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Alzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Alzheimer's disease (AD) is the leading cause of dementia worldwide. The recent announcement that lecanemab, a monoclonal antibody targeting amyloid-b, can slow down cognitive decline in AD is a great step forward in the battle against the disease. However, the modest success achieved in the clinical trial speak to the need for developing additional pharmaceutical approaches to target other key features of AD.
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December 2024
Queen's University, Kingston, ON, Canada; D'OR Institute for Research and Education, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Physical exercise improves overall brain health, cognition, and stimulates the release of extracellular vesicles (EVs) in humans. Exercise upregulates irisin, a myokine derived from fibronectin type III domain-containing protein 5 (FNDC5) previously shown to mediate the beneficial actions of exercise on memory in mouse models of Alzheimer's disease (AD). Here, we investigated if physical exercise upregulates EVs.
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December 2024
University of Kentucky, Lexington, KY, USA.
Background: Compared with the E3 allele of Apolipoprotein E (APOE), E4 increases late-onset Alzheimer's Disease (AD) risk up to 15-fold, while the E2 allele substantially decreases risk. In the CNS, ApoE is predominantly synthesized by astrocytes and microglia, making these two cell types promising targets for ApoE-directed therapeutic approaches. Our lab has generated an inducible "switch" mouse model (APOE4s2) in which we can conditionally replace E4 with the protective E2 in a cell-specific manner.
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December 2024
Ecole polytechnique - CNRS UMR7654, Palaiseau, Ile-de-France, France; Université Paris Cité - Inserm UMR-S1124, Paris, Ile-de-France, France.
Alzheimer's disease (AD) is the most common dementia in humans that today concerns 50 million individuals worldwide and will affect more than 100 million people in 2050. Except for familial AD cases (<5% of AD patients) for which AD pathology connects to mutations in critical genes involved in the processing of the amyloid precursor protein into neurotoxic Aß peptides, it remains unknown what provokes the overproduction and deposition of Aß peptides in the brain of sporadic AD cases (>95% of AD patients). Some nanosized materials, e.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Centre for Ageing and Health (AgeCap) at the University of Gothenburg, Gothenburg, Sweden., Gothenburg, Vastra Gotaland, Sweden.
Background: C-reactive protein (CRP) is an inflammatory biomarker that has been associated with an increased risk of future cognitive decline, alongside other biomarkers such as β-amyloid (Aβ). We sought to explore the relationship between CRP levels and the amyloid/tau/neurodegeneration (A/T/N) groups in elderly individuals with and without APOE-ε4.
Method: From 1203 participants of the Gothenburg H70 Birth Cohort study, born in 1944, plasma CRP levels were collected among 300 participants (159 men & 141 women) who did not have dementia.
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