12 research outputs found
Morphological and Pathological Evolution of the Brain Microcirculation in Aging and Alzheimer’s Disease
Key pathological hallmarks of Alzheimer’s disease (AD), including amyloid plaques, cerebral amyloid angiopathy (CAA) and neurofibrillary tangles do not completely account for cognitive impairment, therefore other factors such as cardiovascular and cerebrovascular pathologies, may contribute to AD. In order to elucidate the microvascular changes that contribute to aging and disease, direct neuropathological staining and immunohistochemistry, were used to quantify the structural integrity of the microvasculature and its innervation in three oldest-old cohorts: 1) nonagenarians with AD and a high amyloid plaque load; 2) nonagenarians with no dementia and a high amyloid plaque load; 3) nonagenarians without dementia or amyloid plaques. In addition, a non-demented (ND) group (average age 71 years) with no amyloid plaques was included for comparison. While gray matter thickness and overall brain mass were reduced in AD compared to ND control groups, overall capillary density was not different. However, degenerated string capillaries were elevated in AD, potentially suggesting greater microvascular “dysfunction” compared to ND groups. Intriguingly, apolipoprotein ε4 carriers had significantly higher string vessel counts relative to non-ε4 carriers. Taken together, these data suggest a concomitant loss of functional capillaries and brain volume in AD subjects. We also demonstrated a trend of decreasing vesicular acetylcholine transporter staining, a marker of cortical cholinergic afferents that contribute to arteriolar vasoregulation, in AD compared to ND control groups, suggesting impaired control of vasodilation in AD subjects. In addition, tyrosine hydroxylase, a marker of noradrenergic vascular innervation, was reduced which may also contribute to a loss of control of vasoconstriction. The data highlight the importance of the brain microcirculation in the pathogenesis and evolution of AD
Direct susceptibility testing by disk diffusion on clinical samples: a rapid and accurate tool for antibiotic stewardship
Subcortical ischaemic changes in young hypertensive patients: frequency, effect on cognitive performance and relationship with markers of endothelial and haemostatic activation
Rapid detection of tetracycline resistance in bovine Pasteurella multocida isolates by MALDI Biotyper antibiotic susceptibility test rapid assay (MBT-ASTRA)
An infectious disease and pharmacokinetic perspective on oral antibiotic treatment of uncomplicated urinary tract infections due to multidrug-resistant Gram-negative uropathogens: the importance of urinary antibiotic concentrations and urinary pH
The effect of egg versus seston quality on hatching success, naupliar metabolism and survival of Calanus finmarchicus in mesocosms dominated by Phaeocystis and diatoms
We studied the effect of a developing Skeletonema marinoi/Phaeocystis spp. bloom on Calanus finmarchicus hatching success, early naupliar survival and metabolism. Our focus was (1) on the development of reproductive rates during a bloom initiation, peak and decline in relation to the production of potentially toxic algal metabolites and (2) on the proportional importance of female nutrition versus naupliar food environment for the production of viable nauplii. Despite polyunsaturated aldehyde (PUA) production by both S. marinoi and Phaeocystis sp., we did not observe any harmful effects on hatching success or naupliar survival and condition in any stages of the short-term (<1 week) algal bloom. Hatching success appeared to be controlled by egg lipid composition, while the beneficial effect of a high food concentration was reflected in naupliar RNA: DNA ratio, protein content and total production of viable nauplii. The egg lipids reflected seston lipids, indicating that the egg fatty acid composition was not modified by the females. Our results suggest that unselective feeding and/or retention of specific lipids can induce qualitative food limitation, although recruitment during the S. marinoi/Phaeocystis sp. bloom was high
Temperature and food quantity effects on the harpacticoid copepod Nitocra spinipes: Combining in vivo bioassays with population modeling
Structural Imaging Measures of Brain Aging
During the course of normal aging, biological changes occur in the brain that are associated with changes in cognitive ability. This review presents data from neuroimaging studies of primarily “normal” or healthy brain aging. As such, we focus on research in unimpaired or nondemented older adults, but also include findings from lifespan studies that include younger and middle aged individuals as well as from populations with prodromal or clinically symptomatic disease such as cerebrovascular or Alzheimer’s disease. This review predominantly addresses structural MRI biomarkers, such as volumetric or thickness measures from anatomical images, and measures of white matter injury and integrity respectively from FLAIR or DTI, and includes complementary data from PET and cognitive or clinical testing as appropriate. The findings reveal highly consistent age-related differences in brain structure, particularly frontal lobe and medial temporal regions that are also accompanied by age-related differences in frontal and medial temporal lobe mediated cognitive abilities. Newer findings also suggest that degeneration of specific white matter tracts such as those passing through the genu and splenium of the corpus callosum may also be related to age-related differences in cognitive performance. Interpretation of these findings, however, must be tempered by the fact that comorbid diseases such as cerebrovascular and Alzheimer’s disease also increase in prevalence with advancing age. As such, this review discusses challenges related to interpretation of current theories of cognitive aging in light of the common occurrence of these later-life diseases. Understanding the differences between “Normal” and “Healthy” brain aging and identifying potential modifiable risk factors for brain aging is critical to inform potential treatments to stall or reverse the effects of brain aging and possibly extend cognitive health for our aging society