Inflammaging as a prodrome to Alzheimer's disease

Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five...
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Autor*in:	Giunta, Brian [verfasserIn] Fernandez, Francisco Nikolic, William V Obregon, Demian Rrapo, Elona Town, Terrence Tan, Jun

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2008

Schlagwörter:	Flavonoid Adaptive Immune Response Adaptive Immunity Cerebral Amyloid Angiopathy Flavonoid Intake

Anmerkung:	© Giunta et al; licensee BioMed Central Ltd. 2008

Übergeordnetes Werk:	Enthalten in: Journal of neuroinflammation - London : BioMed Central, 2004, 5(2008), 1 vom: 11. Nov.
Übergeordnetes Werk:	volume:5 ; year:2008 ; number:1 ; day:11 ; month:11

Links:	Volltext

DOI / URN:	10.1186/1742-2094-5-51

Katalog-ID:	SPR029089204

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allfields	10.1186/1742-2094-5-51 doi (DE-627)SPR029089204 (SPR)1742-2094-5-51-e DE-627 ger DE-627 rakwb eng Giunta, Brian verfasserin aut Inflammaging as a prodrome to Alzheimer's disease 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Giunta et al; licensee BioMed Central Ltd. 2008 Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. Flavonoid (dpeaa)DE-He213 Adaptive Immune Response (dpeaa)DE-He213 Adaptive Immunity (dpeaa)DE-He213 Cerebral Amyloid Angiopathy (dpeaa)DE-He213 Flavonoid Intake (dpeaa)DE-He213 Fernandez, Francisco aut Nikolic, William V aut Obregon, Demian aut Rrapo, Elona aut Town, Terrence aut Tan, Jun aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 5(2008), 1 vom: 11. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:5 year:2008 number:1 day:11 month:11 https://dx.doi.org/10.1186/1742-2094-5-51 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2008 1 11 11
spelling	10.1186/1742-2094-5-51 doi (DE-627)SPR029089204 (SPR)1742-2094-5-51-e DE-627 ger DE-627 rakwb eng Giunta, Brian verfasserin aut Inflammaging as a prodrome to Alzheimer's disease 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Giunta et al; licensee BioMed Central Ltd. 2008 Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. Flavonoid (dpeaa)DE-He213 Adaptive Immune Response (dpeaa)DE-He213 Adaptive Immunity (dpeaa)DE-He213 Cerebral Amyloid Angiopathy (dpeaa)DE-He213 Flavonoid Intake (dpeaa)DE-He213 Fernandez, Francisco aut Nikolic, William V aut Obregon, Demian aut Rrapo, Elona aut Town, Terrence aut Tan, Jun aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 5(2008), 1 vom: 11. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:5 year:2008 number:1 day:11 month:11 https://dx.doi.org/10.1186/1742-2094-5-51 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2008 1 11 11
allfields_unstemmed	10.1186/1742-2094-5-51 doi (DE-627)SPR029089204 (SPR)1742-2094-5-51-e DE-627 ger DE-627 rakwb eng Giunta, Brian verfasserin aut Inflammaging as a prodrome to Alzheimer's disease 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Giunta et al; licensee BioMed Central Ltd. 2008 Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. Flavonoid (dpeaa)DE-He213 Adaptive Immune Response (dpeaa)DE-He213 Adaptive Immunity (dpeaa)DE-He213 Cerebral Amyloid Angiopathy (dpeaa)DE-He213 Flavonoid Intake (dpeaa)DE-He213 Fernandez, Francisco aut Nikolic, William V aut Obregon, Demian aut Rrapo, Elona aut Town, Terrence aut Tan, Jun aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 5(2008), 1 vom: 11. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:5 year:2008 number:1 day:11 month:11 https://dx.doi.org/10.1186/1742-2094-5-51 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2008 1 11 11
allfieldsGer	10.1186/1742-2094-5-51 doi (DE-627)SPR029089204 (SPR)1742-2094-5-51-e DE-627 ger DE-627 rakwb eng Giunta, Brian verfasserin aut Inflammaging as a prodrome to Alzheimer's disease 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Giunta et al; licensee BioMed Central Ltd. 2008 Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. Flavonoid (dpeaa)DE-He213 Adaptive Immune Response (dpeaa)DE-He213 Adaptive Immunity (dpeaa)DE-He213 Cerebral Amyloid Angiopathy (dpeaa)DE-He213 Flavonoid Intake (dpeaa)DE-He213 Fernandez, Francisco aut Nikolic, William V aut Obregon, Demian aut Rrapo, Elona aut Town, Terrence aut Tan, Jun aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 5(2008), 1 vom: 11. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:5 year:2008 number:1 day:11 month:11 https://dx.doi.org/10.1186/1742-2094-5-51 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2008 1 11 11
allfieldsSound	10.1186/1742-2094-5-51 doi (DE-627)SPR029089204 (SPR)1742-2094-5-51-e DE-627 ger DE-627 rakwb eng Giunta, Brian verfasserin aut Inflammaging as a prodrome to Alzheimer's disease 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Giunta et al; licensee BioMed Central Ltd. 2008 Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. Flavonoid (dpeaa)DE-He213 Adaptive Immune Response (dpeaa)DE-He213 Adaptive Immunity (dpeaa)DE-He213 Cerebral Amyloid Angiopathy (dpeaa)DE-He213 Flavonoid Intake (dpeaa)DE-He213 Fernandez, Francisco aut Nikolic, William V aut Obregon, Demian aut Rrapo, Elona aut Town, Terrence aut Tan, Jun aut Enthalten in Journal of neuroinflammation London : BioMed Central, 2004 5(2008), 1 vom: 11. Nov. (DE-627)391784781 (DE-600)2156455-3 1742-2094 nnns volume:5 year:2008 number:1 day:11 month:11 https://dx.doi.org/10.1186/1742-2094-5-51 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2008 1 11 11
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author	Giunta, Brian
spellingShingle	Giunta, Brian misc Flavonoid misc Adaptive Immune Response misc Adaptive Immunity misc Cerebral Amyloid Angiopathy misc Flavonoid Intake Inflammaging as a prodrome to Alzheimer's disease
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topic_title	Inflammaging as a prodrome to Alzheimer's disease Flavonoid (dpeaa)DE-He213 Adaptive Immune Response (dpeaa)DE-He213 Adaptive Immunity (dpeaa)DE-He213 Cerebral Amyloid Angiopathy (dpeaa)DE-He213 Flavonoid Intake (dpeaa)DE-He213
topic	misc Flavonoid misc Adaptive Immune Response misc Adaptive Immunity misc Cerebral Amyloid Angiopathy misc Flavonoid Intake
topic_unstemmed	misc Flavonoid misc Adaptive Immune Response misc Adaptive Immunity misc Cerebral Amyloid Angiopathy misc Flavonoid Intake
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title	Inflammaging as a prodrome to Alzheimer's disease
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title_full	Inflammaging as a prodrome to Alzheimer's disease
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title_sort	inflammaging as a prodrome to alzheimer's disease
title_auth	Inflammaging as a prodrome to Alzheimer's disease
abstract	Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. © Giunta et al; licensee BioMed Central Ltd. 2008
abstractGer	Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. © Giunta et al; licensee BioMed Central Ltd. 2008
abstract_unstemmed	Abstract Recently, the term "inflammaging" was coined by Franceshci and colleagues to characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly from the traditional five cardinal features of acute inflammation in that it is characterized by a relative decline in adaptive immunity and T-helper 2 responses and is associated with increased innate immunity by cells of the mononuclear phagocyte lineage. While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. We and others have found that IFN-γ and other pro-inflammatory cytokines interact with processing and production of Aβ peptide, the pathological hallmark feature of Alzheimer's disease (AD), suggesting that inflammaging may be a "prodrome" to AD. Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Aβ vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models. © Giunta et al; licensee BioMed Central Ltd. 2008
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title_short	Inflammaging as a prodrome to Alzheimer's disease
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author2	Fernandez, Francisco Nikolic, William V Obregon, Demian Rrapo, Elona Town, Terrence Tan, Jun
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up_date	2024-07-03T23:24:21.087Z
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Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age "well" demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immune response of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD. In this review, we fully characterize the aging immune system. 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