Regional cerebral blood flow in down's syndrome

Melamed, Eldad; Mildworf, Bracha; Sharav, Tereza; Belenky, Lev; Wertman, Eliahu

doi:10.1002/ana.410220215

Cited by 10 publications

(1 citation statement)

References 16 publications

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“…Schwartz et al (1983) and Cutler (1986) reported higher than normal cerebral GMR in a small number of young DS individuals, but Schapiro et al (1990) failed to find any GMR differences between DS and a control sample. Melamed, Mildworf, Sharav, Belenky, and Wertman (1987) reported a decrease in cerebral blood flow in DS. Both the Schapiro et al and the Melamed et al studies, however, were conducted with subjects at rest, a condition not likely to accentuate any functional differences.…”

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Brain size and cerebral glucose metabolic rate in nonspecific mental retardation and down syndrome

et al. 1995

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Brain size and cerebral glucose metabolic rate (GMR) were determined with magnetic resonance imaging (MRI) and positron emission tomography (PET) in individuals with mild mental retardation (MR), individuals with Down syndrome (DS) without dementia and in matched controls. The MRI data showed that the MR and the DS groups both had brain volumes of about 80% of controls; variance was greatest within the MR group. PET was obtained with [ 18F]-fluorodeoxyglucose (FDG) as the tracer during a test of attention (Continuous Performance Test; CPT). Whole brain cortex GMR was higher than the controls in both the MR and the DS groups. For all subjects combined, the correlation between brain size and IQ was .65 @ < ,005). Brain imaging with magnetic resonance imaging (MRI) and positron emission tomography (PET) provides an opportunity to characterize brain abnormalities in viva. Structural analyses in severe mental retardation (MR) often reveal brain damage of varying degrees (

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Brain size and cerebral glucose metabolic rate in nonspecific mental retardation and down syndrome

et al. 1995

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A unifying hypothesis of Alzheimer's disease. III. Risk factors

Heininger

2000

Hum. Psychopharmacol. Clin. Exp.

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Normal ageing and Alzheimer's disease (AD) have many features in common and, in many respects, both conditions only differ by quantitative criteria. A variety of genetic, medical and environmental factors modulate the ageing-related processes leading the brain into the devastation of AD. In accordance with the concept that AD is a metabolic disease, these risk factors deteriorate the homeostasis of the Ca(2+)-energy-redox triangle and disrupt the cerebral reserve capacity under metabolic stress. The major genetic risk factors (APP and presenilin mutations, Down's syndrome, apolipoprotein E4) are associated with a compromise of the homeostatic triangle. The pathophysiological processes leading to this vulnerability remain elusive at present, while mitochondrial mutations can be plausibly integrated into the metabolic scenario. The metabolic leitmotif is particularly evident with medical risk factors which are associated with an impaired cerebral perfusion, such as cerebrovascular diseases including stroke, cardiovascular diseases, hypo- and hypertension. Traumatic brain injury represents another example due to the persistent metabolic stress following the acute event. Thyroid diseases have detrimental sequela for cerebral metabolism as well. Furthermore, major depression and presumably chronic stress endanger susceptible brain areas mediated by a host of hormonal imbalances, particularly the HPA-axis dysregulation. Sociocultural and lifestyle factors like education, physical activity, diet and smoking may also modulate the individual risk affecting both reserve capacity and vulnerability. The pathophysiological relevance of trace metals, including aluminum and iron, is highly controversial; at any rate, they may adversely affect cellular defences, antioxidant competence in particular. The relative contribution of these factors, however, is as individual as the pattern of the factors. In familial AD, the genetic factors clearly drive the sequence of events. A strong interaction of fat metabolism and apoE polymorphism is suggested by intercultural epidemiological findings. In cultures, less plagued by the 'blessings' of the 'cafeteria diet-sedentary' Western lifestyle, apoE4 appears to be not a risk factor for AD. This intriguing evidence suggests that, analogous to cardiovascular diseases, apoE4 requires a hyperlipidaemic lifestyle to manifest as AD risk factor. Overall, the etiology of AD is a key paradigm for a gene-environment interaction. Copyright 2000 John Wiley & Sons, Ltd.

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