P3-383: TNF expressing cells in the subependymal zone of the third ventricle of aged mouse and human brain with Alzheimer's disease pathology

2008 ◽  
Vol 4 ◽  
pp. T633-T634
Author(s):  
Ivica Granic ◽  
Csaba Nyakas ◽  
Gabor G. Kovacs ◽  
Paul G.M. Luiten ◽  
Ulrich L.M. Eisel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Third Ventricle ◽  
Aged Mouse ◽  
The Third ◽  
Subependymal Zone

scholarly journals Diagnostic Ability of Structural Transcranial Sonography in Patients with Alzheimer’s Disease

Diagnostics ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 471
Author(s):  
Daiva Rastenyte ◽  
Vaidas Matijosaitis ◽  
Ovidijus Laucius ◽  
Rymante Gleizniene ◽  
Simonas Jesmanas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Medial Temporal Lobe ◽  
Third Ventricle ◽  
Linear Measurement ◽  
Hippocampal Volume ◽  
Transcranial Sonography ◽  
Parahippocampal Gyrus ◽  
Diagnostic Ability ◽  
The Third

The aim of this study was to assess the diagnostic ability of transcranial sonography (TCS) for the evaluation of the medial temporal lobe (MTL) in Alzheimer’s disease (AD). Standard neuropsychological evaluation, TCS and 1.5 T MRI were performed for 20 patients with AD and for 20 age- and sex-matched healthy controls in a prospective manner. Measurements of the size of the third ventricle and heights of the MTL (A) and the choroidal fissure (B) were performed twice on each side by two independent neurosonologists for all participants. On MRI, both conventional and volumetric analyses of the third ventricle and hippocampus were performed. Receiver operating characteristic (ROC) curves analyses were applied. Height of the MTL on TCS had sensitivities of 73.7% (right)/63.2%(left) and specificities of 65% (right)/65–70% (left) Area under a curve (AUC) 75.4–77.2% (right), 60.4–67.8% (left)) for AD. A/B ratio on TCS had sensitivities of 73.7% (right)/57.9% (left) and specificities of 70.0% (right)/55.0% (left) (AUC 73.3% (right), 60.4% (left)) by the experienced neurosonologist, and sensitivities of 78.9% (right and left) and specificities of 60.0% (right)/65.0% (left) (AUC 77.8–80.0%) by the inexperienced neurosonologist for AD. On MRI, linear measurement of the hippocampus and parahippocampal gyrus height had sensitivities of 84.2% (right)/89.5% (left) and specificities of 80.0% (right)/85% (left) (AUC 86.1–92.9%) for AD. Hippocampal volume had sensitivities of 70% (right and left) and specificities of 75% (right)/80% (left) (AUC 77.5–78%) for AD. Atrophy of the right MTL in AD could be detected on TCS with a good diagnostic ability, however MRI performed better on the left.

Psychiatric Phenomena in Alzheimer's Disease. IV: Disorders of Behaviour

1990 ◽  
Vol 157 (1) ◽  
pp. 86-94 ◽  
Author(s):  
Alastair Burns ◽  
Robin Jacoby ◽  
Raymond Levy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Urinary Incontinence ◽  
Binge Eating ◽  
Temporal Lobe ◽  
Third Ventricle ◽  
Severe Dementia ◽  
The Third ◽  
Sexual Disinhibition ◽  
Lobe Atrophy

Out of a sample of 178 patients with AD, aggression was present in 20%, wandering in 19%, binge-eating in 10%, hyperorality in 6%, urinary incontinence in 48%, and sexual disinhibition in 7%. Behavioural abnormalities were greater in those with more severe dementia. Temporal-lobe atrophy correlated with aggression, and widening of the third ventricle with hyperorality. Features of the Kluver–Bucy syndrome were commonly seen, but the full syndrome occurred in only one subject. Patients with at least one feature of the Kluver–Bucy syndrome had greater temporal-lobe atropy than those without any of the features.

Phenylalanine Metabolism is Dysregulated in Human Hippocampus with Alzheimer’s Disease Related Pathological Changes

2021 ◽  
pp. 1-14
Author(s):  
Pan Liu ◽  
Qian Yang ◽  
Ning Yu ◽  
Yan Cao ◽  
Xue Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Pathological Examination ◽  
Pathological Changes ◽  
Targeted Metabolomics ◽  
Phenylpyruvic Acid ◽  
Postmortem Human Brain ◽  
Metabolic Dysregulation ◽  
Phenylalanine Metabolism

Background: Alzheimer’s disease (AD) is one of the most challenging diseases causing an increasing burden worldwide. Although the neuropathologic diagnosis of AD has been established for many years, the metabolic changes in neuropathologic diagnosed AD samples have not been fully investigated. Objective: To elucidate the potential metabolism dysregulation in the postmortem human brain samples assessed by AD related pathological examination. Methods: We performed untargeted and targeted metabolomics in 44 postmortem human brain tissues. The metabolic differences in the hippocampus between AD group and control (NC) group were compared. Results: The results show that a pervasive metabolic dysregulation including phenylalanine metabolism, valine, leucine, and isoleucine biosynthesis, biotin metabolism, and purine metabolism are associated with AD pathology. Targeted metabolomics reveal that phenylalanine, phenylpyruvic acid, and N-acetyl-L-phenylalanine are upregulated in AD samples. In addition, the enzyme IL-4I1 catalyzing transformation from phenylalanine to phenylpyruvic acid is also upregulated in AD samples. Conclusion: There is a pervasive metabolic dysregulation in hippocampus with AD-related pathological changes. Our study suggests that the dysregulation of phenylalanine metabolism in hippocampus may be an important pathogenesis for AD pathology formation.

scholarly journals Luminex-based quantification of Alzheimer’s disease neuropathologic change in formalin-fixed post-mortem human brain tissue

2018 ◽  
Vol 99 (7) ◽  
pp. 1056-1067
Author(s):  
C. Dirk Keene ◽  
Angela M. Wilson ◽  
Mitchell D. Kilgore ◽  
Lauren T. Bruner ◽  
Nadia O. Postupna ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Brain Tissue ◽  
Post Mortem ◽  
Human Brain Tissue ◽  
Formalin Fixed

scholarly journals Dimensional Changes in Lipid Rafts from Human Brain Cortex Associated to Development of Alzheimer’s Disease. Predictions from an Agent-Based Mathematical Model

2021 ◽  
Vol 22 (22) ◽  
pp. 12181
Author(s):  
Guido Santos ◽  
Mario Díaz
Keyword(s):  
Alzheimer’S Disease ◽  
Mathematical Model ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Lipid Rafts ◽  
Brain Cortex ◽  
Clinical Symptoms ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Human Brain Cortex

Alzheimer’s disease (AD) is a neurodegenerative disease caused by abnormal functioning of critical physiological processes in nerve cells and aberrant accumulation of protein aggregates in the brain. The initial cause remains elusive—the only unquestionable risk factor for the most frequent variant of the disease is age. Lipid rafts are microdomains present in nerve cell membranes and they are known to play a significant role in the generation of hallmark proteinopathies associated to AD, namely senile plaques, formed by aggregates of amyloid β peptides. Recent studies have demonstrated that human brain cortex lipid rafts are altered during early neuropathological phases of AD as defined by Braak and Braak staging. The lipid composition and physical properties of these domains appear altered even before clinical symptoms are detected. Here, we use a coarse grain molecular dynamics mathematical model to predict the dimensional evolution of these domains using the experimental data reported by our group in human frontal cortex. The model predicts significant size and frequency changes which are detectable at the earliest neuropathological stage (ADI/II) of Alzheimer’s disease. Simulations reveal a lower number and a larger size in lipid rafts from ADV/VI, the most advanced stage of AD. Paralleling these changes, the predictions also indicate that non-rafts domains undergo simultaneous alterations in membrane peroxidability, which support a link between oxidative stress and AD progression. These synergistic changes in lipid rafts dimensions and non-rafts peroxidability are likely to become part of a positive feedback loop linked to an irreversible amyloid burden and neuronal death during the evolution of AD neuropathology.

scholarly journals Genetic Overlap Between Alzheimer’s Disease and Depression Mapped Onto the Brain

2021 ◽  
Vol 15 ◽  
Author(s):  
Jennifer Monereo-Sánchez ◽  
Miranda T. Schram ◽  
Oleksandr Frei ◽  
Kevin O’Connell ◽  
Alexey A. Shadrin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genome Wide Association Study ◽  
Third Ventricle ◽  
Brain Mri ◽  
Genetic Correlations ◽  
Gaussian Mixture ◽  
Brain Morphology ◽  
Genetic Overlap ◽  
Ventricle Volume

Background: Alzheimer’s disease (AD) and depression are debilitating brain disorders that are often comorbid. Shared brain mechanisms have been implicated, yet findings are inconsistent, reflecting the complexity of the underlying pathophysiology. As both disorders are (partly) heritable, characterising their genetic overlap may provide aetiological clues. While previous studies have indicated negligible genetic correlations, this study aims to expose the genetic overlap that may remain hidden due to mixed directions of effects.Methods: We applied Gaussian mixture modelling, through MiXeR, and conjunctional false discovery rate (cFDR) analysis, through pleioFDR, to genome-wide association study (GWAS) summary statistics of AD (n = 79,145) and depression (n = 450,619). The effects of identified overlapping loci on AD and depression were tested in 403,029 participants of the UK Biobank (UKB) (mean age 57.21, 52.0% female), and mapped onto brain morphology in 30,699 individuals with brain MRI data.Results: MiXer estimated 98 causal genetic variants overlapping between the 2 disorders, with 0.44 concordant directions of effects. Through pleioFDR, we identified a SNP in the TMEM106B gene, which was significantly associated with AD (B = −0.002, p = 9.1 × 10–4) and depression (B = 0.007, p = 3.2 × 10–9) in the UKB. This SNP was also associated with several regions of the corpus callosum volume anterior (B > 0.024, p < 8.6 × 10–4), third ventricle volume ventricle (B = −0.025, p = 5.0 × 10–6), and inferior temporal gyrus surface area (B = 0.017, p = 5.3 × 10–4).Discussion: Our results indicate there is substantial genetic overlap, with mixed directions of effects, between AD and depression. These findings illustrate the value of biostatistical tools that capture such overlap, providing insight into the genetic architectures of these disorders.

Sign in / Sign up

Export Citation Format

Share Document