion: The effects of blood pressure on cognition in old age are finely nuanced. Multivariate repeated measures models reveal a differential effect of blood pressure on verbal recall.

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“…Hypoxia has often been proposed as a factor contributing to or even causing varicose vein formation [61]. Although varicose vein wall hypoxia has been investigated for several decades, the evidence supporting or refuting this theory remains debatable.…”

Section: Discussionmentioning

confidence: 99%

“…Similar observations were also observed in whole-vein explants exposed to hypoxia. Michiels et al [61] described an in vitro model that assessed the effect of hypoxia on saphenous vein explants in the presence of non-stimulated PMN cells. Non-varicose segments of GSV incubated in hypoxic and normoxic environments were perfused with radiolabeled PMN cells.…”

Section: Molecular Studiesmentioning

confidence: 99%

Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins

et al. 2010

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Venous hypoxia has long been postulated as a potential cause of varicosity formation. This article aimed to review the development of this hypothesis, including evidence supporting and controversies surrounding it. Vein wall oxygenation is achieved by oxygen diffusing from luminal blood and vasa vasorum. The whole media of varicosities is oxygenated by vasa vasorum as compared to only the outer two-thirds of media of normal veins. There was no evidence that differences exist between oxygen content of blood from varicose and non-varicose veins, although the former demonstrated larger fluctuations with postural changes. Studies using cell culture and ex vivo explants demonstrated that hypoxia activated leucocytes and endothelium which released mediators regulating vein wall remodelling similar to those observed in varicosities. Venoactive drugs may improve venous oxygenation, and inhibit hypoxia activation of leucocytes and endothelium. The evidence for hypoxia as a causative factor in varicosities remains inconclusive, mainly due to heterogeneity and poor design of published in vivostudies. However, molecular studies have shown that hypoxia was able to cause inflammatory changes and vein wall remodelling similar to those observed in varicosities. Further studies are needed to improve our understanding of the role of hypoxia and help identify potential therapeutic targets.

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Survival in Early Onset Dementia: Effects of Urbanization and Socio-Economic Deprivation

Cited by 12 publications

References 11 publications

Epidemiology of early-onset dementia: a review of the literature

Epidemiology of early-onset dementia: a review of the literature

Blood Pressure and Cognition in the Aberdeen 1936 Birth Cohort

Venous Hypoxia: A Poorly Studied Etiological Factor of Varicose Veins

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