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Book: Neuropathology of dementing disorders

Markesbery, William R.

1998

Author's details	ed. by William R. Markesbery
Keywords	Senile Demenz ; Neuropathologie
Subject	Altersdemenz ; Dementia senilis ; Altersverwirrtheit ; Altersverwirrung ; Alter ; Greisenalter ; Altersschwachsinn ; Altersblödsinn
Language	English
Size	X, 404 S. : Ill., graph. Darst.
Publisher	Arnold
Publishing place	London u.a.
Publishing country	Great Britain
Document type	Book
HBZ-ID	HT008073467
ISBN	0-340-59037-8 ; 978-0-340-59037-9
Database	Catalogue ZB MED Medicine, Health

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1998 A 3714	order for loan	Magazin

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Article ; Online: Neuropathologic alterations in mild cognitive impairment: a review.

Markesbery, William R

Journal of Alzheimer's disease : JAD

2010 Volume 19, Issue 1, Page(s) 221–228

Abstract: Mild cognitive impairment (MCI), the earliest clinically detectable phase of the trajectory toward dementia and Alzheimer's disease (AD), led to the need for even earlier detection and prevention of AD. Although it is a clinical diagnosis, its underlying ...

Abstract	Mild cognitive impairment (MCI), the earliest clinically detectable phase of the trajectory toward dementia and Alzheimer's disease (AD), led to the need for even earlier detection and prevention of AD. Although it is a clinical diagnosis, its underlying neuropathological findings are just being defined. MCI is best studied in longitudinally followed patients in centers that are experienced in dementing disorders. In this review of the few major clinical-pathological reports of longitudinally followed patients, it appears that most autopsied amnestic MCI (aMCI) patients are on a pathway toward AD. Neurofibrillary pathology in entorhinal cortex, hippocampus, and amygdala--not amyloid plaques--is the major substrate for aMCI and for memory decline. In addition, many MCI patients have other concomitant pathological alterations, the most common of which are strokes, but also include argyrophilic grains and Lewy bodies. These findings are not surprising because most MCI autopsied cases have been in the older (80 to 90 year) range where these findings are common. In early AD, the phase following MCI, the significant change is an increase in neurofibrillary tangles in the neocortex that correlates with an increase in Braak score and the observed clinical progression.
MeSH term(s)	Age Factors ; Alzheimer Disease/pathology ; Alzheimer Disease/psychology ; Animals ; Cognition Disorders/pathology ; Cognition Disorders/psychology ; Disease Progression ; Humans ; Neurofibrillary Tangles/pathology
Language	English
Publishing date	2010-01-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-2010-1220
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Article ; Online: Commentary on "Vascular cognitive impairment: today and tomorrow".

Markesbery, William R

Alzheimer's & dementia : the journal of the Alzheimer's Association

2006 Volume 2, Issue 3, Page(s) 205–206

Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1016/j.jalz.2006.04.004
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Article ; Online: Omega-3 fatty acids: potential role in the management of early Alzheimer's disease.

Jicha, Gregory A / Markesbery, William R

Clinical interventions in aging

2010 Volume 5, Page(s) 45–61

Abstract: Omega-3 fatty acids are essential for brain growth and development. They play an important role throughout life, as critical modulators of neuronal function and regulation of oxidative stress mechanisms, in brain health and disease. Docosahexanoic acid ( ... ...

Abstract	Omega-3 fatty acids are essential for brain growth and development. They play an important role throughout life, as critical modulators of neuronal function and regulation of oxidative stress mechanisms, in brain health and disease. Docosahexanoic acid (DHA), the major omega-3 fatty acid found in neurons, has taken on a central role as a target for therapeutic intervention in Alzheimer's disease (AD). A plethora of in vitro, animal model, and human data, gathered over the past decade, highlight the important role DHA may play in the development of a variety of neurological and psychiatric disorders, including AD. Cross sectional and prospective cohort data have demonstrated that reduced dietary intake or low brain levels of DHA are associated with accelerated cognitive decline or the development of incipient dementia, including AD. Several clinical trials investigating the effects of omega-3 fatty acid supplementation in AD have been completed and all failed to demonstrate its efficacy in the treatment of AD. However, these trials produced intriguing data suggesting that the beneficial effects of omega-3 fatty acid supplementation may depend on the stage of disease, other dietary mediators, and apolipoprotein E status.
MeSH term(s)	Alzheimer Disease/diet therapy ; Clinical Trials as Topic ; Cross-Sectional Studies ; Docosahexaenoic Acids/administration & dosage ; Docosahexaenoic Acids/pharmacology ; Humans ; Oxidative Stress/physiology ; Prospective Studies
Chemical Substances	Docosahexaenoic Acids (25167-62-8)
Language	English
Publishing date	2010-04-07
Publishing country	New Zealand
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2364924-0
ISSN	1178-1998 ; 1176-9092
ISSN (online)	1178-1998
ISSN	1176-9092
DOI	10.2147/cia.s5231
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Article: Oxidative damage in mild cognitive impairment and early Alzheimer's disease.

Lovell, Mark A / Markesbery, William R

Journal of neuroscience research

2007 Volume 85, Issue 14, Page(s) 3036–3040

Abstract: Increasing evidence supports a role for oxidative damage in the pathogenesis of Alzheimer's disease (AD). Multiple studies show significantly increased levels of lipid peroxidation and protein, DNA, and RNA oxidation in vulnerable regions of the brain of ...

Abstract	Increasing evidence supports a role for oxidative damage in the pathogenesis of Alzheimer's disease (AD). Multiple studies show significantly increased levels of lipid peroxidation and protein, DNA, and RNA oxidation in vulnerable regions of the brain of patients with late-stage AD (LAD). More recent studies of patients with amnestic mild cognitive impairment (MCI), the earliest clinical manifestation of AD, show similar patterns of oxidative damage. These observations suggest that oxidative damage to critical biomolecules occurs early in the pathogenesis of AD and precedes pronounced neuropathologic alterations. Because oxidative damage begins early in the progress of the disease, it represents a potential therapeutic target for slowing the onset and progression of AD.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Animals ; Cognition Disorders/etiology ; Cognition Disorders/metabolism ; Humans ; Lipid Peroxidation/physiology ; Oxidation-Reduction ; Oxidative Stress/physiology
Language	English
Publishing date	2007-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/jnr.21346
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Article: Damage to lipids, proteins, DNA, and RNA in mild cognitive impairment.

Markesbery, William R / Lovell, Mark A

Archives of neurology

2007 Volume 64, Issue 7, Page(s) 954–956

Abstract: Free radical-mediated oxidative damage is thought to play a role in the pathogenesis of Alzheimer disease. Previous studies have shown oxidative damage to lipids, proteins, DNA, and RNA in multiple brain regions in late-stage Alzheimer disease. Recent ... ...

Abstract	Free radical-mediated oxidative damage is thought to play a role in the pathogenesis of Alzheimer disease. Previous studies have shown oxidative damage to lipids, proteins, DNA, and RNA in multiple brain regions in late-stage Alzheimer disease. Recent studies on patients with amnestic mild cognitive impairment who have undergone autopsy have shown increased lipid peroxidation as well as protein, DNA, and RNA oxidation in multiple brain regions. These studies establish oxidative damage as an early event in the pathogenesis of Alzheimer disease that can serve as a therapeutic target to slow the progression or perhaps the onset of the disease.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Brain/drug effects ; Brain/metabolism ; Brain/physiopathology ; Cognition Disorders/genetics ; Cognition Disorders/metabolism ; Cognition Disorders/physiopathology ; DNA Damage/genetics ; Disease Progression ; Humans ; Lipid Peroxidation ; Nerve Tissue Proteins/metabolism ; Nucleic Acids/metabolism ; Oxidative Stress/drug effects ; Oxidative Stress/genetics
Chemical Substances	Antioxidants ; Nerve Tissue Proteins ; Nucleic Acids
Language	English
Publishing date	2007-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80049-1
ISSN	1538-3687 ; 0003-9942
ISSN (online)	1538-3687
ISSN	0003-9942
DOI	10.1001/archneur.64.7.954
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Article: Oxidatively modified RNA in mild cognitive impairment.

Lovell, Mark A / Markesbery, William R

Neurobiology of disease

2007 Volume 29, Issue 2, Page(s) 169–175

Abstract: Studies show increased oxidative damage in the brains of subjects with Alzheimer's disease (AD) and mild cognitive impairment (MCI). To determine if RNA oxidation occurs in MCI, sections of hippocampus/parahippocampal gyrus (HPG) from 5 MCI, 5 late stage ...

Abstract	Studies show increased oxidative damage in the brains of subjects with Alzheimer's disease (AD) and mild cognitive impairment (MCI). To determine if RNA oxidation occurs in MCI, sections of hippocampus/parahippocampal gyrus (HPG) from 5 MCI, 5 late stage AD (LAD) and 5 age-matched normal control (NC) subjects were subjected to immunohistochemistry using antibodies against 8-hydroxyguanine (8-OHG) and 1-N2-propanodeoxyguanosine (NPrG). Confocal microscopy showed 8-OHG and NPrG immunostaining was significantly (p<0.05) elevated in MCI and LAD HPG compared with NC subjects and was predominately associated with neurons identified using the MC-1 antibody that recognizes conformational alterations of tau, which are associated with early neurofibrillary tangle formation. Pretreating sections with RNase or DNase-I showed immunostaining for both adducts was primarily associated with RNA. In addition, levels of both adducts in MCI were comparable to those measured in LAD, suggesting RNA oxidation may be an early event in the pathogenesis of neuron degeneration in AD.
MeSH term(s)	Adenosine Triphosphatases/metabolism ; Aged, 80 and over ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Analysis of Variance ; Brain/metabolism ; Brain/pathology ; Cation Transport Proteins/metabolism ; Cognition Disorders/genetics ; Cognition Disorders/metabolism ; Cognition Disorders/pathology ; Copper-Transporting ATPases ; Deoxyguanosine/metabolism ; Female ; Guanine/analogs & derivatives ; Guanine/metabolism ; Humans ; Male ; Microscopy, Confocal ; Oxidation-Reduction ; Oxidative Stress ; Postmortem Changes ; RNA/metabolism ; Statistics, Nonparametric
Chemical Substances	Cation Transport Proteins ; 8-hydroxyguanine (5614-64-2) ; Guanine (5Z93L87A1R) ; RNA (63231-63-0) ; Adenosine Triphosphatases (EC 3.6.1.-) ; ATP7A protein, human (EC 7.2.2.8) ; Copper-Transporting ATPases (EC 7.2.2.8) ; Deoxyguanosine (G9481N71RO)
Language	English
Publishing date	2007-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2007.07.030
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Zs.A 4444: Show issues

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Article ; Online: Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer's disease.

Lovell, Mark A / Markesbery, William R

Nucleic acids research

2007 Volume 35, Issue 22, Page(s) 7497–7504

Abstract: Increasing evidence supports a role for oxidative DNA damage in aging and several neurodegenerative diseases including Alzheimer's disease (AD). Attack of DNA by reactive oxygen species (ROS), particularly hydroxyl radicals, can lead to strand breaks, ... ...

Abstract	Increasing evidence supports a role for oxidative DNA damage in aging and several neurodegenerative diseases including Alzheimer's disease (AD). Attack of DNA by reactive oxygen species (ROS), particularly hydroxyl radicals, can lead to strand breaks, DNA-DNA and DNA-protein cross-linking, and formation of at least 20 modified bases adducts. In addition, alpha,beta-unsaturated aldehydic by-products of lipid peroxidation including 4-hydroxynonenal and acrolein can interact with DNA bases leading to the formation of bulky exocyclic adducts. Modification of DNA bases by direct interaction with ROS or aldehydes can lead to mutations and altered protein synthesis. Several studies of DNA base adducts in late-stage AD (LAD) brain show elevations of 8-hydroxyguanine (8-OHG), 8-hydroxyadenine (8-OHA), 5-hydroxycytosine (5-OHC), and 5-hydroxyuracil, a chemical degradation product of cytosine, in both nuclear and mitochondrial DNA (mtDNA) isolated from vulnerable regions of LAD brain compared to age-matched normal control subjects. Previous studies also show elevations of acrolein/guanine adducts in the hippocampus of LAD subjects compared to age-matched controls. In addition, studies of base excision repair show a decline in repair of 8-OHG in vulnerable regions of LAD brain. Our recent studies show elevated 8-OHG, 8-OHA, and 5,6-diamino-5-formamidopyrimidine in both nuclear and mtDNA isolated from vulnerable brain regions in amnestic mild cognitive impairment, the earliest clinical manifestation of AD, suggesting that oxidative DNA damage is an early event in AD and is not merely a secondary phenomenon.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Cognition Disorders/diagnosis ; Cognition Disorders/genetics ; DNA/chemistry ; DNA/metabolism ; DNA Damage ; DNA Repair ; Humans ; Oxidation-Reduction ; Oxidative Stress
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2007-10-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkm821
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Article: Amyloid beta peptide, 4-hydroxynonenal and apoptosis.

Lovell, Mark A / Markesbery, William R

Current Alzheimer research

2006 Volume 3, Issue 4, Page(s) 359–364

Abstract: Considerable evidence suggests a role for oxidative stress in the pathogenesis of neuron degeneration in several neurodegenerative disorders including Alzheimer's disease (AD). Although debated, increasing evidence suggests that oxidative stress/damage ( ... ...

Abstract	Considerable evidence suggests a role for oxidative stress in the pathogenesis of neuron degeneration in several neurodegenerative disorders including Alzheimer's disease (AD). Although debated, increasing evidence suggests that oxidative stress/damage (amyloid beta peptide, iron/hydrogen peroxide) or neurotoxic by-products of lipid peroxidation (4-hydroxy-2-nonenal, acrolein) lead to cell death through apoptosis or programmed cell death in AD. This review discusses current evidence supporting the role of oxidative stress/damage mediated apoptosis in in vitro models of neurodegeneration.
MeSH term(s)	Aldehydes/metabolism ; Aldehydes/toxicity ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Peptides/toxicity ; Animals ; Apoptosis/physiology ; Brain/metabolism ; Brain/physiopathology ; Cells, Cultured/metabolism ; Humans ; Lipid Peroxidation/physiology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/physiopathology ; Neurons/metabolism ; Neurons/pathology ; Oxidative Stress/physiology
Chemical Substances	Aldehydes ; Amyloid beta-Peptides ; 4-hydroxy-2-nonenal (K1CVM13F96)
Language	English
Publishing date	2006-08-25
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2205170-3
ISSN	1567-2050
ISSN	1567-2050
DOI	10.2174/156720506778249506
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Article: DNA oxidation in Alzheimer's disease.

Markesbery, William R / Lovell, Mark A

Antioxidants & redox signaling

2006 Volume 8, Issue 11-12, Page(s) 2039–2045

Abstract: Oxidative damage to DNA may play an important role in aging and neurodegenerative diseases such as Alzheimer's disease (AD). Attack on DNA by reactive oxygen species, particularly hydroxyl radicals, can lead to strand breaks, DNA-DNA and DNA-protein ... ...

Abstract	Oxidative damage to DNA may play an important role in aging and neurodegenerative diseases such as Alzheimer's disease (AD). Attack on DNA by reactive oxygen species, particularly hydroxyl radicals, can lead to strand breaks, DNA-DNA and DNA-protein cross-linking, sister chromatid exchange and translocation, and formation of at least 20 oxidized base adducts. Modification of DNA bases can lead to mutation and altered protein synthesis. In late-stage AD brain, several studies have shown an elevation of the base adducts 8 hydroxyguanine (8-OHG), 8-hydroxyadenine (8-OHA), 5-hydroxycytosine (5-OHC), and 5-hydroxyuracil, a chemical degradation product of cytosine. Several studies have shown a decline in repair of 8-OHG in AD. Most recently, our studies have shown elevated 8-OHG, 8-OHA, and 5,6-diamino-5-formamidopyrimidine in nuclear and mitochondrial DNA in mild cognitive impairment, the earliest detectable form of AD, suggesting that oxidative damage to DNA is an early event in AD and not a secondary phenomenon.
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/chemistry ; Adenine/metabolism ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Cytosine/analogs & derivatives ; Cytosine/chemistry ; Cytosine/metabolism ; DNA/chemistry ; DNA/metabolism ; DNA Damage ; DNA Repair ; Guanine/analogs & derivatives ; Guanine/chemistry ; Guanine/metabolism ; Humans ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism ; Uracil/analogs & derivatives ; Uracil/chemistry ; Uracil/metabolism
Chemical Substances	Reactive Oxygen Species ; 8-hydroxyadenine (21149-26-8) ; 5-hydroxyuracil (496-76-4) ; 8-hydroxyguanine (5614-64-2) ; Uracil (56HH86ZVCT) ; Guanine (5Z93L87A1R) ; 5-hydroxycytosine (75321-30-1) ; Cytosine (8J337D1HZY) ; DNA (9007-49-2) ; Adenine (JAC85A2161)
Language	English
Publishing date	2006-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2006.8.2039
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