Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer's disease

The hippocampus is one of the most affected areas in Alzheimer's disease (AD) . Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life . This process, called adult hippocampal neurogenesis (AHN), confers...

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Veröffentlicht in:	Nature medicine Jg. 25; H. 4; S. 554 - 560
Hauptverfasser:	Moreno-Jiménez, Elena P, Flor-García, Miguel, Terreros-Roncal, Julia, Rábano, Alberto, Cafini, Fabio, Pallas-Bazarra, Noemí, Ávila, Jesús, Llorens-Martín, María
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Nature Publishing Group 01.04.2019
Schlagworte:	Adult Aging Alzheimer Disease - pathology Alzheimer's disease Biomarkers - metabolism Brain Cell Differentiation Controlled conditions Dentate gyrus Dentate Gyrus - pathology Doublecortin Domain Proteins Hippocampal plasticity Hippocampus Hippocampus - pathology Humans Identification methods Maturation Microtubule-Associated Proteins - metabolism Neurogenesis Neurons Neuropeptides - metabolism Physiology
ISSN:	1078-8956, 1546-170X, 1546-170X
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Abstract	The hippocampus is one of the most affected areas in Alzheimer's disease (AD) . Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life . This process, called adult hippocampal neurogenesis (AHN), confers an unparalleled degree of plasticity to the entire hippocampal circuitry . Nonetheless, direct evidence of AHN in humans has remained elusive. Thus, determining whether new neurons are continuously incorporated into the human dentate gyrus (DG) during physiological and pathological aging is a crucial question with outstanding therapeutic potential. By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the DG of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages of AHN. In sharp contrast, the number and maturation of these neurons progressively declined as AD advanced. These results demonstrate the persistence of AHN during both physiological and pathological aging in humans and provide evidence for impaired neurogenesis as a potentially relevant mechanism underlying memory deficits in AD that might be amenable to novel therapeutic strategies.
AbstractList	The hippocampus is one of the most affected areas in Alzheimer’s disease (AD)1. Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life2. This process, called adult hippocampal neurogenesis (AHN), confers an unparalleled degree of plasticity to the entire hippocampal circuitry3,4. Nonetheless, direct evidence of AHN in humans has remained elusive. Thus, determining whether new neurons are continuously incorporated into the human dentate gyrus (DG) during physiological and pathological aging is a crucial question with outstanding therapeutic potential. By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the DG of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages of AHN. In sharp contrast, the number and maturation of these neurons progressively declined as AD advanced. These results demonstrate the persistence of AHN during both physiological and pathological aging in humans and provide evidence for impaired neurogenesis as a potentially relevant mechanism underlying memory deficits in AD that might be amenable to novel therapeutic strategies.Newborn neurons are continuously incorporated into the healthy adult human hippocampus up to the ninth decade of life. However, robust adult hippocampal neurogenesis sharply declines during the progression of Alzheimer’s disease. The hippocampus is one of the most affected areas in Alzheimer's disease (AD)1. Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life2. This process, called adult hippocampal neurogenesis (AHN), confers an unparalleled degree of plasticity to the entire hippocampal circuitry3,4. Nonetheless, direct evidence of AHN in humans has remained elusive. Thus, determining whether new neurons are continuously incorporated into the human dentate gyrus (DG) during physiological and pathological aging is a crucial question with outstanding therapeutic potential. By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the DG of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages of AHN. In sharp contrast, the number and maturation of these neurons progressively declined as AD advanced. These results demonstrate the persistence of AHN during both physiological and pathological aging in humans and provide evidence for impaired neurogenesis as a potentially relevant mechanism underlying memory deficits in AD that might be amenable to novel therapeutic strategies.The hippocampus is one of the most affected areas in Alzheimer's disease (AD)1. Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life2. This process, called adult hippocampal neurogenesis (AHN), confers an unparalleled degree of plasticity to the entire hippocampal circuitry3,4. Nonetheless, direct evidence of AHN in humans has remained elusive. Thus, determining whether new neurons are continuously incorporated into the human dentate gyrus (DG) during physiological and pathological aging is a crucial question with outstanding therapeutic potential. By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the DG of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages of AHN. In sharp contrast, the number and maturation of these neurons progressively declined as AD advanced. These results demonstrate the persistence of AHN during both physiological and pathological aging in humans and provide evidence for impaired neurogenesis as a potentially relevant mechanism underlying memory deficits in AD that might be amenable to novel therapeutic strategies. The hippocampus is one of the most affected areas in Alzheimer's disease (AD) . Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life . This process, called adult hippocampal neurogenesis (AHN), confers an unparalleled degree of plasticity to the entire hippocampal circuitry . Nonetheless, direct evidence of AHN in humans has remained elusive. Thus, determining whether new neurons are continuously incorporated into the human dentate gyrus (DG) during physiological and pathological aging is a crucial question with outstanding therapeutic potential. By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the DG of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages of AHN. In sharp contrast, the number and maturation of these neurons progressively declined as AD advanced. These results demonstrate the persistence of AHN during both physiological and pathological aging in humans and provide evidence for impaired neurogenesis as a potentially relevant mechanism underlying memory deficits in AD that might be amenable to novel therapeutic strategies.
Author	Llorens-Martín, María Moreno-Jiménez, Elena P Flor-García, Miguel Terreros-Roncal, Julia Rábano, Alberto Cafini, Fabio Ávila, Jesús Pallas-Bazarra, Noemí
Author_xml	– sequence: 1 givenname: Elena P surname: Moreno-Jiménez fullname: Moreno-Jiménez, Elena P organization: Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Madrid, Spain – sequence: 2 givenname: Miguel surname: Flor-García fullname: Flor-García, Miguel organization: Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Madrid, Spain – sequence: 3 givenname: Julia surname: Terreros-Roncal fullname: Terreros-Roncal, Julia organization: Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Madrid, Spain – sequence: 4 givenname: Alberto surname: Rábano fullname: Rábano, Alberto organization: Neuropathology Department, CIEN Foundation, Madrid, Spain – sequence: 5 givenname: Fabio surname: Cafini fullname: Cafini, Fabio organization: Universidad Europea de Madrid, Faculty of Biomedical and Health Sciences, Madrid, Spain – sequence: 6 givenname: Noemí orcidid: 0000-0002-0175-5080 surname: Pallas-Bazarra fullname: Pallas-Bazarra, Noemí organization: Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Madrid, Spain – sequence: 7 givenname: Jesús surname: Ávila fullname: Ávila, Jesús organization: Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Madrid, Spain – sequence: 8 givenname: María orcidid: 0000-0001-9129-5198 surname: Llorens-Martín fullname: Llorens-Martín, María email: m.llorens@csic.es, m.llorens@csic.es, m.llorens@csic.es organization: Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), Madrid, Spain. m.llorens@csic.es
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/30911133$$D View this record in MEDLINE/PubMed
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PublicationDate_xml	– month: 04 year: 2019 text: 2019-04-01 day: 01
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PublicationTitle	Nature medicine
PublicationTitleAlternate	Nat Med
PublicationYear	2019
Publisher	Nature Publishing Group
Publisher_xml	– name: Nature Publishing Group
References	31514645 - Neuroscientist. 2019 Aug;25(4):285 30911138 - Nat Med. 2019 Apr;25(4):542-543 31007011 - ACS Chem Neurosci. 2019 May 15;10(5):2091-2093 31271749 - Cell Stem Cell. 2019 Jul 3;25(1):7-8 30953034 - Nat Rev Neurol. 2019 May;15(5):245
References_xml	– reference: 30953034 - Nat Rev Neurol. 2019 May;15(5):245 – reference: 31007011 - ACS Chem Neurosci. 2019 May 15;10(5):2091-2093 – reference: 31271749 - Cell Stem Cell. 2019 Jul 3;25(1):7-8 – reference: 30911138 - Nat Med. 2019 Apr;25(4):542-543 – reference: 31514645 - Neuroscientist. 2019 Aug;25(4):285
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Snippet	The hippocampus is one of the most affected areas in Alzheimer's disease (AD) . Moreover, this structure hosts one of the most unique phenomena of the adult... The hippocampus is one of the most affected areas in Alzheimer’s disease (AD)1. Moreover, this structure hosts one of the most unique phenomena of the adult... The hippocampus is one of the most affected areas in Alzheimer's disease (AD)1. Moreover, this structure hosts one of the most unique phenomena of the adult...
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SubjectTerms	Adult Aging Alzheimer Disease - pathology Alzheimer's disease Biomarkers - metabolism Brain Cell Differentiation Controlled conditions Dentate gyrus Dentate Gyrus - pathology Doublecortin Domain Proteins Hippocampal plasticity Hippocampus Hippocampus - pathology Humans Identification methods Maturation Microtubule-Associated Proteins - metabolism Neurogenesis Neurons Neuropeptides - metabolism Physiology
Title	Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer's disease
URI	https://www.ncbi.nlm.nih.gov/pubmed/30911133 https://www.proquest.com/docview/2203124905 https://www.proquest.com/docview/2197897137
Volume	25
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