Research articleIncreased density of senile plaques (SP), but not neurofibrillary tangles (NFT), in non-demented individuals with the apolipoprotein E4 allele: comparison to confirmed Alzheimer's disease patients
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Cited by (42)
Development of new treatments for Alzheimer's disease based on the modulation of translocator protein (TSPO)
2019, Ageing Research ReviewsCitation Excerpt :Several studies have shown that changes in cholesterol levels and turnover may be involved in the development of AD. One key protein involved in cholesterol homeostasis is apolipoprotein E (apoE), which is also able to regulate Aβ aggregation and clearance in the brain (Sparks et al., 1996). The apoE gene presents three major alleles in humans: apoE ε2, apoE ε3, apoE ε4.
Episodic memory in normal aging and Alzheimer disease: Insights from imaging and behavioral studies
2015, Ageing Research ReviewsCitation Excerpt :However, ϵ4-carrier status is associated with greater longitudinal declines in memory performance, which become evident by the sixth decade of life (Caselli et al., 2009). A recent study by Kantarci et al. (2012) showed for the first time that the ApoE genotype modifies the association between cognition and the Aβ load, which is measured with PIB-Pittsburgh compound B and constitutes the senile plaques in cognitively normal older adults (see also Sparks et al., 1996). While PIB retention was modestly associated with cognitive function even after the data were adjusted for age, sex, and education, the presence of the ApoE ϵ4 allele significantly increased the Aβ load and influenced the relationship between the Aβ load and cognitive function, increasing the risk of cognitive decline in healthy individuals.
Epidemiology and clinical diagnosis: Alzheimer disease
2013, PET ClinicsCitation Excerpt :Unfortunately, despite evidence of some success at lessening brain amyloid with vaccine strategies, clinical success has eluded all approaches.6 These therapeutic disappointments, together with findings that EOAD and LOAD can have differences in their clinical presentations and rates of progression, that mutations in the tau gene (MAPT) can also produce dementia, and that abnormal tau regional brain distribution does not parallel amyloid deposition but has a stronger association with degree of cognitive impairment,7 have led to a questioning of the underlying assumption of the amyloid cascade hypothesis for LOAD; that is, that LOAD shares the same fundamental cause as autosomal dominant forms of EOAD. Two very different paradigms have been proposed to fill the perceived void.
Blood pressure is associated with higher brain amyloid burden and lower glucose metabolism in healthy late middle-age persons
2012, Neurobiology of AgingCitation Excerpt :Findings from FDG PET studies suggest that even those with medically-controlled hypertension have reduced cerebral glucose metabolism in brain regions related to AD and aging (Beason-Held et al., 2007; Salerno et al., 1995). Autopsy studies have reported that elevated BP is associated with the hallmark neuropathological markers of AD, including increased neurofibrillary tangles, amyloid plaques, and brain atrophy compared with age-matched normotensive individuals (Petrovitch et al., 2000; Sparks et al., 1995, 1996). The pathophysiological mechanism by which elevated BP or increased arterial stiffness influences the development of AD has not been elucidated.
The enigma of mixed dementia
2007, Alzheimer's and DementiaCitation Excerpt :The occurrence of cerebral infarcts in AD increases significantly with age but has little influence on the clinical features in progressed stages of AD and can hardly be predicted from common vascular risk factors. However, persons with hypertension have increased NFTs and brain atrophy at autopsy [122,123], and CVD or atherosclerosis is strongly associated with the presence of plaques [121]. Therefore, prevention of CVD may be critically important in preventing late-life cognitive function [33].
Midlife blood pressure and neuritic plaques, neurofibrillary tangles, and brain weight at death: the HAAS
2000, Neurobiology of Aging