βA4 deposits are constant in the brain of the oldest old: An immunocytochemical study of 20 french centenarians

Delaère, P.; He, Yi; Fayet, Guy; Duyckaerts, Charles; Hauw, J. J.

doi:10.1016/0197-4580(93)90096-t

Cited by 133 publications

(58 citation statements)

References 32 publications

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“…Depending on age and genetic status, 20%-40% of older adults may exhibit amyloid burden at death despite antemortem normal cognition (2,3). However, amyloid plaque accumulation continues with increasing age and may be present in up to 100% of the oldest old (ie centenarians) (4,5). The preclinical phase of the AD continuum represents a critical opportunity for therapeutic intervention; however, robust methods to detect AD-related pathophysiological changes during life must first be established.…”

Section: Introductionmentioning

confidence: 99%

Late-Life Vascular Risk Factors and Alzheimer Disease Neuropathology in Individuals with Normal Cognition

Besser

Alosco

Gómez

et al. 2016

J Neuropathol Exp Neurol

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Vascular risk factors (VRFs) have been associated with clinically diagnosed Alzheimer disease (AD), but few studies have examined the association between VRF and AD neuropathology (ADNP) in cognitively normal individuals. We used longitudinal data from the National Alzheimer's Disease Center's Uniform Data Set and Neuropathology Data Set to examine the association between VRF and ADNP (moderate to frequent neuritic plaques; Braak stage III-VI) in those with normal cognition. Our sample included 53 participants with ADNP and 140 without ADNP. Body mass index (BMI), resting heart rate (HR), and pulse pressure (PP) were measured at each visit; values were averaged across participant visits and examined annual change in BMI, PP, and HR. Hypertension, diabetes, and hypercholesterolemia were self-reported. In the multivariable logistic regression analyses, average BMI and HR were associated with lower odds of ADNP, and annual increases in HR and BMI were associated with higher odds of ADNP. A previously experienced decline in BMI or HR in late-life (therefore, currently low BMI and low HR) as well as a late-life increase in BMI and HR may indicate underlying AD pathology. Additional clinicopathological research is needed to elucidate the role of changes in late-life VRF and AD pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Late-Life Vascular Risk Factors and Alzheimer Disease Neuropathology in Individuals with Normal Cognition

Besser

Alosco

Gómez

et al. 2016

J Neuropathol Exp Neurol

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“…The pattern of clustering of Ab deposits was also similar in control and AD cases, i.e., in cortical gyri, deposits were aggregated into clusters regularly distributed parallel to the pia mater, suggesting a similar pathogenesis [9]. In a further study of centenarians [56], Ab deposits were recorded in the parahippocampal gyrus (PHG) of patients, whether demented or not, but the hippocampus was unaffected, suggesting a little relationship between lesion density and severity of mental deficits.…”

Section: Theories Based On Agingmentioning

confidence: 86%

Review article What causes alzheimer’s disease?

Armstrong¹

2013

158

119

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A b s t r a c t Since the earliest descriptions of Alzheimer's disease (AD), many theories have been advanced as to its cause. These include: (1) exacerbation of aging, (2) degeneration of anatomical pathways, including the cholinergic and cortico-cortical pathways, (3) an environmental factor such as exposure to aluminium, head injury, or malnutrition, (4) genetic factors including mutations of amyloid precursor protein (APP) and presenilin (PSEN) genes and allelic variation in apolipoprotein E (Apo E), (5) mitochondrial dysfunction, (6) a compromised blood brain barrier, (7) immune system dysfunction, and (8) infectious agents. This review discusses the evidence for and against each of these theories and concludes that AD is a multifactorial disorder in which genetic and environmental risk factors interact to increase the rate of normal aging ('allostatic load'). The consequent degeneration of neurons and blood vessels results in the formation of abnormally aggregated 'reactive' proteins such as b-amyloid (Ab) and tau. Gene mutations influence the outcome of age-related neuronal degeneration to cause early onset familial AD (EO-FAD

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“…The major molecular constituent of the SP is Aβ [53] and hence, Aβ deposition in the form of diffuse ('pre-amyloid'), primitive, and classic ('dense-cored') deposits is often regarded as a 'signature' pathological feature of AD [36,53]. Nevertheless, studies of Aβ deposition have also demonstrated overlaps between AD and normal brain [37,94]. In addition, there are overlaps reported between the various entities which comprise FTD [16], and within and between the disorders comprising the tauopathies and synucleinopathies [16].…”

Section: Overlap Modelmentioning

confidence: 99%

On the ‘classification’ of neurodegenerative disorders: discrete entities, overlap or continuum?

Armstrong¹

2012

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A b s t r a c t ('overlap' model) , and (3) that distinct diseases do not exist and neurodegenerative disease is a 'continuum' in which there is continuous variation in clinical/pathological features from one case to another ('continuum' model). Third, to distinguish between models, the distribution of the most important molecular 'signature' lesions across the different diseases is reviewed. Such lesions often have poor

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βA4 deposits are constant in the brain of the oldest old: An immunocytochemical study of 20 french centenarians

Cited by 133 publications

References 32 publications

Late-Life Vascular Risk Factors and Alzheimer Disease Neuropathology in Individuals with Normal Cognition

Late-Life Vascular Risk Factors and Alzheimer Disease Neuropathology in Individuals with Normal Cognition

Review article What causes alzheimer’s disease?

On the ‘classification’ of neurodegenerative disorders: discrete entities, overlap or continuum?

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