Title: Restoration of cervical lymphatic vessel function in aging rescues cerebrospinal fluid drainage
Abstract: Cervical lymphatic vessels (cLVs) have been shown to drain solutes and cerebrospinal fluid (CSF) from the brain. However, their hydrodynamical properties have never been evaluated in vivo. Here, we developed two-photon optical imaging with particle tracking in vivo of CSF tracers (2P-OPTIC) in superficial and deep cLVs of mice, characterizing their flow and showing that the major driver is intrinsic pumping by contraction of the lymphatic vessel wall. Moreover, contraction frequency and flow velocity were reduced in aged mice, which coincided with a reduction in smooth muscle actin expression. Slowed flow in aged mice was rescued using topical application of prostaglandin F2α, a prostanoid that increases smooth muscle contractility, which restored lymphatic function in aged mice and enhanced central nervous system clearance. We show that cLVs are important regulators of CSF drainage and that restoring their function is an effective therapy for improving clearance in aging.
https://www.nature.com/articles/s43587-024-00691-3
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Title: Untreated high blood pressure may raise Alzheimer’s disease risk
Abstract:
Previous research shows several health concerns can increase a person’s risk of developing Alzheimer’s disease, including high blood pressure.
Researchers estimate 46% of adults worldwide do not know they have hypertension.
Researchers from the University of New South Wales have found people with untreated high blood pressure may have an increased risk of developing Alzheimer’s disease compared to people who have been or are being treated for hypertension.
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Title: Aging: a biology problem, or a question of physics?
Abstract:
Dr Leonard Hayflick explains why he believes most research into aging and longevity isn’t asking the right questions.
https://longevity.technology/news/aging-a-biology-problem-or-a-question-of-physics/
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Title: Epigenome editing technologies for discovery and medicine
Abstract:
Given the ubiquitous role of epigenetics in complex phenotypes, epigenome editing has unique potential to impact a broad spectrum of diseases. By leveraging powerful DNA-targeting technologies, such as CRISPR, epigenome editing exploits the heritable and reversible mechanisms of epigenetics to alter gene expression without introducing DNA breaks, inducing DNA damage or relying on DNA repair pathways.
https://www.nature.com/articles/s41587-024-02320-1
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Title: Nanotoxicology: An Overview
Abstract: Nanotoxicology is a specialized branch of nanotechnology focused on assessing the harmful effects of nanoparticles (NPs) on human health and the environment.1 NPs exhibit unique properties compared to their bulk counterparts due to their quantum size effects and high surface-to-volume ratio, which affect their toxicity.
https://www.azonano.com/article.aspx?ArticleID=6792
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Title: Changes in the Extracellular Matrix with Aging: A Larger Role in Alzheimer's Disease
Abstract:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia (2023). Aging is a leading risk factor for sporadic onset of AD. During normal aging, regulatory signaling pathways that are critical for cellular health gradually become less effective, leading to impairment of physiological functions across all tissue systems (Zia et al., 2021). For example, in the healthy brain, the production and clearance of amyloid-β (Aβ) peptides are balanced to maintain appropriate levels of Aβ in the cells, vasculature, and extracellular space. However, with aging, the body loses the ability to maintain this process, leading to an increase of misfolded Aβ peptides and the generation of extracellular plaques (Hampel et al., 2021). These plaques are one of the characteristic pathological features of AD.
Insulin/insulin growth factor-1 (IGF-1) signaling, a major pathway implicated in the regulation of aging, may also play a pivotal role in Aβ pathogenesis (Sano et al., 2023). Insulin signaling begins when insulin secreted by the pancreas binds to an IGF-1 receptor, leading to phosphorylation of insulin receptor substrate proteins, IRS1-4 (Zia et al., 2021). These modified substrates independently control distinct intracellular cascades. Genetic deletion of one of these substrates, Irs2, in mice causes severe type 2 diabetes mellitus, with associated behavioral changes, impairments
#aging