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1. Synaptic density is correlated with Aβ plaques and neurofibrillary tau tangles across the clinical and biologic Alzheimer’s disease continuum

Author

DiFilippo, Alexandra H, primary, McLachlan, Max, additional, McVea, Andrew K, additional, Bettcher, Brecca, additional, Jonaitis, Erin M., additional, Ennis, Gilda E., additional, Pasquesi, Mary‐Elizabeth, additional, Davenport, Nancy J, additional, Thor, Yer, additional, Grover, Ethan, additional, Hudson, Sarah, additional, Barnhart, Todd E, additional, Engle, Jonathan W, additional, Betthauser, Tobey J, additional, Johnson, Sterling C, additional, Bendlin, Barbara B, additional, and Christian, Bradley T., additional

Published
2023
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2. Regional correlation analysis between neuronal metabolism and synaptic density using [18F]FDG and [11C]UCB‐J

Author

DiFilippo, Alexandra H, primary, McLachlan, Max, additional, Jonaitis, Erin M., additional, Ennis, Gilda E., additional, McVea, Andrew K, additional, Bettcher, Brecca, additional, Pasquesi, Mary‐Elizabeth, additional, Thor, Yer, additional, Davenport, Nancy J, additional, Grover, Ethan, additional, Hudson, Sarah, additional, Barnhart, Todd E, additional, Betthauser, Tobey J, additional, Engle, Jonathan W, additional, Johnson, Sterling C, additional, Bendlin, Barbara B, additional, and Christian, Bradley T., additional

Published
2023
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3. Lower synaptic density and higher neurofibrillary tau are associated with worse cognitive performance

Author

DiFilippo, Alexandra H, primary, Xin, Yangchun, additional, Jonaitis, Erin M., additional, Kohli, Akshay, additional, Ennis, Gilda E., additional, McVea, Andrew K, additional, McLachlan, Max, additional, Pasquesi, Mary‐Elizabeth, additional, Davenport, Nancy J, additional, Betthauser, Tobey J, additional, Barnhart, Todd E, additional, Engle, Jonathan W, additional, Johnson, Sterling C., additional, Bendlin, Barbara B., additional, and Christian, Bradley T, additional

Published
2022
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4. Regional correlation analysis between neuronal metabolism and synaptic density using [18F]FDG and [11C]UCB‐J.

Author

DiFilippo, Alexandra H, McLachlan, Max, Jonaitis, Erin M., Ennis, Gilda E., McVea, Andrew K, Bettcher, Brecca, Pasquesi, Mary‐Elizabeth, Thor, Yer, Davenport, Nancy J, Grover, Ethan, Hudson, Sarah, Barnhart, Todd E, Betthauser, Tobey J, Engle, Jonathan W, Johnson, Sterling C, Bendlin, Barbara B, and Christian, Bradley T.

Abstract

Background: Neuronal hypometabolism measured with [18F]FDG PET scans can be used to identify neurodegeneration as part of the AT(N) (amyloid, tau, neurodegeneration) framework in AD. PET imaging of synaptic vesicle glycoprotein SV2A using [11C]UCB‐J provides an index of synaptic density, which has been shown to decrease during neurodegeneration. The purpose of this study was to examine the regional relationship between neuronal metabolism and synaptic density in participants across the continuum of AD‐related pathology. Method: Participants were recruited from the Wisconsin ADRC and the Wisconsin Registry for Alzheimer's Prevention (WRAP) study. A subset of 13 participants (Table 1) were selected who had completed cognitive testing, structural MR imaging, and PET imaging with the following: [11C]PiB centiloid (CL) for amyloid +/‐ status, [18F]MK‐6240 SUVR for tau +/‐ status, [11C]UCB‐J DVR for regional synaptic density burden, and [18F]FDG SUVR for regional glucose metabolism. UCB‐J and FDG analysis used a whole cerebellum reference region; PiB and MK‐6240 analysis used cerebellar GM reference regions. Inter‐tracer (UCB‐J/FDG) correlations were performed in Freesurfer‐defined bilateral Braak‐associated ROIs (Medial Temporal Lobe [MTL]: entorhinal cortex, hippocampus, and amygdala; Ventral Temporal Lobe [VTL]: fusiform, lingual, and inferior temporal gyri), signature regions of hypometabolism in AD (posterior cingulate, parietal, and frontal cortices) and a region with only marginal hypometabolism in AD (occipital cortex). Associations were determined using Pearson correlations (r). Result: All ROIs demonstrate a positive association between FDG SUVR and UCB‐J DVR, with r > 0.7 and p < 0.01 (Figure 1). The occipital, frontal, and posterior cingulate cortices demonstrate the strongest correlations (r = 0.84, 0.83, and 0.81, respectively). Conclusion: In cognitively impaired and unimpaired participants showing varying degrees of β‐amyloid and neurofibrillary tau burden, strong positive correlations are observed in regions associated with AD tau pathology and hypometabolism. Correlations are also observed in regions not typically associated with hypometabolism. This suggests that a relationship may exist between synaptic density and neuronal metabolism in the presence of AD neuropathology. [ABSTRACT FROM AUTHOR]

Published
2023
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6. In vivo analysis of synaptic degeneration with Aβ plaque and NFT accumulation in cognitive decline

Author

DiFilippo, Alexandra H., primary, Tullis, Tyler, additional, Zammit, Matthew D., additional, Murali, Dhanabalan, additional, Kohli, Akshay, additional, Ennis, Gilda E., additional, Davenport, Nancy J., additional, Barnhart, Todd E., additional, Engle, Jonathan W., additional, Betthauser, Tobey J., additional, Stone, Charles K., additional, Johnson, Sterling C., additional, Bendlin, Barbara B, additional, and Christian, Bradley T., additional

Published
2021
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7. Synaptic vesicle protein SV2A imaging with [11C]UCB‐J as a novel biomarker of neurodegeneration in Alzheimer's disease

Author

Bendlin, Barbara B, primary, DiFilippo, Alexandra H, additional, Betthauser, Tobey J, additional, Chin, Nathaniel A, additional, Murali, Dhanabalan, additional, Vogt, Nicholas M, additional, McKinney, Grace, additional, Davenport, Nancy J, additional, Barnhart, Todd E, additional, Engle, Jonathan W, additional, Johnson, Sterling C, additional, and Christian, Bradley T, additional

Published
2020
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10. Elevated Insulin and Insulin Resistance are Associated with Altered Myelin in Cognitively Unimpaired Middle‐Aged Adults

Author

O’Grady, J. Patrick, primary, Dean, Douglas C., additional, Yang, Kao Lee, additional, Canda, Cristybelle‐Marie, additional, Hoscheidt, Siobhan M., additional, Starks, Erika J., additional, Merluzzi, Andrew, additional, Hurley, Samuel, additional, Davenport, Nancy J., additional, Okonkwo, Ozioma C., additional, Anderson, Rozalyn M., additional, Asthana, Sanjay, additional, Johnson, Sterling C., additional, Alexander, Andrew L., additional, and Bendlin, Barbara B., additional

Published
2019
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12. P4‐375: CEREBRAL GLUCOSE UPTAKE DIFFERS BY LEVEL OF HOMA‐IR AND INSULIN SECRETION IN NONDIABETIC ADULTS

Author

Ennis, Gilda E., primary, Koscik, Rebecca L., additional, Davenport, Nancy J., additional, Taylor, Chase E., additional, Oh, Jennifer M., additional, Christian, Brad T., additional, Chin, Nathaniel A., additional, Asthana, Sanjay, additional, Johnson, Sterling C., additional, Okonkwo, Ozioma C., additional, and Bendlin, Barbara B., additional

Published
2018
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13. P1‐318: OBSTRUCTIVE SLEEP APNEA IS ASSOCIATED WITH LOWER MEMORY FUNCTION IN MIDDLE‐AGED ADULTS

Author

Derynda, Brittany R., primary, Shouel, Heather L., additional, Sprecher, Kate E., additional, Taylor, Chase E., additional, Davenport, Nancy J., additional, Carlsson, Cynthia M., additional, Bazalakova, Mihaela H., additional, Asthana, Sanjay, additional, Johnson, Sterling C., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Riedner, Brady A., additional, Benca, Ruth M., additional, and Bendlin, Barbara B., additional

Published
2018
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14. IC‐P‐089: OBSTRUCTIVE SLEEP APNEA IS ASSOCIATED WITH LOWER MEMORY FUNCTION IN MIDDLE‐AGED ADULTS

Author

Derynda, Brittany R., primary, Shouel, Heather L., additional, Sprecher, Kate E., additional, Taylor, Chase E., additional, Davenport, Nancy J., additional, Carlsson, Cynthia M., additional, Bazalakova, Mihaela H., additional, Asthana, Sanjay, additional, Johnson, Sterling C., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Riedner, Brady A., additional, Benca, Ruth M., additional, and Bendlin, Barbara B., additional

Published
2018
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15. Elevated Insulin and Insulin Resistance are Associated with Altered Myelin in Cognitively Unimpaired Middle-Aged Adults.

Author

O'Grady, J. Patrick, Dean, Douglas C., Yang, Kao Lee, Canda, Cristybelle‐Marie, Hoscheidt, Siobhan M., Starks, Erika J., Merluzzi, Andrew, Hurley, Samuel, Davenport, Nancy J., Okonkwo, Ozioma C., Anderson, Rozalyn M., Asthana, Sanjay, Johnson, Sterling C., Alexander, Andrew L., Bendlin, Barbara B., Dean, Douglas C 3rd, and Canda, Cristybelle-Marie

Subjects
MIDDLE-aged persons, MYELIN, INSULIN resistance, TYPE 2 diabetes, DISEASE risk factors, INSULIN, NERVE tissue, RESEARCH funding, NEURODEGENERATION
Abstract

Objective: Insulin regulates metabolism and influences neural health. Insulin resistance (IR) and type II diabetes have been identified as risk factors for Alzheimer disease (AD). Evidence has also suggested that myelinated white matter alterations may be involved in the pathophysiology of AD; however, it is unknown whether insulin or IR affect the underlying myelin microstructure. The relationships between insulin, IR, and myelin were examined, with the hypothesis that IR would be associated with reduced myelin.Methods: Cognitively unimpaired adults enriched for risk factors for AD underwent multicomponent driven equilibrium single pulse observation of T1 and T2 imaging, a myelin-sensitive neuroimaging technique. Linear regressions were used to test the relationship between homeostatic model assessment of IR, insulin, and myelin water fraction (MWF) as well as interactions with APOE ε4.Results: Both IR and insulin level were associated with altered myelin content, wherein a significant negative association with MWF was observed in white matter regions and a positive association with MWF was observed in gray matter.Conclusions: The results suggest that insulin and IR influence white matter myelination in a cognitively unimpaired population. Additional studies are needed to determine the extent to which this may contribute to cognitive decline or vulnerability to neurodegenerative disease. [ABSTRACT FROM AUTHOR]

Published
2019
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19. P3-156: Elevated cardiovascular risk is associated with altered myelin content

Author

Dean, Douglas C., primary, Sojkova, Jitka, additional, Hurley, Samuel, additional, O'Grady, Patrick, additional, Canda, Christybelle-Marie, additional, Burke, Katie-Grace, additional, Davenport, Nancy J., additional, Asthana, Sanjay, additional, Sager, Mark A., additional, Johnson, Sterling C., additional, Alexander, Andrew L., additional, and Bendlin, Barbara B., additional

Published
2015
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20. P4-264: Amyloid pathology is associated with extensive myelin alteration in preclinical Alzheimer's disease: New insights into disease process with novel brain imaging

Author

Dean, Douglas C., primary, Sojkova, Jitka, additional, Hurley, Samuel, additional, O'Grady, Patrick, additional, Canda, Christybelle-Marie, additional, Davenport, Nancy J., additional, DeRungs, LeAnn, additional, Carlsson, Cynthia M., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Sager, Mark A., additional, Asthana, Sanjay, additional, Johnson, Sterling C., additional, Alexander, Andrew L., additional, and Bendlin, Barbara B., additional

Published
2015
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21. IC-P-096: Insulin resistance is associated with altered microstructure in the medial temporal lobe and fornix of cognitively healthy APOE4 carriers

Author

Starks, Erika Jane, primary, O'Grady, Joseph Patrick, additional, Hoscheidt, Siobhan M., additional, Racine, Annie M., additional, Okonkwo, Ozioma C., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Carlsson, Cynthia M., additional, Rowley, Howard A., additional, Asthana, Sanjay, additional, Adluru, Nagesh, additional, Alexander, Andrew L., additional, Gleason, Carey E., additional, Dowling, N Maritza, additional, DeRungs, LeAnn, additional, Davenport, Nancy J., additional, Sager, Mark A., additional, Johnson, Sterling C., additional, and Bendlin, Barbara B., additional

Published
2015
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22. IC-P-128: Alterations in myelin content are related to cognitive performance in nondemented older adults: Findings from the wisconsin registry for Alzheimer's prevention study

Author

Sojkova, Jitka, primary, Dean, Douglas C., additional, Hurley, Samuel, additional, O'Grady, Patrick, additional, Canda, Cristybelle, additional, Davenport, Nancy J., additional, Asthana, Sanjay, additional, Sager, Mark A., additional, Johnson, Sterling C., additional, Gallagher, Catherine L., additional, Alexander, Andrew L., additional, and Bendlin, Barbara B., additional

Published
2015
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23. P1‐204: Insulin resistance is associated with altered microstructure in the medial temporal lobe and fornix of cognitively healthy ApoE ε4 carriers

Author

Starks, Erika Jane, primary, O'Grady, Joseph Patrick, additional, Hoscheidt, Siobhan M., additional, Racine, Annie M., additional, Okonkwo, Ozioma C., additional, Zetterberg, Henrik, additional, Carlsson, Cynthia M., additional, Rowley, Howard A., additional, Blennow, Kaj, additional, Asthana, Sanjay, additional, Adluru, Nagesh, additional, Alexander, Andrew L., additional, Gleason, Carey E., additional, Dowling, N. Maritza, additional, DeRungs, LeAnn, additional, Davenport, Nancy J., additional, Sager, Mark A., additional, Johnson, Sterling C., additional, and Bendlin, Barbara B., additional

Published
2015
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24. P1-199: ApoE-e4 is associated with altered myelin content in preclinical ad

Author

Dean, Douglas C., primary, Sojkova, Jitka, additional, Hurley, Samuel, additional, O'Grady, Patrick, additional, Canda, Christybelle-Marie, additional, Davenport, Nancy J., additional, Asthana, Sanjay, additional, Sager, Mark A., additional, Johnson, Sterling C., additional, Alexander, Andrew L., additional, and Bendlin, Barbara B., additional

Published
2015
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28. Myocardial proteolysis during acute myocardial ischaemia.

Author

BOLLI, ROBERTO, DAVENPORT, NANCY J, GOLDSTEIN, ROBERT E, and EPSTEIN, STEPHEN E

Abstract

To investigate the role of cellular proteinases in acute myocardial infarction, we measured the rate of total proteolysis (ie, degradation of proteins to amino acids and oligopeptides) in slices obtained from nonischaemic myocardium, 1 h ischaemic endocardium, 3 h ischaemic epicardium, and 3 h ischaemic endocardium in open-chest dogs. Slices were incubated either in high pO2 or in low pO2 Krebs-Ringer-bicarbonate buffer with cycloheximide; proteolysis was estimated from tyrosine production. Tyrosine production in each of the ischaemic tissues incubated in low pO2 medium was lower than that in nonischaemic myocardium incubated in high pO2 medium. This suggests that proteolysis is inhibited during acute myocardial infarction both before (3 h ischaemic epicardium) and shortly after (1 h ischaemic endocardium, 3 h ischaemic endocardium) irreversible damage is believed to occur. Tyrosine production in 1 h and 3 h ischaemic endocardium was similar to that in 3 h ischaemic epicardium, indicating that no increase in proteolytic activity accompanies the progression of ischaemic damage from the phase of reversibility to that of presumed irreversibility. Ischaemic tissues did not exhibit a rebound increase in proteolysis when incubated in high pO2 medium, suggesting that reperfusion of acutely ischaemic myocardium is not associated with activation of proteolytic enzymes. Leupeptin, an inhibitor of thiol-proteinases, produced similar decreases of proteolysis in nonischaemic and ischaemic myocardium: thus, lysosomal thiol-proteinases (cathepsins B, L and H) do not appear to be activated in acute myocardial ischaemia. The data provide evidence that total proteolysis decreases throughout the phase of acute myocardial infarction during which irreversible injury develops, suggesting that cellular proteinases may not play a causal role in ischaemic myocellular death. [ABSTRACT FROM PUBLISHER]

Published
1983

31. Relative Effects of Sulfinpyrazone and Ibuprofen on Canine Platelet Function and ProstaglandinMediated Coronary Vasodilation

Author

Goldstein, Robert E., Davenport, Nancy J., Capurro, Norine L., Lipson, Lewis C., Bonow, Robert O., Shulman, N. Raphael, and Epstein, Stephen E.

Abstract

Recent evidence suggests that the platelet-inhibitory drugs sulfin-pyrazone and ibuprofen may have value in treatment of coronary artery disease. However, these drugs do not only block platelet aggregation, but also block synthesis by blood vessels of prostaglandins that promote vasodilation. Platelets may differ from blood vessels in their sensitivity to sulfinpyrazone or ibuprofen. In theory, optimal doses for coronary disease would inhibit potentially deleterious platelet aggregation but not interfere with synthesis of possibly beneficial vasodilator prostaglandins. To determine whether it was possible to identify such optimal doses we measured the effects of intravenous sulfinpyrazone, 0.3–100 mg/kg (n= 9), or sodium ibuprofen, 0.1–3 mg/kg (n= 7), on vasodilation induced by the protaglandin precursor arachidonic acid. We also assessed drug effects on in vitroplatelet aggregation in the same animals. Both sulfinpyrazone and ibuprofen caused a dose-related reduction in flow increment after arachidonic acid. Sulfinpyrazone, ≥10 mg/kg, and ibuprofen, ≥1 mg/kg, produced a mean reduction of least 60 (p< 0.02 for each) in the vasodilator response to 1 mg arachidonic acid. Sulfinpyrazone, 0.3 mg/kg, and ibuprofen, 0.1 mg/kg, had no consistent effects on flow. Flow rise after intracoronary prostaglandin E2was undiminished by sulfinpyrazone or ibuprofen. Sulfinpyrazone, ≥10 mg/kg, and ibuprofen, ≥1 mg/kg, markedly inhibited platelet aggregation induced by adenosine diphosphate, 2.3 x 10-5M (p< 0.01 for each). Sulfinpyrazone, 0.3 mg/kg, and ibuprofen, 0.1 mg/kg, failed to alter platelet aggregation. Hence, sulfinpyrazone and ibuprofen doses inhibiting platelet function also produced comparable inhibition of arachidonic acid-induced coronary vasodilation, presumably by interfering with arachidonic acid conversion to vasodilator prostaglandins. Neither sulfinpyrazone nor ibuprofen, administered acutely, appears to have an “optimal” dose that in

Published
1980

32. In Vivo Enhancement of Platelet Activating FactorInduced Prostacyclin Production by OKY046 a Selective Inhibitor of Thromboxane A2Synthase

Author

Davenport, Nancy J., Goldstein, Robert E., and Feuerstein, Giora Z.

Abstract

Platelet-activating factor (PAF) a likely mediator of endototin action. causes thromhovane A, (TXA2) release and pulmonary hypertension in pigs. We examined the effect of selective TXA2synthase inhihition with OKY 046 on cyclooxygenase metabolites during PAF-induced pulmonary hypertension. Sig closed-chest pigs received PAF in escalating doses (0.1, 0.3, and 3.0 nmol intravenously, i.v.) before and after (E)-3[4-(1-imidazolyl methyl) phenyl]-Z-propenoic acid hydrochloride monohydrate OKY-046. 10-mg kg i.v. bolus plus 20-mg kg h infusion. Plasma samples at peak PAF effect had radioimmunoassay (RAI) for the stahle metabolites of TXA2(TXB2) and prostacyclin (6-keto-PGF1α). Tachyphylaxis was not noted in 5 control pigs given sequential repeats of the PAF dosing series. Pulmonary vascular resistance (PVR) was 240 ± 30 (SE) dynesem at baseline and increased to 3.100 ± 1.300 alter 1.0 nmol PAF (p 0.05). When the same amount of PAF was given after OKY-046. PVR increased only to 820 ± 280 dynes 8 cm TXB2was 34 ± 7 pg 0.1 ml at baseline and increased to 70 ± 4 pg 0.1 ml with PAF 1.0 nmol (p 0.001). TXB2levels were unchanged from 34 ± 4 pg 0.1 ml when PAP 1.0 nmol was administered alter OKY-046 INS vs. pre-OKY-046). In contrast. 6-keto-PGF1α6 ± 2 pg 0.1 ml at baseline increased to 24 ± 4 pg 0.1 ml after PAF 1.0 nmol and increased further to 50 ± 4 pg 0.1 ml when PAF 1.0 nmol was given after OKY-046 (p 0.05 vs. pre-OKY-046). Thus, OKY-046 attenuation ofa PAF induced increase in PVR was associated with a 50 reduction in plasma TXB2and 100 increase in plasma 6-keto-PGF1α. The latter may reflect arachidonate shunting to prostacyclin production with dual beneficial effects at the site of PAF action: decrease in vasomotor tone, and dispersion of platelet aggregates.

Published
1991

34. Insulin resistance is associated with altered microstructure in the medial temporal lobe and fornix of cognitively healthy ApoE4 carriers.

Author

Starks, Erika Jane, O'Grady, Joseph Patrick, Hoscheidt, Siobhan M., Racine, Annie M., Okonkwo, Ozioma C., Zetterberg, Henrik, Blennow, Kaj, Carlsson, Cynthia M., Rowley, Howard A., Asthana, Sanjay, Adluru, Nagesh, Alexander, Andrew L., Gleason, Carey E., Dowling, N Maritza, DeRungs, LeAnn, Davenport, Nancy J., Sager, Mark A., Johnson, Sterling C., and Bendlin, Barbara B.

Published
2015
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35. Insulin resistance is associated with altered microstructure in the medial temporal lobe and fornix of cognitively healthy ApoE ε4 carriers.

Author

Starks, Erika Jane, O'Grady, Joseph Patrick, Hoscheidt, Siobhan M., Racine, Annie M., Okonkwo, Ozioma C., Zetterberg, Henrik, Carlsson, Cynthia M., Rowley, Howard A., Blennow, Kaj, Asthana, Sanjay, Adluru, Nagesh, Alexander, Andrew L., Gleason, Carey E., Dowling, N. Maritza, DeRungs, LeAnn, Davenport, Nancy J., Sager, Mark A., Johnson, Sterling C., and Bendlin, Barbara B.

Published
2015
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37. Amyloid pathology is associated with extensive myelin alteration in preclinical Alzheimer’s disease: New insights into disease process with novel brain imaging.

Author

IIIDean, Douglas C., Sojkova, Jitka, Hurley, Samuel, O'Grady, Patrick, Canda, Christybelle-Marie, Davenport, Nancy J., DeRungs, LeAnn, Carlsson, Cynthia M., Zetterberg, Henrik, Blennow, Kaj, Sager, Mark A., Asthana, Sanjay, Johnson, Sterling C., Alexander, Andrew L., and Bendlin, Barbara B.

Published
2015
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