Apo E allele frequencies in Alzheimerʼs disease, Lewy body dementia, Alzheimerʼs disease with cerebrovascular disease and vascular dementia

Bétard, Christine; Robitaille, Yves; Gee, Michayla E.; Tiberghien, D.; Larrivee, Denis; Roy, Patrice; Mortimer, James A.; Gauvreau, D.

doi:10.1097/00001756-199410000-00013

Cited by 68 publications

(21 citation statements)

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“…Increased rates of the Apo E ε4 isoform have been detected in some studies of patients with vascular dementia (Shimano et al 1989 ;Pedro-Botet et al 1992 ;Noguchi et al 1993 ;Frisoni et al 1994), but not others (Betard et al 1994 ;Kawamata et al 1994 ;Sakoda et al 1994). Most importantly, the Apo ε4 isoform has also been detected with increased frequency in a small group of patients with late-life depression (Krishnan et al 1994).…”

Section: Identifying Genetically-determined Risk Factorsmentioning

confidence: 95%

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Hickie¹,

Scott²

1998

Psychol. Med.

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The severe depressive disorders of late life are associated with high rates of medical morbidity and mortality, cognitive impairment, suicide, disability, complex treatment regimens, institutionalization and high costs to the community (Murphy, 1983; Murphy et al. 1988; Bruce & Leaf, 1989; NIH Consensus Development Panel, 1992; Alexopoulos et al. 1993a, b; Brodaty et al. 1993; Bruce et al. 1994; Forsell et al. 1994; Hickie et al. 1995; Blazer, 1996). Those disorders that are accompanied by cognitive impairment and/or concurrent medical morbidity have a particularly poor outcome (Bruce & Leaf, 1989; Alexopoulos et al. 1993b; Hickie et al. 1995, 1997a). Although psychosocial models of late-life depression place considerable importance on age-related psychological and social risk factors, those who survive into later life may actually be characterized by psychological resilience (Henderson, 1994; Blazer, 1997).Current aetiological research in late-life depression, therefore, places particular emphasis on the potential role of biological risk factors. The potential importance of vascular risk factors is receiving renewed attention and may provide opportunities for specific prevention and intervention strategies in high-risk populations. This emphasis on possible vascular risk factors, and the wider importance of vascular pathologies in late-life neuropsychiatric disorders, mirrors the emphasis of much earlier clinico-pathological studies (Binswanger, 1894; Alzheimer, 1895). The specific focus on the importance of small progressive changes within the subcortical white matter, as distinct from more discrete cortical infarcts (Olszewski, 1962), is now supported by the emerging neuroimaging literature and theoretical constructs in late-life depression (Krishnan, 1991, 1993; Hickie et al. 1996, 1997b; Krishnan et al. 1997).

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Section: Identifying Genetically-determined Risk Factorsmentioning

confidence: 95%

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Hickie¹,

Scott²

1998

Psychol. Med.

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“…We feel this can answer the inconsistency in reproducing the manifestation of Al in Al-treated animal models. The methodology followed for the estimation of Al has also been a matter of 152 Veer Bala Gupta et al Aluminium and Alzheimer's disease Figure 5. Complexity of Al involvement, and various targets of its action in causing neuronal cell death.…”

Section: Al Speciation: a Fundamental Prerequisite For Understanding mentioning

confidence: 99%

“…Recent progress in genetic analysis has made it possible to identify three genes that cause familial AD, which are the genes for APP on chromosome 21 [146 , 147], presenilin 1 (PS-1) on chromosome 14 [148,149] and presenilin 2 (PS-2) on chromosome 1 [150,151]. In addition, the e4 allele of the ApoE gene present on chromosome 19 is found to be an important risk factor for senile [152,153] and presenile [154] AD. The genetic components account for only a part of AD cases [155], suggesting that interaction of environmental risk factors and genes could be a possible hallmark in the etiology of AD.…”

Section: Cross-talk Between Genetic Susceptibility and Al In Admentioning

confidence: 99%

Aluminium in Alzheimer?s disease: are we still at a crossroad?

Gupta

Anitha

Hegde

et al. 2005

CMLS, Cell. Mol. Life Sci.

275

143

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Aluminium, an environmentally abundant non-redox trivalent cation has long been implicated in the pathogenesis of Alzheimer's disease (AD). However, the definite mechanism of aluminium toxicity in AD is not known. Evidence suggests that trace metal homeostasis plays a crucial role in the normal functioning of the brain, and any disturbance in it can exacerbate events associated with AD. The present paper reviews the scientific literature linking aluminium with AD. The focus is on aluminium levels in brain, region-specific and subcellular distribution, its relation to neurofibrillary tangles, amyloid beta, and other metals. A detailed mechanism of the role of aluminium in oxidative stress and cell death is highlighted. The importance of complex speciation chemistry of aluminium in relation to biology has been emphasized. The debatable role of aluminium in AD and the cross-talk between aluminium and genetic susceptibility are also discussed. Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in AD cannot be discarded. However, whether aluminium is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood.

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“…Since the presence of the apolipoprotein E (apoE) Â4 allele was shown to be a genetic risk factor for late-onset AD [1][2][3][4][5][6][7][8], several areas of investigation have been directed toward possible biological roles of apoE in neurodegenerative processes and in neuronal repair [8][9][10][11][12][13][14][15][16]. However, the known association of apoE polymorphism with serum lipids and vascular abnormalities might also reflect a role for abnormal lipids in the development of AD.…”

Section: Introductionmentioning

confidence: 99%

Elevated Serum Total and LDL Cholesterol in Very Old Patients with Alzheimer’s Disease

Lesser

Kandiah

Libow

et al. 2001

Dement Geriatr Cogn Disord

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The relationships of serum lipids with Alzheimer’s disease (AD) and other dementias in very old patients are not clear. All residents of an academic nursing home were studied clinically for dementia and for serum lipids. All those autopsied over a 7.7-year period had apolipoprotein E (apoE) genotyping and detailed neuropathological examination. Those with pathologically defined criteria for AD (n = 84) were compared to all others who also had clinical dementia but did not show AD changes (n = 22). In contrast to most other reports of serum lipids in very old patients with AD, total cholesterol (TC) and low density lipoprotein cholesterol levels were each significantly higher for those with AD. The lipid-AD associations were progressively stronger with increasing pathological certainty of AD diagnosis. These relationships remained significant after adjustment for apoE genotype and for other known risk factors. The lipid-AD associations in a very old cohort, and prior evidence that elevated TC in middle life is a risk factor for later dementia, prompt consideration of factors associated with lipid metabolism in the development of Alzheimer’s dementia.

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Apo E allele frequencies in Alzheimerʼs disease, Lewy body dementia, Alzheimerʼs disease with cerebrovascular disease and vascular dementia

Cited by 68 publications

References 0 publications

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Late-onset depressive disorders: a preventable variant of cerebrovascular disease?

Aluminium in Alzheimer?s disease: are we still at a crossroad?

Elevated Serum Total and LDL Cholesterol in Very Old Patients with Alzheimer’s Disease

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