Risultati per: Studio chiarisce come l’Alzheimer si diffonde nel cervello

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Stroke, Ahead of Print. BACKGROUND:Species-specific differences in astrocytes and their Alzheimer disease-associated pathology may influence cellular responses to other insults. Herein, human glial chimeric mice were generated to evaluate how Alzheimer disease predisposing genetic background in human astrocytes contributes to behavioral outcome and brain pathology after cortical photothrombotic ischemia.METHODS:Neonatal (P0) immunodeficient mice of both sexes were transplanted with induced pluripotent stem cell–derived astrocyte progenitors from Alzheimer disease patients carryingPSEN1exon 9 deletion (PSEN1ΔE9), with isogenic controls, with cells from a healthy donor, or with mouse astrocytes or vehicle. After 14 months, a photothrombotic lesion was produced with Rose Bengal in the motor cortex. Behavior was assessed before ischemia and 1 and 4 weeks after the induction of stroke, followed by tissue perfusion for histology.RESULTS:Open field, cylinder, and grid-walking tests showed a persistent locomotor and sensorimotor impairment after ischemia and female mice had larger infarct sizes; yet, these were not affected by astrocytes withPSEN1ΔE9 background. Staining for human nuclear antigen confirmed that human cells successfully engrafted throughout the mouse brain. However, only a small number of human cells were positive for astrocytic marker GFAP (glial fibrillary acidic protein), mostly located in the corpus callosum and retaining complex human-specific morphology with longer processes compared with host counterparts. While host astrocytes formed the glial scar, human astrocytes were scattered in small numbers close to the lesion boundary. Aβ (beta-amyloid) deposits were not present inPSEN1ΔE9 astrocyte-transplanted mice.CONCLUSIONS:Transplanted human cells survived and distributed widely in the host brain but had no impact on severity of ischemic damage after cortical photothrombosis in chimeric mice. Only a small number of transplanted human astrocytes acquired GFAP-positive glial phenotype or migrated toward the ischemic lesion forming glial scar.PSEN1ΔE9 astrocytes did not impair behavioral recovery after experimental stroke.

This JAMA Internal Medicine Patient Page describes use of aducanumab for treatment of Alzheimer disease, including potential benefits, harms, and concerns about use.

Stroke, Volume 53, Issue Suppl_1, Page ATP203-ATP203, February 1, 2022. Introduction:Alzheimer’s disease and related dementias (ADRD) are a leading cause of disability and premature death in the U.S. The aim of this study was to identify demographic and clinical predictors (age, sex race/ ethnicity, marital status, education level, history of heart disease, myocardial infarction, stroke, hypertension, diabetes, anxiety and depression symptoms, subjective memory rating, clock drawing results) of ADRD in a cohort of adults over age 65.Methods:We obtained data for 2011 to 2020 from the National Health and Aging Trends Study (NHATS). NHATS contains a nationally representative sample of Medicare beneficiaries aged 65 years and older. We included participants with complete data (N=6161).Results:Logistic regression analysis (see Table 1) suggested that the odds of having ADRD were 2.24 times higher in participants who had a stroke than in those who had not (p