Childhood mental ability and dementia

Whalley, Lawrence J.; Starr, John M.; Athawes, R. W. B.; Hunter, David; Pattie, Alison; Deary, Ian J.

doi:10.1212/wnl.55.10.1455

Cited by 237 publications

(194 citation statements)

References 34 publications

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“…No such association has been detected for early onset dementia, but lower IQ at age 11 has been associated with increased risk of late-onset dementia. 15 However, this study comprised only 50 late-onset cases, so was inadequately powered to determine effects of childhood IQ on AD and VaD separately. The Nun Study also found an association between linguistic ability at about 22 years of age and late-onset dementia, but this was based on just 39 neuropathology cases, only 59% of whom fulfilled clinical diagnostic criteria for dementia.…”

Section: Discussionmentioning

confidence: 99%

Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia

McGurn¹,

Deary²,

Starr³

2008

Neurology

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112

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Section: Discussionmentioning

confidence: 99%

Childhood cognitive ability and risk of late-onset Alzheimer and vascular dementia

McGurn¹,

Deary²,

Starr³

2008

Neurology

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112

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“…Braak and Braak (1999) showed that AD-related pathology can be seen as early as in the third decade of life. However, AD pathology is unlikely to be a major factor in 11-year-olds (Whalley et al, 2000).Another possibility is that these findings reflect the consequences of early life environment, which has been linked to the later development of such chronic adult diseases as heart disease and diabetes (Osmond & Barker, 2000). Nutrient limitation in utero and infancy leads to changes of structure and metabolism that are the origin of hypertension and diabetes in adulthood.…”

mentioning

confidence: 93%

The apolipoprotein E gene, attention, and brain function.

Parasuraman¹,

Greenwood²,

Sunderland³

2002

Neuropsychology

109

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The ɛ4 allele of the apolipoprotein E (ApoE) gene is associated with alterations in brain function and is a risk factor for Alzheimer's disease (AD). Changes in components of visuospatial attention with ApoE-ɛ4, aging, and AD are described. Healthy middle-aged adults without dementia who have the ApoE-ɛ4 gene show deficits in spatial attention and working memory that are qualitatively similar to those seen in clinically diagnosed AD patients. The findings support an association between ApoE polymorphism and specific components of visuospatial attention. Molecular mechanisms that may mediate the ApoE-attention link by modulating cholinergic neurotransmission to the posterior parietal cortex are discussed. Studies of attention and brain function in ApoE-ɛ4 carriers without dementia can advance knowledge of the genetics of visual attention, may enhance understanding of the preclinical phase of AD, and may lead to better methods for early AD detection.Apolipoprotein E (ApoE) is an amino acid glycoprotein that is important in lipid storage, transport, and metabolism (Mahley, 1988). Although synthesized mainly in the liver, ApoE is also found in the peripheral and central nervous systems, including the brain. ApoE has long been of interest in medicine, but its importance in neuroscience increased dramatically with the identification of the ɛ4 allele of the ApoE gene on chromosome 19 as a major risk factor for the development of late-onset Alzheimer's disease (AD) in older adults Strittmatter et al., 1993). This discovery led to a growing number of studies examining the role of the ApoE gene in normal brain function and cognition, as well as in disorders such as AD, brain injury, and stroke (Higgins, Large, Rupniak, & Barnes, 1997;Horsburgh, McCarron, White, & Nicol, 2000; J. D. Smith, 2000).Polymorphisms of the ApoE gene are associated with significant alterations in brain morphology (Plassman et al., 1997) and cognitive functioning, including attention (Greenwood, Sunderland, Friz, & Parasuraman, 2000) and memory (Bondi et al., 1995). Studies of ApoE may thus reveal information relevant to the genetics of attention and memory in normal individuals. At the same time, such studies may identify cognitive and neural changes that may be characteristic of preclinical stages of AD. In this article, we review the role of the ApoE gene in normal cognition and in the development of deficits indicative of early AD.Currently, no reliable methods exist for the early detection and treatment of AD. New techniques for preventing, slowing the progression of, and treating AD are being urgently sought. Such efforts would be aided considerably if AD could be detected prior to the clinical diagnosis of AD and before irreversible brain changes occur (Daffner & Scinto, 2000). Postmortem studies show that neuropathological changes occur decades before the onset of NIH Public Access Author ManuscriptNeuropsychology. Author manuscript; available in PMC 2006 January 25. Published in final edited form as:Neuropsychology. 2002 April ; ...

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“…The participants have been followed up for mortality and cancer since inception, and have recently been linked with the Scottish Morbidity Records (SMR) system, enabling data on physical and mental illness to be investigated. 16 , related to lifetime psychiatric contact 17 , and a risk factor for mortality 18 and for senile but not pre-senile dementia in later life 19 .…”

Section: Introductionmentioning

confidence: 99%