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| http://dx.doi.org/10.1085/jgp.20171187501122018c | DOI Listing |
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Reversal of neuronal tau pathology via adiponectin receptor activation.
Commun Biol
January 2025
Division of Geriatrics, Department of Medicine, SMPH, University of Wisconsin-Madison, Madison, WI, USA.
Changes in brain mitochondrial metabolism are coincident with functional decline; however, direct links between the two have not been established. Here, we show that mitochondrial targeting via the adiponectin receptor activator AdipoRon (AR) clears neurofibrillary tangles (NFTs) and rescues neuronal tauopathy-associated defects. AR reduced levels of phospho-tau and lowered NFT burden by a mechanism involving the energy-sensing kinase AMPK and the growth-sensing kinase GSK3b.
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Alzheimers Dement
December 2024
Vanderbilt Memory & Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, USA.
Background: "SuperAgers" are older adults (ages 80+) whose cognitive performance resembles that of adults in their 50s to mid-60s. Factors underlying their exemplary aging are underexplored in large, racially diverse cohorts. Using eight cohorts, we investigated the frequency of APOE genotypes in SuperAgers compared to middle-aged and older adults.
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Alzheimers Dement
December 2024
National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
Background: Lewy body dementia (LBD) is the second most prevalent dementia in the United States after Alzheimer's disease (AD). Recent studies have implicated rare mutations in two lipid transport genes, ABCA1 and ATP8B4, in Alzheimer's disease. Substantial co-pathology and shared risk factors indicate an intersectional genetic architecture between LBD and AD; therefore, we investigated the association of rare mutations in ABCA1 and ATP8B4 with LBD.
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Alzheimers Dement
December 2024
Northwestern University, Chicago, IL, USA.
Background: Apolipoprotein E4 (E4) is the strongest genetic risk factor for sporadic Alzheimer's Disease (AD), and aging is the greatest overall risk factor for AD. Many cellular and molecular changes occur within the brain throughout aging, one of which being the increased bone morphogenetic protein 4 (BMP4) signaling. As APOE and BMPs are known to interact in non-neuronal organs, we hypothesized that enhanced BMP signaling in the brain may interact with APOE in a genotype-dependent manner to initiate or exacerbate neuropathological cascades relevant to AD.
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Alzheimers Dement
December 2024
Washington University School of Medicine in St Louis, St. Louis, MO, USA.
As part of the goal of the ADSP to develop effect therapeutic for AD, it has become imperative to develop therapeutic targets for APOE4. The Apolipoprotein E4 gene (APOE4) strongest genetic risk factor for AD and is present in 64% of sporadic, late-onset AD, with a recent prevalence estimate of 245 million carriers worldwide. A key question is whether APOE4 is a toxic or gain of function allele or alternatively if its effect is due to a loss or partial loss of function.
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