Life Extension Factor Klotho Enhances Cognition
Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhance...
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| Veröffentlicht in: | Cell reports (Cambridge) Jg. 7; H. 4; S. 1065 - 1076 |
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| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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United States
Elsevier Inc
01.05.2014
Elsevier |
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| ISSN: | 2211-1247, 2211-1247 |
| Online-Zugang: | Volltext |
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| Abstract | Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages.
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•KLOTHO variant elevates klotho levels and is associated with enhanced human cognition•Elevation of klotho in mice enhances normal cognition, independent of age•Klotho elevation leads to greater synaptic GluN2B (NMDAR subunit) levels and plasticity•GluN2B blockade abolishes klotho-mediated effects on NMDAR functions and cognition
Klotho extends lifespan. Whether aging regulators like klotho can counteract aging-related cognitive decline and promote brain health is unknown. Here, Dubal, Mucke, and colleagues demonstrate that a variant of the KLOTHO gene that increases klotho levels in the circulation is associated with better cognition in normal aging individuals. Elevating klotho in mice also enhanced cognition and synaptic plasticity, even in the young life stage, through mechanisms that involve regulation of NMDA receptors, key players in learning and memory. |
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| AbstractList | Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages.
[Display omitted]
•KLOTHO variant elevates klotho levels and is associated with enhanced human cognition•Elevation of klotho in mice enhances normal cognition, independent of age•Klotho elevation leads to greater synaptic GluN2B (NMDAR subunit) levels and plasticity•GluN2B blockade abolishes klotho-mediated effects on NMDAR functions and cognition
Klotho extends lifespan. Whether aging regulators like klotho can counteract aging-related cognitive decline and promote brain health is unknown. Here, Dubal, Mucke, and colleagues demonstrate that a variant of the KLOTHO gene that increases klotho levels in the circulation is associated with better cognition in normal aging individuals. Elevating klotho in mice also enhanced cognition and synaptic plasticity, even in the young life stage, through mechanisms that involve regulation of NMDA receptors, key players in learning and memory. Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages. Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a life span-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an NMDA receptor subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition at different life stages and counteract cognitive decline. Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages. Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages.Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages. |
| Author | Kramer, Joel H. Zhu, Lei Yu, Gui-Qiu Broestl, Lauren Wang, Dan Bennett, David A. De Jager, Philip L. Sturm, Virginia E. Yu, Lei Ho, Kaitlyn Kuro-o, Makoto Kim, Daniel Coppola, Giovanni Miller, Bruce L. Mucke, Lennart Klein, Eric Small, Gary W. Abraham, Carmela R. Yokoyama, Jennifer S. Dubal, Dena B. Eilertson, Kirsten E. Worden, Kurtresha |
| AuthorAffiliation | 6 Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390 8 Program in Translational NeuroPsychiatric Genomics, Institute for Neurosciences, Departments of Neurology & Psychiatry, Brigham and Women’s Hospital, Boston, MA 02115 5 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 10 Program in Medical and Population Genetics, Broad Institute, Cambridge, MA 02142 1 Gladstone Institute of Neurological Disease, San Francisco, CA 94158 4 Gladstone Institutes Bioinformatics Core, San Francisco, CA 94158 3 Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90024 2 Department of Neurology, University of California, San Francisco, CA 94158 11 Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118 7 Center for Molecular Medicine, Jichi Medical University, Tochigi 329-0498, Japan 9 Harvard Medical School, Boston, MA 02115 |
| AuthorAffiliation_xml | – name: 4 Gladstone Institutes Bioinformatics Core, San Francisco, CA 94158 – name: 1 Gladstone Institute of Neurological Disease, San Francisco, CA 94158 – name: 5 Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612 – name: 10 Program in Medical and Population Genetics, Broad Institute, Cambridge, MA 02142 – name: 11 Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118 – name: 3 Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90024 – name: 6 Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390 – name: 7 Center for Molecular Medicine, Jichi Medical University, Tochigi 329-0498, Japan – name: 8 Program in Translational NeuroPsychiatric Genomics, Institute for Neurosciences, Departments of Neurology & Psychiatry, Brigham and Women’s Hospital, Boston, MA 02115 – name: 9 Harvard Medical School, Boston, MA 02115 – name: 2 Department of Neurology, University of California, San Francisco, CA 94158 |
| Author_xml | – sequence: 1 givenname: Dena B. surname: Dubal fullname: Dubal, Dena B. email: dena.dubal@ucsf.edu organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA – sequence: 2 givenname: Jennifer S. surname: Yokoyama fullname: Yokoyama, Jennifer S. organization: Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA – sequence: 3 givenname: Lei surname: Zhu fullname: Zhu, Lei organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA – sequence: 4 givenname: Lauren surname: Broestl fullname: Broestl, Lauren organization: Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA – sequence: 5 givenname: Kurtresha surname: Worden fullname: Worden, Kurtresha organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA – sequence: 6 givenname: Dan surname: Wang fullname: Wang, Dan organization: Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA – sequence: 7 givenname: Virginia E. surname: Sturm fullname: Sturm, Virginia E. organization: Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA – sequence: 8 givenname: Daniel surname: Kim fullname: Kim, Daniel organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA – sequence: 9 givenname: Eric surname: Klein fullname: Klein, Eric organization: Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA 90024, USA – sequence: 10 givenname: Gui-Qiu surname: Yu fullname: Yu, Gui-Qiu organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA – sequence: 11 givenname: Kaitlyn surname: Ho fullname: Ho, Kaitlyn organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA – sequence: 12 givenname: Kirsten E. surname: Eilertson fullname: Eilertson, Kirsten E. organization: Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA – sequence: 13 givenname: Lei surname: Yu fullname: Yu, Lei organization: Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612, USA – sequence: 14 givenname: Makoto surname: Kuro-o fullname: Kuro-o, Makoto organization: Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA – sequence: 15 givenname: Philip L. surname: De Jager fullname: De Jager, Philip L. organization: Program in Translational NeuroPsychiatric Genomics, Institute for Neurosciences, Departments of Neurology & Psychiatry, Brigham and Women’s Hospital, Boston, MA 02115, USA – sequence: 16 givenname: Giovanni surname: Coppola fullname: Coppola, Giovanni organization: Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA 90024, USA – sequence: 17 givenname: Gary W. surname: Small fullname: Small, Gary W. organization: Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA 90024, USA – sequence: 18 givenname: David A. surname: Bennett fullname: Bennett, David A. organization: Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, IL 60612, USA – sequence: 19 givenname: Joel H. surname: Kramer fullname: Kramer, Joel H. organization: Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA – sequence: 20 givenname: Carmela R. surname: Abraham fullname: Abraham, Carmela R. organization: Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118, USA – sequence: 21 givenname: Bruce L. surname: Miller fullname: Miller, Bruce L. organization: Department of Neurology, University of California, San Francisco, San Francisco, CA 94158, USA – sequence: 22 givenname: Lennart surname: Mucke fullname: Mucke, Lennart email: lmucke@gladstone.ucsf.edu organization: Gladstone Institute of Neurological Disease, San Francisco, CA 94158, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24813892$$D View this record in MEDLINE/PubMed |
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| Title | Life Extension Factor Klotho Enhances Cognition |
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