Age-related total gray matter and white matter changes in normal adult brain. Part I: volumetric MR imaging analysis. Am. J
A technique of segmenting total gray matter (GM) and total white matter (WM) in human brain is now available. We investigated the effects of age and sex on total fractional GM (%GM) and total fractional WM (%WM) volumes by using volumetric MR imaging in healthy adults.
Fifty-four healthy volunteers (22 men, 32 women) aged 20-86 years underwent dual-echo fast spin-echo MR imaging. Total GM, total WM, and intracranial space volumes were segmented by using MR image-based computerized semiautomated software. Volumes were normalized as a percentage of intracranial volume (%GM and %WM) to adjust for variations in head size. Age and sex effects were then assessed.
Both %GM and %WM in the intracranial space were significantly less in older subjects (> or =50 years) than in younger subjects (<50 years) (P <.0001 and P =.02, respectively). Consistently, %GM decreased linearly with age, beginning in the youngest subjects. %WM decreased in a quadratic fashion, with a greater rate beginning only in adult midlife. Although larger GM volumes were observed in men before adjustments for cranium size, no significant differences in %GM or %WM were observed between the sexes.
GM volume loss appears to be a constant, linear function of age throughout adult life, whereas WM volume loss seems to be delayed until middle adult life. Both appear to be independent of sex. Quantitative analysis of %GM and %WM volumes can improve our understanding of brain atrophy due to normal aging; this knowledge may be valuable in distinguishing atrophy of disease patterns from characteristics of the normal aging process.
Available from: Zsigmond Tamás Kincses
- "Two studies using voxel-based techniques that reported no overall significant effect of aging on WM volume did reveal a decline with age in some areas (Good et al. 2001; Taki et al. 2004). The combined effects of age and gender on the human brain have been assessed suggesting a more profound decline in GM volume in males (Ge et al. 2002a; Raz et al. 1997; Taki et al. 2004). However, research evidence is inconsistent on one hand (Lemaitre et al. 2005) and sparse on the other, especially considering the subcortical GM structures. "
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ABSTRACT: Effects of gender on grey matter (GM) volume differences in subcortical structures of the human brain have consistently been reported. Recent research evidence suggests that both gender and brain size influences volume distribution in subcortical areas independently. The goal of this study was to determine the effects of the interplay between brain size, gender and age contributing to volume differences of subcortical GM in the human brain. High-resolution T1-weighted images were acquired from 53 healthy males and 50 age-matched healthy females. Total GM volume was determined using voxel-based morphometry. We used model-based subcortical segmentation analysis to measure the volume of subcortical nuclei. Main effects of gender, brain volume and aging on subcortical structures were examined using multivariate analysis of variance. No significant difference was found in total brain volume between the two genders after correcting for total intracranial volume. Our analysis revealed significantly larger hippocampus volume for females. Additionally, GM volumes of the caudate nucleus, putamen and thalamus displayed a significant age-related decrease in males as compared to females. In contrast to this only the thalamic volume loss proved significant for females. Strikingly, GM volume decreases faster in males than in females emphasizing the interplay between aging and gender on subcortical structures. These findings might have important implications for the interpretation of the effects of unalterable factors (i.e. gender and age) in cross-sectional structural MRI studies. Furthermore, the volume distribution and changes of subcortical structures have been consistently related to several neuropsychiatric disorders (e.g. Parkinson's disease, attention deficit hyperactivity disorder, etc.). Understanding these changes might yield further insight in the course and prognosis of these disorders.
Brain Imaging and Behavior 11/2015; DOI:10.1007/s11682-015-9468-3 · 4.60 Impact Factor
- "We tested for a positive correlation between euphoric experience and OFC volume in each of the three OFC ROIs across both cerebral hemispheres (adjusted a = 0.0083; i.e., P = 0.05/6 comparisons, 3 ROIs 9 2 hemispheres). Using Pearson's partial correlations, we controlled for the effects of age, gender, handedness, scanner, state anxiety, sensation seeking, and intracranial volume (Ge et al. 2002; Tisserand et al. 2004; Welborn et al. 2009; Carlson et al. 2015). Given that mOFC processing of threat versus safety cues (Greenberg et al. 2013a, b) has been linked to structural variability across a broader circuit (Cha et al. 2014), we performed a stepwise linear regression (P \ 0.05 to enter and P [ 0.10 for removal) analysis to test (1) the degree to which the correlation between the mOFC and euphoria holds when additional brain regions are considered and if so, (2) whether additional variance can be explained by adding other components of the circuit. "
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ABSTRACT: The medial orbitofrontal cortex has been linked to the experience of positive affect. Greater medial orbitofrontal cortex volume is associated with greater expression of positive affect and reduced medial orbital frontal cortex volume is associated with blunted positive affect. However, little is known about the experience of euphoria, or extreme joy, and how this state may relate to variability in medial orbitofrontal cortex structure. To test the hypothesis that variability in euphoric experience correlates with the volume of the medial orbitofrontal cortex, we measured individuals' (N = 31) level of self-reported euphoria in response to a highly anticipated first time skydive and measured orbitofrontal cortical volumes with structural magnetic resonance imaging. Skydiving elicited a large increase in self-reported euphoria. Participants' euphoric experience was predicted by the volume of their left medial orbitofrontal cortex such that, the greater the volume, the greater the euphoria. Further analyses indicated that the left medial orbitofrontal cortex and amygdalo-hippocampal complex independently explain variability in euphoric experience and that medial orbitofrontal cortex volume, in conjunction with other structures within the mOFC-centered corticolimbic circuit, can be used to predict individuals' euphoric experience.
Brain Structure and Function 11/2015; DOI:10.1007/s00429-015-1139-z · 5.62 Impact Factor
Available from: Jaime L Eugenin
- "A key hallmark is the progressive decline in physiological functions and behavioral capacity, which is observed at various levels of the organism, in particular at the central nervous system (CNS; Smith et al., 2005). These changes can lead to altered behavior, memory impairment, or loss of several control functions (Lipsitz and Goldberger, 1992; Lipsitz, 2002; Glenn et al., 2004). In addition, some responses of the immune system, in special "
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ABSTRACT: Aging is the main risk factor for neurodegenerative diseases. In aging, microglia undergo phenotypic changes compatible with their activation. Glial activation can lead to neuroinflammation, which is increasingly accepted as part of the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD). We hypothesize that in aging, aberrant microglia activation leads to a deleterious environment and neurodegeneration. In aged mice, microglia exhibit an increased expression of cytokines and an exacerbated inflammatory response to pathological changes. Whereas LPS increases nitric oxide secretion in microglia from young mice, induction of reactive oxygen species (ROS) predominates in older mice. Furthermore, there is accumulation of DNA oxidative damage in mitochondria of microglia during aging, and also an increased intracellular ROS production. Increased ROS activates the redox-sensitive nuclear factor kappa B, which promotes more neuroinflammation, and can be translated in functional deficits, such as cognitive impairment. Mitochondria-derived ROS and cathepsin B, are also necessary for the microglial cell production of interleukin-1β, a key inflammatory cytokine. Interestingly, whereas the regulatory cytokine TGFβ1 is also increased in the aged brain, neuroinflammation persists. Assessing this apparent contradiction, we have reported that TGFβ1 induction and activation of Smad3 signaling after inflammatory stimulation are reduced in adult mice. Other protective functions, such as phagocytosis, although observed in aged animals, become not inducible by inflammatory stimuli and TGFβ1. Here, we discuss data suggesting that mitochondrial and endolysosomal dysfunction could at least partially mediate age-associated microglial cell changes, and, together with the impairment of the TGFβ1-Smad3 pathway, could result in a reduction of protective activation and a facilitation of cytotoxic activation of microglia, resulting in the promotion of neurodegeneration.
Frontiers in Aging Neuroscience 08/2015; 7:124. DOI:10.3389/fnagi.2015.00124 · 4.00 Impact Factor
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