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To perform brain asymmetry studies in large neuroimaging archives, reliable and automatic detection of the interhemispheric fissure (IF) is needed to first extract the cerebral hemispheres. The detection of the IF is often referred to as mid-sagittal plane estimation, as this plane separates the two cerebral hemispheres. However, traditional planar estimation techniques fail when the IF presents a curvature caused by existing pathology or a natural phenomenon known as brain torque. As a result, midline estimates can be inaccurate. In this study, a fully unsupervised midline estimation technique is proposed that is comprised of three main stages head angle correction, control point estimation and midline generation. The control points are estimated using a combination of intensity, texture, gradient, and symmetry-based features. As shown, the proposed method automatically adapts to IF curvature, is applied on a slice-to-slice basis for more accurate results and also provides accurate delineation of the midlinent differences in biomarker means were found across SCI and MCI and SCI and AD.Background Older adults with hypertension often had diminished walking performance. The underlying mechanism through which hypertension affects walking performance, however, has not been fully understood. We here measured the complexity of the continuous systolic (SBP) and diastolic (DBP) blood pressure fluctuation, grade of white matter lesions (WMLs), and cognitive function and used structural equation modeling (SEM) to examine the interrelationships between hypertension, BP complexity, WMLs, cognitive function, and walking speed in single- and dual-task conditions. Methods A total of 152 older adults with age > 60 years (90 hypertensive and 62 normotensive participants) completed one MRI scan of brain structure, a finger BP assessment of at least 10 min, Mini-Mental State Examination (MMSE) to assess cognitive function, and 10-meter walking tests in single (i.e., normal walking) and dual tasks (i.e., walking while performing a serial subtraction of three from a random three-digit number). The grade of WMLslking speed in hypertensive and normotensive older adults, revealing a potential mechanism that hypertension may affect walking performance in older adults through diminished BP complexity, increased WML grade, and decreased cognitive function, and BP complexity is an important factor for such effects. selleck chemical Future longitudinal studies are warranted to confirm the findings in this study.Alzheimer disease (AD) is an aging-related disorder linked to endoplasmic reticulum (ER) stress. The main pathologic feature of AD is the presence of extracellular senile plaques and intraneuronal neurofibrillary tangles (NFTs) in the brain. In neurodegenerative diseases, the unfolded protein response (UPR) induced by ER stress ensures cell survival. Mesencephalic astrocyte-derived neurotrophic factor (MANF) protects against ER stress and has been implicated in the pathogenesis of AD. MANF is expressed in neurons of the brain and spinal cord. However, there have been no investigations on MANF expression in the brain of AD patients. This was addressed in the present study by immunohistochemistry, western blotting, and quantitative analyses of postmortem brain specimens. We examined the localization and expression levels of MANF in the inferior temporal gyrus of the cortex (ITGC) in AD patients (n = 5), preclinical (pre-)AD patients (n = 5), and age-matched non-dementia controls (n = 5) by double immunofluorescence labeling with antibodies against the neuron-specific nuclear protein neuronal nuclei (NeuN), ER chaperone protein 78-kDa glucose-regulated protein (GRP78), and MANF. The results showed that MANF was mainly expressed in neurons of the ITGC in all 3 groups; However, the number of MANF-positive neurons was significantly higher in pre-AD (Braak stage III/IV) and AD (Braak stage V/VI) patients than that in the control group. Thus, MANF is overexpressed in AD and pre-AD, suggesting that it can serve as a diagnostic marker for early stage disease.There is a growing evidence describing a decline in adaptive homeostasis in aging-related diseases affecting the central nervous system (CNS), many of which are characterized by the appearance of non-native protein aggregates. One signaling pathway that allows cell adaptation is the integrated stress response (ISR), which senses stress stimuli through four kinases. ISR activation promotes translational arrest through the phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2α) and the induction of a gene expression program to restore cellular homeostasis. However, depending on the stimulus, ISR can also induce cell death. One of the ISR sensors is the double-stranded RNA-dependent protein kinase [protein kinase R (PKR)], initially described as a viral infection sensor, and now a growing evidence supports a role for PKR on CNS physiology. PKR has been largely involved in the Alzheimer’s disease (AD) pathological process. Here, we reviewed the antecedents supporting the role of PKR on the efficiency of synaptic transmission and cognition. Then, we review PKR’s contribution to AD and discuss the possible participation of PKR as a player in the neurodegenerative process involved in aging-related pathologies affecting the CNS.Delirium is an acute neuropsychiatric syndrome and one of the most common presenting symptoms of acute medical illnesses in older people. Delirium can be triggered by a single cause, but in most cases, it is multifactorial as it depends on the interaction between predisposing and precipitating factors. Delirium is highly prevalent in older patients across various settings of care and correlates with an increased risk of adverse clinical outcomes. Several pathophysiological mechanisms may contribute to its onset, including neurotransmitter imbalance, neuroinflammation, altered brain metabolism, and impaired neuronal network connectivity. Several screening and diagnostic tools for delirium exist, but they are unfortunately underutilized. Additionally, the diagnosis of delirium superimposed on dementia poses a formidable challenge – especially if dementia is severe. Non-pharmacological approaches for the prevention and multidomain interventions for the treatment of delirium are recommended, given that there is currently no robust evidence of drugs that can prevent or resolve delirium.