Marker Of Brain Atrophy Research Articles

Postural Instability Is Associated with Brain Atrophy and Cognitive Impairment in the Elderly: The J-SHIPP Study

Background/Aims: Mobility impairment in older adults has been suggested to be a marker of subclinical structural and functional brain abnormalities. We investigated a possible association between static postural instability and brain abnormalities and cognitive decline. Methods: The study subjects were 390 community residents without definitive dementia (67 ± 7 years old) and 21 patients with Alzheimer’s disease (AD). Brain atrophy was measured by MRI. Results: The mobility of the posturography-measured center of gravity (COG) was positively associated with the temporal horn area (THA; r = 0.260; p < 0.001). Subjects who could not stand on one leg for >40 s (n = 102) showed a significantly larger THA (22 ± 18 vs. 14 ± 11 × 10^–2 cm²; p < 0.001). Multiple regression analysis identified COG path length (β = 0.118; p = 0.032) and one-leg standing time (β = 0.176; p = 0.001) as independent determinants of THA. Mild cognitive impairment (MCI) subjects (n = 61) had a significantly enlarged THA compared to that of normal cognitive subjects (22 ± 16 vs. 16 ± 13 × 10^–2 cm²; p = 0.002). AD patients showed a more enlarged THA (78 ± 55 × 10^–2 cm²). Subjects with cognitive decline showed a significantly shorter one-leg standing time (normal: 50 ± 17 s; MCI: 42 ± 21 s; AD: 18 ± 20s; p < 0.001). Conclusion: Reduced postural stability was an independent marker of brain atrophy and pathological cognitive decline in the elderly.

Consumo de pescado y riesgo de anomalías cerebrales subclínicas detectadas mediante resonancia magnética en adultos de edad avanzada

To investigate the association between fish consumption and subclinical brain abnormalities. In the population-based cardiovascular health study, 3660 participants age > or = 65 underwent an MRI scan in 1992-1994. Five years later, 2313 were scanned. Neuroradiologists assessed MRI scans in a standardized and blinded manner. Food frequency questionnaires were used to assess dietary intakes. Participants with known cerebrovascular disease were excluded from the analyses. After adjustment for multiple risk factors, the risk for having one or more prevalent subclinical infarcts was lower among those consuming tuna/other fish > or 3 times/week, compared to < 1/month (relative risk 0.74, 95 % CI = 0.54-1.01, p = 0.06, p trend = 0.03). Tuna/other fish consumption was also associated with trends toward lower incidence of subclinical infarcts. Additionally, tuna/ other fish intake was associated with better white matter grade, but not with sulcal and ventricular grades, markers of brain atrophy. No significant association were found between fried fish consumption and any subclinical brain abnormalities. Among older adults, modest consumption of tuna/other fish, but not fried fish, was associated with lower prevalence of subclinical infarcts and white matter abnormalities on MRI examinations. Our results add to prior evidence that suggest that dietary intake of fish with higher eicosapentaenoic acid and docosahexaenoic acid content, and not fried fish intake, may have clinically important health benefits.

Association of White-Matter Lesions with Brain Atrophy Markers: The Three-City Dijon MRI Study

Background: Brain atrophy and white-matter lesions (WML) are common features at cerebral MRI of both normal and demented elderly people. In a population-based study of 1,792 elderly subjects aged 65–80 years, free of dementia, who had a cerebral MRI at entry, we investigated the relationship between WML volume and brain atrophy markers estimated by hippocampal, gray matter (GM) and cerebrospinal fluid (CSF) volumes. Methods: An automated algorithm of detection and quantification of WML was developed, and voxel-based morphometry methods were used to estimate GM, CSF and hippocampal volumes. To evaluate the relation between those volumes and WML load, we used analysis of covariance and multiple linear regression models adjusting for potential confounders and total intracranial volumes. Results: Age was highly correlated with WML load and all brain atrophy markers. Total WML volume was negatively associated with both GM (β = –0.03, p < 0.0001) and hippocampal volumes (β = –0.75, p = 0.0009) and positively with CSF volumes (β = 0.008, p = 0.02) after controlling for sex, age, education level, hypertension and apolipoprotein E genotype. Evidence for a relationship between brain atrophy markers and WML was stronger for periventricular WML. We found that the relationship between WML and hippocampal volumes was independent of other brain tissue volumes. Conclusion: These results suggest that, in the brain of nondemented elderly subjects, degenerative processes and vascular changes co-occur and are related independently of vascular risk factors.

Fish consumption and risk of subclinical brain abnormalities on MRI in older adults

To investigate the association between fish consumption and subclinical brain abnormalities. In the population-based Cardiovascular Health Study, 3,660 participants age > or =65 underwent an MRI scan in 1992-1994. Five years later, 2,313 were scanned. Neuroradiologists assessed MRI scans in a standardized and blinded manner. Food frequency questionnaires were used to assess dietary intakes. Participants with known cerebrovascular disease were excluded from the analyses. After adjustment for multiple risk factors, the risk of having one or more prevalent subclinical infarcts was lower among those consuming tuna/other fish > or =3 times/week, compared to <1/month (relative risk 0.74, 95% CI = 0.54-1.01, p = 0.06, p trend = 0.03). Tuna/other fish consumption was also associated with trends toward lower incidence of subclinical infarcts. Additionally, tuna/other fish intake was associated with better white matter grade, but not with sulcal and ventricular grades, markers of brain atrophy. No significant associations were found between fried fish consumption and any subclinical brain abnormalities. Among older adults, modest consumption of tuna/other fish, but not fried fish, was associated with lower prevalence of subclinical infarcts and white matter abnormalities on MRI examinations. Our results add to prior evidence that suggest that dietary intake of fish with higher eicosapentaenoic acid and docosahexaenoic acid content, and not fried fish intake, may have clinically important health benefits.

Validation of linear cerebral atrophy markers in multiple sclerosis

Linear measures of cerebral ventricular enlargement may act as surrogate measures of cerebral atrophy in multiple sclerosis (MS). Linear atrophy markers were measured from routine MRI scans during a population survey of 171 Tasmanian MS patients and 91 healthy controls. Thirty-five Victorian MS clinic patients were recruited as a validation cohort with 14 of these re-assessed 4 years later. In the population survey, we measured three linear brain atrophy markers: inter-caudate distance (ICD), third ventricle width (TVW) and frontal horn width (FHW). TVW (OR 2.0, p = 0.001) and ICD (OR 16.1, p < 0.001) differentiated between MS cases and controls. In the validation study, we correlated the intercaudate ratio (ICR = ICD/brain width) and third ventricular ratio (TVR = TVW/brain width) with brain parenchymal volume. Cross-sectionally, ICR ( R = −0.453, p < 0.01) and TVR ( R = −0.653, p < 0.01) were correlated with brain parenchymal volume. Longitudinally, brain parenchymal volume loss was inversely correlated with increased ICD ( R = −0.77, p < 0.01) and TVW ( R = −0.71, p < 0.01). This study shows that ICD measurements obtained from clinical MRI scans are valid brain atrophy measures for use in monitoring MS progression.

Bicaudate ratio as a magnetic resonance imaging marker of brain atrophy in multiple sclerosis.

Brain atrophy has emerged as a useful surrogate marker of disease involvement in multiple sclerosis (MS). The relationship between whole-brain or regional atrophy and cognitive dysfunction is poorly understood. To determine whether the bicaudate ratio (BCR)-the minimum intercaudate distance divided by brain width along the same line-is increased in MS and to compare the ability of the BCR, whole-brain atrophy, and other magnetic resonance imaging markers to predict cognitive dysfunction. Case-control study. University-affiliated clinic. Sixty patients with MS and 50 age- and sex-matched control subjects. Bicaudate ratio, whole-brain atrophy, T2 lesion load, T1 ("black hole") lesion load, and caudate volume were measured quantitatively using fluid-attenuated inversion recovery, T1-weighted, and gradient-echo magnetic resonance imaging scans. Symbol Digit Modalities Test was used to assess cognitive function. The BCR (mean [SD]) was higher in patients with MS (0.11 [0.03]) than in controls (0.09 [0.02]) (P<.001), suggesting subcortical atrophy in MS. The BCR was related to total T2 (r = 0.56, P<.001) and T1 (r = 0.40, P<.002) lesion volumes, but not caudate volume in patients with MS. Regression modeling selected BCR (P<.05), but not whole-brain atrophy, T1 or T2 lesion volume, or caudate volume as predictive of Symbol Digit Modalities Test score in patients with MS. The BCR is increased in MS and is more closely associated with cognitive dysfunction than are other magnetic resonance imaging surrogate markers including whole-brain atrophy. Increased BCR is best explained by frontal horn ventricular enlargement due to atrophy of deep frontal subcortical white matter. This highlights the close relationship between subcortical atrophy and cognitive impairment in patients with MS.

The correlation between ventricular diameter measured by transcranial sonography and clinical disability and cognitive dysfunction in patients with multiple sclerosis.

Magnetic resonance imaging (MRI) data suggest that the extent of brain atrophy in patients with multiple sclerosis (MS) is related to the severity of disease. To evaluate whether ventricular diameter determined by transcranial sonography (TCS) is a marker of brain atrophy and is correlated with disability, cognitive performance, and mood. We examined 74 subjects with MS and 74 age- and sex-matched control subjects with TCS and assessed the transverse diameter of the third ventricle and the frontal horns of the lateral ventricles. Quantitative neurological examination was performed in subjects with MS using the Expanded Disability Status Scale. All subjects with MS underwent MRI, the Brief Repeatable Battery of Neuropsychological Tests for MS, and standardized tests for mood disorders. Transcranial sonographic measurements of ventricular diameter closely matched MRI measurements (Spearman rank correlation, r=0.7-0.9; P<.01). The ventricular diameters were significantly larger in subjects with MS than in healthy age- and sex-matched control subjects. The measurement of the diameter of the third ventricle obtained by TCS or MRI and the measurement of disability obtained with the Expanded Disability Status Scale were significantly correlated (Spearman rank correlation, r = 0.4; P<.01). The correlation between the diameter of the frontal horns and disability was substantially lower for both neuroimaging techniques. In addition, TCS and MRI data correlated significantly with the majority of neuropsychological tests; no correlation was found between the diameter of the ventricles and depression scales. As ventricular diameter is related to the status of disability and may also indicate disease progression, we propose measurement of the diameter of the third ventricle with TCS as a quick and easy surrogate marker for serial follow-up examinations in patients with MS.

Are there any body fluid markers of brain atrophy in multiple sclerosis?

The weak correlation between inflammatory activity and disease progression in patients with multiple sclerosis has shifted the emphasis from inflammatory monitoring to the investigation of the pathological processes of demyelination, axonal loss, and gliosis. New magnetic resonance imaging (MRI) techniques that have been developed to measure these processes appear very promising. This paper will briefly discuss potential body fluid markers of axonal loss, gliosis and demyelination, as the pathological substrates of brain atrophy, their function and the principles behind their future study in patients with multiple sclerosis.

Age-related brain atrophy enhanced by smoking: a quantitative study with computed tomography.

We examined the chronic effect of smoking on brain atrophy quantitatively with computed tomography (CT). Study was performed on 159 smokers and 194 non-smokers from 40 to 69 years old with neither neurological nor focal abnormality in brain CT. Brain atrophy index (BAI) which was a quantitative marker of brain atrophy reported previously, was calculated from each pixel of brain CT. There was a significant age dependent increase of BAI in both non-smokers and smokers. Smokers showed a significant increase in BAI (atrophic) compared to non-smokers in three age groups, 50-54, 55-59 (p less than 0.01, both) and 65-69 (p less than 0.05). In the male, the mean BAI became high when the smoking index increased (p less than 0.01). The systolic blood pressure and serum triglycerides of smokers were significantly higher than the non-smokers (p less than 0.05 and p less than 0.01). It was suggested that age-related brain atrophy was increased by chronic smoking through advanced atherosclerosis.