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Article: Editorial: Oxidative Stress in Myocardial and Neural Remodeling.

Nguyen, Thao P / Frautschy, Sally A / Eghbali, Mansoureh

2021 Volume 12, Page(s) 606484

Language	English
Publishing date	2021-02-05
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.606484
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Article ; Online: The Chronic Effects of a Single Low-Intensity Blast Exposure on Phosphoproteome Networks and Cognitive Function Influenced by Mutant Tau Overexpression.

Jackson, Marcus / Chen, Shanyan / Nguyen, Thao Thi / Siedhoff, Heather R / Balderrama, Ashley / Zuckerman, Amitai / Li, Runting / Greenlief, C Michael / Cole, Gregory / Frautschy, Sally A / Cui, Jiankun / Gu, Zezong

International journal of molecular sciences

2024 Volume 25, Issue 6

Abstract: Blast-induced neurotrauma (BINT) is a pressing concern for veterans and civilians exposed to explosive devices. Affected personnel may have increased risk for long-term cognitive decline and developing tauopathies including Alzheimer's disease-related ... ...

Abstract	Blast-induced neurotrauma (BINT) is a pressing concern for veterans and civilians exposed to explosive devices. Affected personnel may have increased risk for long-term cognitive decline and developing tauopathies including Alzheimer's disease-related disorders (ADRD) or frontal-temporal dementia (FTD). The goal of this study was to identify the effect of BINT on molecular networks and their modulation by mutant tau in transgenic (Tg) mice overexpressing the human tau P301L mutation (rTg4510) linked to FTD or non-carriers. The primary focus was on the phosphoproteome because of the prominent role of hyperphosphorylation in neurological disorders. Discrimination learning was assessed following injury in the subsequent 6 weeks, using the automated home-cage monitoring CognitionWall platform. At 40 days post injury, label-free phosphoproteomics was used to evaluate molecular networks in the frontal cortex of mice. Utilizing a weighted peptide co-expression network analysis (WpCNA) approach, we identified phosphopeptide networks tied to associative learning and mossy-fiber pathways and those which predicted learning outcomes. Phosphorylation levels in these networks were inversely related to learning and linked to synaptic dysfunction, cognitive decline, and dementia including Atp6v1a and Itsn1. Low-intensity blast (LIB) selectively increased pSer262tau in rTg4510, a site implicated in initiating tauopathy. Additionally, individual and group level analyses identified the Arhgap33 phosphopeptide as an indicator of BINT-induced cognitive impairment predominantly in rTg4510 mice. This study unveils novel interactions between ADRD genetic susceptibility, BINT, and cognitive decline, thus identifying dysregulated pathways as targets in potential precision-medicine focused therapeutics to alleviate the disease burden among those affected by BINT.
MeSH term(s)	Mice ; Humans ; Animals ; tau Proteins/genetics ; tau Proteins/metabolism ; Frontotemporal Dementia/genetics ; Phosphopeptides ; Tauopathies/metabolism ; Mice, Transgenic ; Cognition ; Disease Models, Animal
Chemical Substances	tau Proteins ; Phosphopeptides
Language	English
Publishing date	2024-03-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25063338
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Article ; Online: Thinking outside the box about COX-1 in Alzheimer's disease.

Frautschy, Sally A

Neurobiology of disease

2010 Volume 38, Issue 3, Page(s) 492–494

Abstract: This article from Coma et al. shows that a salicylic acid derivative Triflusal, a platelet aggregation inhibitor and irreversible inhibitor of COX-1, can correct defects in axonal curvature and cognition in an AD transgenic mouse model (Tg2576) (Coma et ... ...

Abstract	This article from Coma et al. shows that a salicylic acid derivative Triflusal, a platelet aggregation inhibitor and irreversible inhibitor of COX-1, can correct defects in axonal curvature and cognition in an AD transgenic mouse model (Tg2576) (Coma et al., 2010). Here we discuss the controversy over the role of COX-1 in AD, which has not been considered carefully in part due to the presumed adverse gastrointestinal effects of COX-1 antagonism. However, recent clinical data from this group as well as other groups challenges this assumption that COX-1 antagonism will be associated with side effects. Most importantly this article raises critical questions about the role of COX-1, versus COX-2 versus both in Abeta pathogenesis. The animal model data in this article as well as the recently published trial data suggest that COX-1 may play an important role in early pathogenesis and should not be ignored as a potential target for early intervention.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/immunology ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Central Nervous System Agents/adverse effects ; Central Nervous System Agents/therapeutic use ; Cognition Disorders/drug therapy ; Cognition Disorders/immunology ; Cognition Disorders/metabolism ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/therapeutic use ; Disease Models, Animal ; Humans ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/metabolism ; Mice ; Salicylates/adverse effects ; Salicylates/therapeutic use
Chemical Substances	Amyloid beta-Peptides ; Central Nervous System Agents ; Cyclooxygenase 2 Inhibitors ; Membrane Proteins ; Salicylates ; triflusal (1Z0YFI05OO) ; Cyclooxygenase 1 (EC 1.14.99.1) ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS1 protein, human (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Ptgs1 protein, mouse (EC 1.14.99.1)
Language	English
Publishing date	2010-06
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2010.02.009
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Article ; Online: What was lost in translation in the DHA trial is whom you should intend to treat.

Frautschy, Sally A / Cole, Greg M

Alzheimer's research & therapy

2011 Volume 3, Issue 1, Page(s) 2

Abstract: The results of a randomized double-blind placebocontrolled trial with docosahexaenoic acid (DHA) supplementation in mild to moderate Alzheimer's disease (AD) published by Quinn and colleagues in JAMA argues against overall efficacy of DHA in slowing ... ...

Abstract	The results of a randomized double-blind placebocontrolled trial with docosahexaenoic acid (DHA) supplementation in mild to moderate Alzheimer's disease (AD) published by Quinn and colleagues in JAMA argues against overall efficacy of DHA in slowing progression. However, certain caveats in the results caution against discarding DHA altogether, raising questions about oxidation, dosage, pharmacogenomics and stage of intervention.One potential misconception is that what works for prevention will slow progression in AD subjects.Preclinical studies with DHA supported the rationale for early stage intervention; and three epidemiological studies indicated DHA intake was associated with reduced risk in non-apolipoprotein E4 (ApoE4) carriers. Putative drugs are initially tested for impact on progression because prevention approaches are problematic. However, should a drug be discarded for prevention if it fails to modify progression? Consistent with epidemiology, DHA significantly benefited two measures of cognition in mild to moderate non-ApoE4 carriers. Although the results of this trial were overall negative, failing to modify other outcomes, this commentary discusses important questions raised by them. Should future trials pursue DHA in non-ApoE4 carriers for slowing progression? Since in vivo oxidation of DHA may have adverse effects, particularly in ApoE4 patients, should preclinical and clinical studies be performed to optimize dose and mitigate oxidation before pursuing intervention or prevention trials with DHA? And finally, should DHA be tested now for mild cognitive impairment or prevention?
Language	English
Publishing date	2011-01-20
Publishing country	England
Document type	Editorial
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/alzrt61
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Article ; Online: DHA may prevent age-related dementia.

Cole, Greg M / Frautschy, Sally A

The Journal of nutrition

2010 Volume 140, Issue 4, Page(s) 869–874

Abstract: The risk for dementia, a major contributor to incapacitation and institutionalization, rises rapidly as we age, doubling every 5 y after age 65. Tens of millions of new Alzheimer's disease (AD) and other dementia cases are projected as elderly ... ...

Abstract	The risk for dementia, a major contributor to incapacitation and institutionalization, rises rapidly as we age, doubling every 5 y after age 65. Tens of millions of new Alzheimer's disease (AD) and other dementia cases are projected as elderly populations increase around the world, creating a projected dementia epidemic for which most nations are not prepared. Thus, there is an urgent need for prevention approaches that are safe, effective, and affordable. This review addresses the potential of one promising candidate, the (n-3) fatty acid docosahexaenoic acid (DHA), which appears to slow pathogenesis of AD and possibly vascular dementia. DHA is pleiotropic, acting at multiple steps to reduce the production of the beta-amyloid peptide, widely believed to initiate AD. DHA moderates some of the kinases that hyperphosphorylate the tau-protein, a component of the neurofibrillary tangle. DHA may help suppress insulin/neurotrophic factor signaling deficits, neuroinflammation, and oxidative damage that contribute to synaptic loss and neuronal dysfunction in dementia. Finally, DHA increases brain levels of neuroprotective brain-derived neurotrophic factor and reduces the (n-6) fatty acid arachidonate and its prostaglandin metabolites that have been implicated in promoting AD. Clinical trials suggest that DHA or fish oil alone can slow early stages of progression, but these effects may be apolipoprotein E genotype specific, and larger trials with very early stages are required to prove efficacy. We advocate early intervention in a prodromal period with nutrigenomically defined subjects with an appropriately designed nutritional supplement, including DHA and antioxidants.
MeSH term(s)	Aged ; Aging ; Dementia/metabolism ; Dementia/prevention & control ; Docosahexaenoic Acids/administration & dosage ; Docosahexaenoic Acids/pharmacology ; Humans
Chemical Substances	Docosahexaenoic Acids (25167-62-8)
Language	English
Publishing date	2010-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	218373-0
ISSN	1541-6100 ; 0022-3166
ISSN (online)	1541-6100
ISSN	0022-3166
DOI	10.3945/jn.109.113910
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Article ; Online: Why pleiotropic interventions are needed for Alzheimer's disease.

Frautschy, Sally A / Cole, Greg M

Molecular neurobiology

2010 Volume 41, Issue 2-3, Page(s) 392–409

Abstract: Alzheimer's disease (AD) involves a complex pathological cascade thought to be initially triggered by the accumulation of beta-amyloid (Abeta) peptide aggregates or aberrant amyloid precursor protein (APP) processing. Much is known of the factors ... ...

Abstract	Alzheimer's disease (AD) involves a complex pathological cascade thought to be initially triggered by the accumulation of beta-amyloid (Abeta) peptide aggregates or aberrant amyloid precursor protein (APP) processing. Much is known of the factors initiating the disease process decades prior to the onset of cognitive deficits, but an unclear understanding of events immediately preceding and precipitating cognitive decline is a major factor limiting the rapid development of adequate prevention and treatment strategies. Multiple pathways are known to contribute to cognitive deficits by disruption of neuronal signal transduction pathways involved in memory. These pathways are altered by aberrant signaling, inflammation, oxidative damage, tau pathology, neuron loss, and synapse loss. We need to develop stage-specific interventions that not only block causal events in pathogenesis (aberrant tau phosphorylation, Abeta production and accumulation, and oxidative damage), but also address damage from these pathways that will not be reversed by targeting prodromal pathways. This approach would not only focus on blocking early events in pathogenesis, but also adequately correct for loss of synapses, substrates for neuroprotective pathways (e.g., docosahexaenoic acid), defects in energy metabolism, and adverse consequences of inappropriate compensatory responses (aberrant sprouting). Monotherapy targeting early single steps in this complicated cascade may explain disappointments in trials with agents inhibiting production, clearance, or aggregation of the initiating Abeta peptide or its aggregates. Both plaque and tangle pathogenesis have already reached AD levels in the more vulnerable brain regions during the "prodromal" period prior to conversion to "mild cognitive impairment (MCI)." Furthermore, many of the pathological events are no longer proceeding in series, but are going on in parallel. By the MCI stage, we stand a greater chance of success by considering pleiotropic drugs or cocktails that can independently limit the parallel steps of the AD cascade at all stages, but that do not completely inhibit the constitutive normal functions of these pathways. Based on this hypothesis, efforts in our laboratories have focused on the pleiotropic activities of omega-3 fatty acids and the anti-inflammatory, antioxidant, and anti-amyloid activity of curcumin in multiple models that cover many steps of the AD pathogenic cascade (Cole and Frautschy, Alzheimers Dement 2:284-286, 2006).
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Alzheimer Disease/therapy ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/metabolism ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Clinical Trials as Topic ; Curcumin/metabolism ; Curcumin/therapeutic use ; Docosahexaenoic Acids/metabolism ; Docosahexaenoic Acids/therapeutic use ; Down Syndrome/genetics ; Energy Metabolism ; Enzyme Inhibitors/metabolism ; Enzyme Inhibitors/therapeutic use ; Humans ; Peptide Fragments/genetics ; Peptide Fragments/metabolism ; Signal Transduction/physiology ; tau Proteins/genetics ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Anti-Inflammatory Agents, Non-Steroidal ; Enzyme Inhibitors ; Peptide Fragments ; amyloid beta-protein (1-42) ; tau Proteins ; Docosahexaenoic Acids (25167-62-8) ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2010-05-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-010-8137-1
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Article ; Online: Mechanisms of action of non-steroidal anti-inflammatory drugs for the prevention of Alzheimer's disease.

Cole, Greg M / Frautschy, Sally A

CNS & neurological disorders drug targets

2009 Volume 9, Issue 2, Page(s) 140–148

Abstract: Alzheimer's disease (AD) is accompanied by an activation of the innate immune system, and many epidemiological studies have shown reduced risk for dementia or AD associated with chronic consumption of non-steroidal anti-inflammatory drugs (NSAIDs). These ...

Abstract	Alzheimer's disease (AD) is accompanied by an activation of the innate immune system, and many epidemiological studies have shown reduced risk for dementia or AD associated with chronic consumption of non-steroidal anti-inflammatory drugs (NSAIDs). These observations led to animal model studies to test the hypothesis that NSAIDs can be disease-modifying for some aspects of AD pathogenesis. NSAIDs cannot only suppress inflammatory targets, which could contribute to neuroprotection, they also slow amyloid deposition by mechanisms that remain unclear. Several large clinical trials with NSAID therapies with AD subjects have failed, and cyclooxygenase-2 does not appear to be a useful target for disease modifying therapy. However, there may be apolipoprotein E E4 pharmacogenomic effects and a real but delayed positive signal in a large primary prevention trial with naproxen. This encourages researchers to re-address possible mechanisms for a stage-dependent NSAID efficacy, the subject of this review.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/physiopathology ; Alzheimer Disease/prevention & control ; Amyloid beta-Peptides/antagonists & inhibitors ; Amyloid beta-Peptides/metabolism ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Apolipoprotein E4/antagonists & inhibitors ; Apolipoprotein E4/metabolism ; Brain/drug effects ; Brain/metabolism ; Brain/physiopathology ; Brain Chemistry/drug effects ; Brain Chemistry/physiology ; Clinical Trials as Topic ; Cyclooxygenase 2 Inhibitors/pharmacology ; Cyclooxygenase 2 Inhibitors/therapeutic use ; Disease Models, Animal ; Encephalitis/drug therapy ; Encephalitis/physiopathology ; Encephalitis/prevention & control ; Humans ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use
Chemical Substances	Amyloid beta-Peptides ; Anti-Inflammatory Agents, Non-Steroidal ; Apolipoprotein E4 ; Cyclooxygenase 2 Inhibitors ; Neuroprotective Agents
Language	English
Publishing date	2009-08-07
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2228394-8
ISSN	1996-3181 ; 1871-5273
ISSN (online)	1996-3181
ISSN	1871-5273
DOI	10.2174/187152710791011991
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Article ; Online: Commentary on "Cytoskeletal modulators and pleiotropic strategies for Alzheimer drug discovery." Pleiotropic approaches to Alzheimer's and other diseases of aging.

Cole, Greg M / Frautschy, Sally A

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

2009 Volume 2, Issue 4, Page(s) 284–286

Language	English
Publishing date	2009-07-09
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.2006.08.006
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Article ; Online: Apolipoprotein E isotype-dependent modulation of microRNA-146a in plasma and brain.

Teter, Bruce / LaDu, Mary Jo / Sullivan, Patrick M / Frautschy, Sally A / Cole, Greg M

Neuroreport

2016 Volume 27, Issue 11, Page(s) 791–795

Abstract: The Apolipoprotein E (ApoE) isotype ApoE4 is a prevalent genetic risk factor for Alzheimer's disease (AD) that can modulate systemic and central inflammation, independent of amyloid accumulation. Although disruption of innate immune toll receptor ... ...

Abstract	The Apolipoprotein E (ApoE) isotype ApoE4 is a prevalent genetic risk factor for Alzheimer's disease (AD) that can modulate systemic and central inflammation, independent of amyloid accumulation. Although disruption of innate immune toll receptor signaling is modulated by ApoE and observed in AD, ApoE isotype-specific effects remain poorly understood. Therefore, we examined the effect of the ApoE isotype on the brain levels of major regulators of TLR signaling including miR146a, a microRNA enriched in the brain. We used 6-month-old ApoE3 or ApoE4 targeted replacement mice with and without mutant familial AD transgenes. ApoE4 reduced the levels of miR146a compared with ApoE3, both in the brain (29%; P<0.0001) and in plasma (47%; P<0.05), which correlated with each other (r=0.74; P<0.05). The presence of 5xFAD transgenes increased brain miR146a in both ApoE3 (E3FAD) and ApoE4 (E4FAD) mice; however, miR146a levels in E4FAD mice remained lower than those in E3FAD mice (62%; P<0.05), despite increased amyloid and inflammation. Supporting these observations, ApoE4 brains showed increased expression of interleukin receptor-associated kinase-1 (160%; P<0.05) (normally downregulated by miR146) that correlated inversely with miR146a levels (r=0.637; P<0.0001). Reduced negative feedback of toll-like receptor signaling (by miRNA146a) can explain early-life hypersensitivity to innate immune stimuli (including Aβ) in ApoE4 carriers. Thus, ApoE4 causes early dysregulation of a central controller of the innate immune system both centrally and systemically. This defect persists with familial AD pathology and may be relevant to ApoE4 AD risk.
Language	English
Publishing date	2016-08-03
Publishing country	England
Document type	Journal Article
ZDB-ID	1049746-8
ISSN	1473-558X ; 0959-4965
ISSN (online)	1473-558X
ISSN	0959-4965
DOI	10.1097/WNR.0000000000000608
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Article: A sensitive LC-MS assay using derivatization with boron trifluoride to quantify curcuminoids in biological samples

Yoon, Alexander J / Wu, Haiqiang / Pan, Roy D / Teter, Bruce / Cipolla, Jack / Chang, Edwin / Avila, Luis Z / Basak, Saroj K / Srivatsan, Eri S / Wang, Marilene B / Cole, Greg M / Frautschy, Sally A / Hampton, Phillip D / Faull, Kym F

Analytical biochemistry. 2020 May 01, v. 596

2020

Abstract: A procedure is described to measure curcumin (C), demethoxycurcumin (DMC), bisdemethoxycurcumin (BDMC), tetrahydrocurcumim (TC) and their glucuronidated metabolites (CG, DMCG, and BDMCG) in plasma, brain, liver and tumor samples. The procedure involves ... ...

Abstract	A procedure is described to measure curcumin (C), demethoxycurcumin (DMC), bisdemethoxycurcumin (BDMC), tetrahydrocurcumim (TC) and their glucuronidated metabolites (CG, DMCG, and BDMCG) in plasma, brain, liver and tumor samples. The procedure involves converting the analytes to their boron difluoride derivatives and analyzing them by combined liquid chromatography coupled to an ion trap mass spectrometer operating in the negative ion MSn scan mode. The method has superb limits of detection of 0.01 nM for all curcuminoids and 0.5 nM for TC and the glucuroniated metabolites, and several representative chromatograms of biological samples containing these analytes are provided. In addition, the pharmacokinetic profile of these compounds in one human who daily consumed an over-the-counter curcuminoid product shows the peak and changes in circulating concentrations achieved by this mode of administration.
Keywords	blood plasma ; boron ; brain ; chemical species ; curcumin ; derivatization ; detection limit ; humans ; liquid chromatography ; liver ; mass spectrometry ; metabolites ; neoplasms ; pharmacokinetics ; spectrometers
Language	English
Dates of publication	2020-0501
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1110-1
ISSN	1096-0309 ; 0003-2697
ISSN (online)	1096-0309
ISSN	0003-2697
DOI	10.1016/j.ab.2020.113636
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