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1. A randomized, double-blind, placebo-controlled trial of resveratrol for Alzheimer disease

Author

Turner, R Scott, Thomas, Ronald G, Craft, Suzanne, van Dyck, Christopher H, Mintzer, Jacobo, Reynolds, Brigid A, Brewer, James B, Rissman, Robert A, Raman, Rema, Aisen, Paul S, Study, For the Alzheimer's Disease Cooperative, Study, Alzheimer's Disease Cooperative, Mintzer, J, Reynolds, BA, Karlawish, J, Galasko, D, Heidebrink, J, Aggarwal, N, Graff-Radford, N, Sano, M, Petersen, R, Bell, K, Doody, R, Smith, A, Bernick, C, Porteinsson, A, Tariot, P, Mulnard, R, Lerner, A, Schneider, L, Burns, J, Raskind, M, Ferris, S, Jicha, G, Quiceno, M, Obisesan, T, Rosenberg, P, Weintraub, D, Kieburtz, K, Miller, B, Kryscio, R, and Alexopoulis, G

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Clinical Sciences, Neurodegenerative, Alzheimer's Disease, Acquired Cognitive Impairment, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Trials and Supportive Activities, Aging, Brain Disorders, Clinical Research, Digestive Diseases, Dementia, Complementary and Integrative Health, Neurosciences, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Neurological, Aged, Aged, 80 and over, Alzheimer Disease, Double-Blind Method, Female, Gastrointestinal Diseases, Humans, Male, Middle Aged, Resveratrol, Stilbenes, Alzheimer's Disease Cooperative Study, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveA randomized, placebo-controlled, double-blind, multicenter 52-week phase 2 trial of resveratrol in individuals with mild to moderate Alzheimer disease (AD) examined its safety and tolerability and effects on biomarker (plasma Aβ40 and Aβ42, CSF Aβ40, Aβ42, tau, and phospho-tau 181) and volumetric MRI outcomes (primary outcomes) and clinical outcomes (secondary outcomes).MethodsParticipants (n = 119) were randomized to placebo or resveratrol 500 mg orally once daily (with dose escalation by 500-mg increments every 13 weeks, ending with 1,000 mg twice daily). Brain MRI and CSF collection were performed at baseline and after completion of treatment. Detailed pharmacokinetics were performed on a subset (n = 15) at baseline and weeks 13, 26, 39, and 52.ResultsResveratrol and its major metabolites were measurable in plasma and CSF. The most common adverse events were nausea, diarrhea, and weight loss. CSF Aβ40 and plasma Aβ40 levels declined more in the placebo group than the resveratrol-treated group, resulting in a significant difference at week 52. Brain volume loss was increased by resveratrol treatment compared to placebo.ConclusionsResveratrol was safe and well-tolerated. Resveratrol and its major metabolites penetrated the blood-brain barrier to have CNS effects. Further studies are required to interpret the biomarker changes associated with resveratrol treatment.Classification of evidenceThis study provides Class II evidence that for patients with AD resveratrol is safe, well-tolerated, and alters some AD biomarker trajectories. The study is rated Class II because more than 2 primary outcomes were designated.

Published
2015

2. A blood-based signature of cerebrospinal fluid A beta(1-42) status

Author

Goudey, B., Fung, B.J., Schieber, C., Faux, N.G., Weiner, M.W., Aisen, P., Petersen, R., Jack, C.R., Jagust, W., Trojanowki, J.Q., Toga, A.W., Beckett, L., Green, R.C., Saykin, A.J., Morris, J., Shaw, L.M., Kaye, J., Quinn, J., Silbert, L., Lind, B., Carter, R., Dolen, S., Schneider, L.S., Pawluczyk, S., Beccera, M., Teodoro, L., Spann, B.M., Brewer, J., Vanderswag, H., Fleisher, A., Heidebrink, J.L., Lord, J.L., Mason, S.S., Albers, C.S., Knopman, D., Johnson, K., Doody, R.S., Villanueva-Meyer, J., Chowdhury, M., Rountree, S., Dang, M., Stern, Y., Honig, L.S., Bell, K.L., Ances, B., Morris, J.C., Carroll, M., Creech, M.L., Franklin, E., Mintun, M.A., Schneider, S., Oliver, A., Marson, D., Griffth, R., Clark, D., Geldmacher, D., Brockington, J., Roberson, E., Natelson Love, M., Grossman, H., Mitsis, E., Shah, R.C., deToledo-Morrell, L., Duara, R., Varon, D., Greig, M.T., Roberts, P., Albert, M., Onyike, C., D'Agostino, D., Kielb, S., Galvin, J.E., Cerbone, B., Michel, C.A., Pogorelec, D.M., Rusinek, H., Leon, M.J. de, Glodzik, L., De Santi, S., Doraiswamy, P.M., Petrella, J.R., Borges-Neto, S., Wong, T.Z., Coleman, E., Smith, C.D., Jicha, G., Hardy, P., Sinha, P., Oates, E., Conrad, G., Porsteinsson, A.P., Goldstein, B.S., Martin, K., Makino, K.M., Ismail, M.S., Brand, C., Mulnard, R.A., Thai, G., McAdams-Ortiz, C., Womack, K., Mathews, D., Quiceno, M., Levey, A.I., Lah, J.J., Cellar, J.S., Burns, J.M., Swerdlow, R.H., Brooks, W.M., Apostolova, L., Tingus, K., Woo, E., Silverman, D.H.S., Lu, P.H., Bartzokis, G., Graff-Radford, N.R., Parftt, F., Kendall, T., Johnson, H., Farlow, M.R., Hake, A.M., Matthews, B.R., Brosch, J.R., Herring, S., Hunt, C., Dyck, .H. van, Carson, R.E., MacAvoy, M.G., Varma, P., Chertkow, H., Bergman, H., Hosein, C., Black, S., Stefanovic, B., Caldwell, C., Hsiung, Ging-Yuek Robin, Feldman, H., Mudge, B., Assaly, M., Finger, E., Pasternack, S., Rachisky, I., Trost, D., Kertesz, A., Bernick, C., Munic, D., Mesulam, M.-M., Lipowski, K., Weintraub, S., Bonakdarpour, B., Kerwin, D., Wu, C.-K., Johnson, N., Sadowsky, C., Villena, T., Turner, R.S., Reynolds, B., Sperling, R.A., Johnson, K.A., Marshall, G., Yesavage, J., Taylor, J.L., Lane, B., Rosen, A., Tinklenberg, J., Sabbagh, M.N., Belden, C.M., Jacobson, S.A., Sirrel, S.A., Kowall, N., Killiany, R., Budson, A.E., Norbash, A., Johnson, P.L., Obisesan, T.O., Wolday, S., Allard, J., Lerner, A., Ogrocki, P., Tatsuoka, C., Fatica, P., Fletcher, E., Maillard, P., Olichney, J., DeCarli, C., Carmichael, O., Kittur, S., Borrie, M., Lee, T.-Y., Bartha, R., Johnson, S., Asthana, S., Carlsson, C.M., Potkin, S.G., Preda, A., Nguyen, D., Tariot, P., Burke, A., Trncic, N., Reeder, S., Bates, V., Capote, H., Rainka, M., Scharre, D.W., Kataki, M., Adeli, A., Zimmerman, E.A., Celmins, D., Brown, A.D., Pearlson, G.D., Blank, K., Anderson, K., Flashman, L.A., Seltzer, M., Hynes, M.L., Santulli, R.B., Sink, K.M., Gordineer, L., Williamson, J.D., Garg, P., Watkins, F., Ott, B.R., Querfurth, H., Tremont, G., Salloway, S., Malloy, P., Correia, S., Rosen, H.J., Miller, B.L., Perry, D., Mintzer, J., Spicer, K., Bachman, D., Pomara, N., Hernando, R., Sarrael, A., Relkin, N., Chaing, G., Lin, M., Ravdin, L., Smith, A., Raj, B.A., Fargher, K., Saykin, A., Nho, K., Kling, M., Toledo, J., Shaw, L., Trojanowski, J., Farrer, L., Kastsenmueller, G., Arnold, M., Wishart, D., Wurtz, P., Bhattcharyya, S., Duijin, C. van, Mangravite, L., Han, X., Hankemeier, T., Fiehn, O., Barupal, D., Thiele, I., Heinken, A., Meikle, P., Price, N., Funk, C., Jia, W., Kueider-Paisley, A., Tenebaum, J., Black, C., Moseley, A., Thompson, W., Mahmoudiandehkorki, S., Baillie, R., Welsh-Bohmer, K., Plassman, B., and Epidemiology

Subjects
Male, 0301 basic medicine, Apolipoprotein E, Oncology, medicine.medical_specialty, Amyloid, Amyloid beta, lcsh:Medicine, Article, 03 medical and health sciences, Apolipoproteins E, 0302 clinical medicine, Cerebrospinal fluid, Alzheimer Disease, Predictive Value of Tests, Internal medicine, medicine, Humans, Dementia, Cognitive decline, lcsh:Science, Aged, Aged, 80 and over, Amyloid beta-Peptides, Multidisciplinary, biology, Chemokine CCL26, business.industry, lcsh:R, Alzheimer’s Disease Metabolomics Consortium, Alzheimer’s Disease Neuroimaging Initiative, medicine.disease, Peptide Fragments, 3. Good health, 030104 developmental biology, biology.protein, Chromogranin A, Female, lcsh:Q, Alzheimer's disease, business, Biomarkers, 030217 neurology & neurosurgery, Alzheimer's Disease Neuroimaging Initiative
Abstract

It is increasingly recognized that Alzheimer’s disease (AD) exists before dementia is present and that shifts in amyloid beta occur long before clinical symptoms can be detected. Early detection of these molecular changes is a key aspect for the success of interventions aimed at slowing down rates of cognitive decline. Recent evidence indicates that of the two established methods for measuring amyloid, a decrease in cerebrospinal fluid (CSF) amyloid β1−42 (Aβ1−42) may be an earlier indicator of Alzheimer’s disease risk than measures of amyloid obtained from Positron Emission Tomography (PET). However, CSF collection is highly invasive and expensive. In contrast, blood collection is routinely performed, minimally invasive and cheap. In this work, we develop a blood-based signature that can provide a cheap and minimally invasive estimation of an individual’s CSF amyloid status using a machine learning approach. We show that a Random Forest model derived from plasma analytes can accurately predict subjects as having abnormal (low) CSF Aβ1−42 levels indicative of AD risk (0.84 AUC, 0.78 sensitivity, and 0.73 specificity). Refinement of the modeling indicates that only APOEε4 carrier status and four plasma analytes (CGA, Aβ1−42, Eotaxin 3, APOE) are required to achieve a high level of accuracy. Furthermore, we show across an independent validation cohort that individuals with predicted abnormal CSF Aβ1−42 levels transitioned to an AD diagnosis over 120 months significantly faster than those with predicted normal CSF Aβ1−42 levels and that the resulting model also validates reasonably across PET Aβ1−42 status (0.78 AUC). This is the first study to show that a machine learning approach, using plasma protein levels, age and APOEε4 carrier status, is able to predict CSF Aβ1−42 status, the earliest risk indicator for AD, with high accuracy.

Published
2019

3. Association of common genetic variants in GPCPD1 with scaling of visual cortical surface area in humans

Author

Bakken, TE, Roddey, JC, Djurovic, S, Akshoomoff, N, Amaral, DG, Bloss, CS, Casey, BJ, Chang, L, Ernst, TM, Gruen, JR, Jernigan, TL, Kaufmann, WE, Kenet, T, Kennedy, DN, Kuperman, JM, Murray, SS, Sowell, ER, Rimol, LM, Mattingsdal, M, Melle, I, Agartz, I, Andreassen, OA, Schork, NJ, Dale, AM, Alzheimer’s Disease Neuroimaging Initiative, Pediatric Imaging, Neurocognition, Genetics Study, Weiner, M, Aisen, P, Petersen, R, Jack, CR, Jr, Jagust, W, Trojanowki, JQ, Toga, AW, Beckett, L, Green, RC, Saykin, AJ, Morris, J, Liu, E, Montine, T, Gamst, A, Thomas, RG, Donohue, M, Walter, S, Gessert, D, Sather, T, Harvey, D, Kornak, J, Dale, A, Bernstein, M, Felmlee, J, Fox, N, Thompson, P, Schuff, N, Alexander, G, DeCarli, C, Bandy, D, Koeppe, RA, Foster, N, Reiman, EM, Chen, K, Mathis, C, Cairns, NJ, Taylor-Reinwald, L, Shaw, L, Lee, VM, Korecka, M, Crawford, K, Neu, S, Foroud, TM, Potkin, S, Shen, L, Kachaturian, Z, Frank, R, Snyder, PJ, Molchan, S, Kaye, J, Quinn, J, Lind, B, Dolen, S, Schneider, LS, Pawluczyk, S, Spann, BM, Brewer, J, Vanderswag, H, Heidebrink, JL, Lord, JL, Johnson, K, Doody, RS, Villanueva-Meyer, J, Chowdhury, M, Stern, Yaakov, Honig, LS, Bell, KL, Morris, JC, Ances, B, Carroll, M, Leon, S, Mintun, MA, Schneider, S, Marson, D, Griffith, R, Clark, D, Grossman, H, Mitsis, E, Romirowsky, A, deToledo-Morrell, L, Shah, RC, Duara, R, Varon, D, Roberts, P, Albert, M, Onyike, C, Kielb, S, Rusinek, H, de, Leon, MJ, Glodzik, L, De, Santi, S, Doraiswamy, PM, Petrella, JR, Coleman, RE, Arnold, SE, Karlawish, JH, Wolk, D, Smith, CD, Jicha, G, Hardy, P, Lopez, OL, Oakley, M, Simpson, DM, Porsteinsson, AP, Goldstein, BS, Martin, K, Makino, KM, Ismail, MS, Brand, C, Mulnard, RA, Thai, G, Mc-Adams-Ortiz, C, Womack, K, Mathews, D, Quiceno, M, Diaz-Arrastia, R, King, R, Martin-Cook, K, DeVous, M, Levey, AI, Lah, JJ, Cellar, JS, Burns, JM, Anderson, HS, Swerdlow, RH, Apostolova, L, Lu, PH, Bartzokis, G, Silverman, DH, Graff-Radford, NR, Parfitt, F, Johnson, H, Farlow, MR, Hake, AM, Matthews, BR, Herring, S, van, Dyck, CH, Carson, RE, MacAvoy, MG, Chertkow, H, Bergman, H, Hosein, C, Black, S, Stefanovic, B, Caldwell, C, Ging-Yuek, Hsiung, R, Feldman, H, Mudge, B, Assaly, M, Kertesz, A, Rogers, J, Trost, D, Bernick, C, Munic, D, Kerwin, D, Mesulam, MM, Lipowski, K, Wu, CK, Johnson, N, Sadowsky, C, Martinez, W, Villena, T, Turner, RS, Reynolds, B, Sperling, RA, Johnson, KA, Marshall, G, Frey, M, Yesavage, J, Taylor, JL, Lane, B, Rosen, A, Tinklenberg, J, Sabbagh, M, Belden, C, Jacobson, S, Kowall, N, Killiany, R, Budson, AE, Norbash, A, Johnson, PL, Obisesan, TO, Wolday, S, Bwayo, SK, Lerner, A, Hudson, L, Ogrocki, P, Fletcher, E, Carmichael, O, Olichney, J, Kittur, S, Borrie, M, Lee, TY, Bartha, R, Johnson, S, Asthana, S, Carlsson, CM, Potkin, SG, Preda, A, Nguyen, D, Tariot, P, Fleisher, A, Reeder, S, Bates, V, Capote, H, Rainka, M, Scharre, DW, Kataki, M, Zimmerman, EA, Celmins, D, Brown, AD, Pearlson, GD, Blank, K, Anderson, K, Santulli, RB, Schwartz, ES, Sink, KM, Williamson, JD, Garg, P, Watkins, F, Ott, BR, Querfurth, H, Tremont, G, Salloway, S, Malloy, P, Correia, S, Rosen, HJ, Miller, BL, Mintzer, J, Longmire, CF, Spicer, K, Finger, E, Rachinsky, I, Drost, D, Jernigan, T, McCabe, C, Grant, E, Ernst, T, Kuperman, J, Chung, Y, Murray, S, Bloss, C, Darst, B, Pritchett, L, Saito, A, Amaral, D, DiNino, M, Eyngorina, B, Sowell, E, Houston, S, Soderberg, L, Kaufmann, W, van, Zijl, P, Rizzo-Busack, H, Javid, M, Mehta, N, Ruberry, E, Powers, A, Rosen, B, Gebhard, N, Manigan, H, Frazier, J, Kennedy, D, Yakutis, L, Hill, M, Gruen, J, Bosson-Heenan, J, and Carlson, H

Subjects
anatomy & histology, pathology [Visual Cortex], Adult, Diagnostic Imaging, Male, Linkage disequilibrium, Visual perception, genetic structures, Adolescent, Genotype, Imaging genetics, methods [Diagnostic Imaging], Single-nucleotide polymorphism, Genome-wide association study, Saccharomyces cerevisiae, Biology, Polymorphism, Single Nucleotide, Cohort Studies, methods [Brain Mapping], pathology [Brain], Cortex (anatomy), Genetic variation, Medicine and Health Sciences, medicine, Humans, genetics [Phosphoric Diester Hydrolases], Aged, Visual Cortex, Genetics, Brain Mapping, Multidisciplinary, Models, Genetic, Phosphoric Diester Hydrolases, metabolism [Saccharomyces cerevisiae], Brain, Genetic Variation, Genomics, Middle Aged, Biological Sciences, Visual cortex, medicine.anatomical_structure, Female, Genome-Wide Association Study
Abstract

Visual cortical surface area varies two- to threefold between human individuals, is highly heritable, and has been correlated with visual acuity and visual perception. However, it is still largely unknown what specific genetic and environmental factors contribute to normal variation in the area of visual cortex. To identify SNPs associated with the proportional surface area of visual cortex, we performed a genome-wide association study followed by replication in two independent cohorts. We identified one SNP (rs6116869) that replicated in both cohorts and had genome-wide significant association ( P combined = 3.2 × 10 −8 ). Furthermore, a metaanalysis of imputed SNPs in this genomic region identified a more significantly associated SNP (rs238295; P = 6.5 × 10 −9 ) that was in strong linkage disequilibrium with rs6116869. These SNPs are located within 4 kb of the 5′ UTR of GPCPD1 , glycerophosphocholine phosphodiesterase GDE1 homolog ( Saccharomyces cerevisiae ), which in humans, is more highly expressed in occipital cortex compared with the remainder of cortex than 99.9% of genes genome-wide. Based on these findings, we conclude that this common genetic variation contributes to the proportional area of human visual cortex. We suggest that identifying genes that contribute to normal cortical architecture provides a first step to understanding genetic mechanisms that underlie visual perception.

Published
2012

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