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2. Maternal and Foetal Outcome of Anti-epileptic Drug Use in Pregnancy in Afro-Caribbean Patients.

Author

Rowe-Gardener, S., Gayle, F., and Johnson, N.

Abstract

Objective: To determine the maternal and foetal outcomes of anti-epileptic drugs (AEDs) use during pregnancy, in women of Afro-Caribbean descent, seen at the University Hospital of the West Indies (UHWI). Methods: A retrospective observational study was conducted for the period of2002-12. From the records received, 40 cases were identified from the labour ward admission books and the Codes and Ethics Department. The controls were sought from the labour ward records and were matched for year of delivery, age ± 6 years and co-morbidities. Results: An adverse foetal outcome was higher in infants exposed to AEDs in utero and was found to be statistically significant (p = 0.04). The occurrence of minor malformations in infants exposed to AED was determined to be more than two-times (14.2%) compared to the occurrence in infants from the control group (6.1%). The maternal outcomes from an exposure to AED in pregnancy were not found to be significantly different between cases and controls. (p = 0.06). Conclusion: There are additional adverse effects of AED use in pregnancy, other than major congenital malformations (MCMs), such as an increased risk of foetal demise. Similar to the previous reports, there are adverse maternal outcomes of AED use, though the differences did not achieve conventional levels of statistical significance in this study. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Plasma amyloid-beta levels in a pre-symptomatic Dutch-type hereditary cerebral amyloid angiopathy pedigree: A cross-sectional and longitudinal investigation

Author

Chatterjee, P., Tegg, M., Pedrini, S., Fagan, A., Xiong, C., Singh, A., Taddei, K., Gardener, S., Masters, C., Schofield, P., Multhaup, G., Benzinger, T., Morris, J., Bateman, R., Greenberg, S., van Buchem, M., Stoops, E., Vanderstichele, H., Teunissen, C., Hankey, G., Wermer, M., Sohrabi, H., Martins, R.N., the Dominantly Inherited Alzheimer Network, Chatterjee, P., Tegg, M., Pedrini, S., Fagan, A., Xiong, C., Singh, A., Taddei, K., Gardener, S., Masters, C., Schofield, P., Multhaup, G., Benzinger, T., Morris, J., Bateman, R., Greenberg, S., van Buchem, M., Stoops, E., Vanderstichele, H., Teunissen, C., Hankey, G., Wermer, M., Sohrabi, H., Martins, R.N., and the Dominantly Inherited Alzheimer Network

Abstract

Plasma amyloid-beta (Aβ) has long been investigated as a blood biomarker candidate for Cerebral Amyloid Angiopathy (CAA), however previous findings have been inconsistent which could be attributed to the use of less sensitive assays. This study investigates plasma Aβ alterations between pre-symptomatic Dutch-type hereditary CAA (D-CAA) mutation-carriers (MC) and non-carriers (NC) using two Aβ measurement platforms. Seventeen pre-symptomatic members of a D-CAA pedigree were assembled and followed up 3–4 years later (NC = 8; MC = 9). Plasma Aβ1-40 and Aβ1-42 were cross-sectionally and longitudinally analysed at baseline (T1) and follow-up (T2) and were found to be lower in MCs compared to NCs, cross-sectionally after adjusting for covariates, at both T1(Aβ1-40: p = 0.001; Aβ1-42: p = 0.0004) and T2 (Aβ1-40: p = 0.001; Aβ1-42: p = 0.016) employing the Single Molecule Array (Simoa) platform, however no significant differences were observed using the xMAP platform. Further, pairwise longitudinal analyses of plasma Aβ1-40 revealed decreased levels in MCs using data from the Simoa platform (p = 0.041) and pairwise longitudinal analyses of plasma Aβ1-42 revealed decreased levels in MCs using data from the xMAP platform (p = 0.041). Findings from the Simoa platform suggest that plasma Aβ may add value to a panel of biomarkers for the diagnosis of pre-symptomatic CAA, however, further validation studies in larger sample sets are required.

Published
2021

6. Amyloid and tau pathology associations with personality traits, neuropsychiatric symptoms, and cognitive lifestyle in the preclinical phases of sporadic and autosomal dominant Alzheimer’s disease

Author

Pichet Binette, A., Vachon-Presseau, É., Morris, J., Bateman, R., Benzinger, T., Collins, D.L., Poirier, J., Breitner, J.C.S., Villeneuve, S., Allegri, R., Amtashar, F., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, Jill, Buckles, V., Chea, S., Chhatwal, J., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D‘Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., DiBari, S.H., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Levin, J., Marcus, D., Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J.H., Salloway, S., Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Tam, A., Labonté, A., Faubert, A-M, Mathieu, A., Madjar, C., Carrier, C.E., Dansereau, C., Kazazian, C., Lepage, C., Picard, C., Maillet, D., Michaud, D., Couture, D., Dea, D., Cuello, C., Barkun, A., Evans, A., Courcot, B., Tardif, C., Debacker, C., Jack, C.R., Fontaine, D., Knopman, D.S., Maultaup, G., Near, J., Leoutsakos, J-M, Maltais, J-R, Brandt, J., Pruessner, J., Morris, J.C., Cheewakriengkrai, L., Münter, L-M, Collins, L., Chakravarty, M., Sager, M.A., Dauar-Tedeschi, M., Eisenberg, M., Rajah, N., Aisen, P., Toussaint, J., Rosa-Neto, P., Bellec, P., Kostopoulos, P., Etienne, P., Tariot, P.N., Orban, P., Sperling, R.A., Hoge, R., Thomas, R.G., Gauthier, S., Craft, S., Montine, T.J., Nair, V., Bohbot, V., Venugopalan, V., Fonov, V., Ituria-Medina, Y., Khachaturian, Z.S., Teigner, E., Anthal, E., Yu, E., Ferdinand, F., Pogossova, G., Mayrand, G., Duclair, G., Gagné, G., Newbold-Fox, H., Leppert, I., Vallée, I., Vogel, J.W., Tremblay-Mercier, J., Frenette, J., Frappier, J., Kat, J., Miron, J., Wan, K., Mahar, L., Carmo, L., Théroux, L., Dadar, M., Dufour, M., Lafaille-Magnan, M-E, Appleby, M., Savard, M., Tuwaig, M., Petkova, M., Rioux, P., Meyer, P-F, El-Khoury, R., Gordon, R., Giles, R., Das, S., Wang, S., Tabrizi, S., Mathotaarachchi, S., Dubuc, S., Lee, T., Beaudry, T., Gervais, V., Pagé, V., Gonneaud, J., Ayranci, G., Pascoal, T.A., Desautels, R., Benbouhoud, F., Saint-Fort, E.F., Verfaillie, S.C.J., Farzin, S., Salaciak, A., Tullo, S., Vachon-Presseau, E., Daoust, L-A, Köbe, T., Spreng, N., McSweeney, M., Nilsson, N., Pishnamazi, M., Bedetti, C., Pichet Binette, A., Vachon-Presseau, É., Morris, J., Bateman, R., Benzinger, T., Collins, D.L., Poirier, J., Breitner, J.C.S., Villeneuve, S., Allegri, R., Amtashar, F., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, Jill, Buckles, V., Chea, S., Chhatwal, J., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D‘Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., DiBari, S.H., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Levin, J., Marcus, D., Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J.H., Salloway, S., Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Tam, A., Labonté, A., Faubert, A-M, Mathieu, A., Madjar, C., Carrier, C.E., Dansereau, C., Kazazian, C., Lepage, C., Picard, C., Maillet, D., Michaud, D., Couture, D., Dea, D., Cuello, C., Barkun, A., Evans, A., Courcot, B., Tardif, C., Debacker, C., Jack, C.R., Fontaine, D., Knopman, D.S., Maultaup, G., Near, J., Leoutsakos, J-M, Maltais, J-R, Brandt, J., Pruessner, J., Morris, J.C., Cheewakriengkrai, L., Münter, L-M, Collins, L., Chakravarty, M., Sager, M.A., Dauar-Tedeschi, M., Eisenberg, M., Rajah, N., Aisen, P., Toussaint, J., Rosa-Neto, P., Bellec, P., Kostopoulos, P., Etienne, P., Tariot, P.N., Orban, P., Sperling, R.A., Hoge, R., Thomas, R.G., Gauthier, S., Craft, S., Montine, T.J., Nair, V., Bohbot, V., Venugopalan, V., Fonov, V., Ituria-Medina, Y., Khachaturian, Z.S., Teigner, E., Anthal, E., Yu, E., Ferdinand, F., Pogossova, G., Mayrand, G., Duclair, G., Gagné, G., Newbold-Fox, H., Leppert, I., Vallée, I., Vogel, J.W., Tremblay-Mercier, J., Frenette, J., Frappier, J., Kat, J., Miron, J., Wan, K., Mahar, L., Carmo, L., Théroux, L., Dadar, M., Dufour, M., Lafaille-Magnan, M-E, Appleby, M., Savard, M., Tuwaig, M., Petkova, M., Rioux, P., Meyer, P-F, El-Khoury, R., Gordon, R., Giles, R., Das, S., Wang, S., Tabrizi, S., Mathotaarachchi, S., Dubuc, S., Lee, T., Beaudry, T., Gervais, V., Pagé, V., Gonneaud, J., Ayranci, G., Pascoal, T.A., Desautels, R., Benbouhoud, F., Saint-Fort, E.F., Verfaillie, S.C.J., Farzin, S., Salaciak, A., Tullo, S., Vachon-Presseau, E., Daoust, L-A, Köbe, T., Spreng, N., McSweeney, M., Nilsson, N., Pishnamazi, M., and Bedetti, C.

Abstract

Background Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. Methods A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. Results In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. Conclusions In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression.

Published
2020

7. A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease

Author

Barthélemy, N.R., Li, Y., Joseph-Mathurin, N., Gordon, B.A., Hassenstab, J., Benzinger, T.L.S., Buckles, V., Fagan, A.M., Perrin, R.J., Goate, A.M., Morris, J.C., Karch, C.M., Xiong, C., Allegri, R., Mendez, P.C., Berman, S.B., Ikeuchi, T., Mori, H., Shimada, H., Shoji, M., Suzuki, K., Noble, J., Farlow, M., Chhatwal, J., Graff-Radford, N.R., Salloway, S., Schofield, P.R., Masters, C.L., Martins, R.N., O’Connor, A., Fox, N.C., Levin, J., Jucker, M., Gabelle, A., Lehmann, S., Sato, C., Bateman, R.J., McDade, E., Bateman, R., Bechara, J., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Chea, S., Chrem Mendez, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Fitzpatrick, C., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Groves, A., Hoechst-Swisher, L., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., Morris, J., Nagamatsu, A., Neimeyer, K., Norton, J., Perrin, R., Raichle, M., Renton, A., Ringman, J., Roh, J.H., Schofield, P., Sigurdson, W., Sohrabi, H., Sparks, P., Taddei, K., Wang, P., Xu, X., Barthélemy, N.R., Li, Y., Joseph-Mathurin, N., Gordon, B.A., Hassenstab, J., Benzinger, T.L.S., Buckles, V., Fagan, A.M., Perrin, R.J., Goate, A.M., Morris, J.C., Karch, C.M., Xiong, C., Allegri, R., Mendez, P.C., Berman, S.B., Ikeuchi, T., Mori, H., Shimada, H., Shoji, M., Suzuki, K., Noble, J., Farlow, M., Chhatwal, J., Graff-Radford, N.R., Salloway, S., Schofield, P.R., Masters, C.L., Martins, R.N., O’Connor, A., Fox, N.C., Levin, J., Jucker, M., Gabelle, A., Lehmann, S., Sato, C., Bateman, R.J., McDade, E., Bateman, R., Bechara, J., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Chea, S., Chrem Mendez, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Fitzpatrick, C., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Groves, A., Hoechst-Swisher, L., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., Morris, J., Nagamatsu, A., Neimeyer, K., Norton, J., Perrin, R., Raichle, M., Renton, A., Ringman, J., Roh, J.H., Schofield, P., Sigurdson, W., Sohrabi, H., Sparks, P., Taddei, K., Wang, P., and Xu, X.

Abstract

Development of tau-based therapies for Alzheimer’s disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer’s disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments.

Published
2020

9. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease

Author

Preische, O., Schultz, S.A., Apel, A., Kuhle, J., Kaeser, S.A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C.L., Martins, R., Schofield, P.R., Rossor, M.N., Graff-Radford, N.R., Salloway, S., Ghetti, B., Ringman, J.M., Noble, J.M., Chhatwal, J., Goate, A.M., Benzinger, T.L.S., Morris, J.C., Bateman, R.J., Wang, G., Fagan, A.M., McDade, E.M., Gordon, B.A., Jucker, M., Allegri, R., Amtashar, F., Bateman, R., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D’Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Lee, J-H, Marcus, D., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Morris, J., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Preische, O., Schultz, S.A., Apel, A., Kuhle, J., Kaeser, S.A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C.L., Martins, R., Schofield, P.R., Rossor, M.N., Graff-Radford, N.R., Salloway, S., Ghetti, B., Ringman, J.M., Noble, J.M., Chhatwal, J., Goate, A.M., Benzinger, T.L.S., Morris, J.C., Bateman, R.J., Wang, G., Fagan, A.M., McDade, E.M., Gordon, B.A., Jucker, M., Allegri, R., Amtashar, F., Bateman, R., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D’Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Lee, J-H, Marcus, D., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Morris, J., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., and Xu, X.

Abstract

Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. Here we leverage the unique characteristics of the Dominantly Inherited Alzheimer Network and ultrasensitive immunoassay technology to demonstrate that NfL levels in the cerebrospinal fluid (n = 187) and serum (n = 405) are correlated with one another and are elevated at the presymptomatic stages of familial Alzheimer’s disease. Longitudinal, within-person analysis of serum NfL dynamics (n = 196) confirmed this elevation and further revealed that the rate of change of serum NfL could discriminate mutation carriers from non-mutation carriers almost a decade earlier than cross-sectional absolute NfL levels (that is, 16.2 versus 6.8 years before the estimated symptom onset). Serum NfL rate of change peaked in participants converting from the presymptomatic to the symptomatic stage and was associated with cortical thinning assessed by magnetic resonance imaging, but less so with amyloid-β deposition or glucose metabolism (assessed by positron emission tomography). Serum NfL was predictive for both the rate of cortical thinning and cognitive changes assessed by the Mini–Mental State Examination and Logical Memory test. Thus, NfL dynamics in serum predict disease progression and brain neurodegeneration at the early presymptomatic stages of familial Alzheimer’s disease, which supports its potential utility as a clinically useful biomarker.

Published
2019

10. An atlas of cortical circular RNA expression in Alzheimer disease brains demonstrates clinical and pathological associations

Author

Dube, U., Del-Aguila, J.L., Li, Z., Budde, J.P., Jiang, S., Hsu, S., Ibanez, L., Fernandez, M.V., Farias, F., Norton, J., Gentsch, J., Wang, F., Allegri, R., Amtashar, F., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., D'Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Kasuga, K., Kawarabayashi, T., Klunk, W., koeppe, R., Kuder-Buletta, E., Laske, C., Levin, J., Marcus, D., Martins, R., Mason, N.S., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Dube, U., Del-Aguila, J.L., Li, Z., Budde, J.P., Jiang, S., Hsu, S., Ibanez, L., Fernandez, M.V., Farias, F., Norton, J., Gentsch, J., Wang, F., Allegri, R., Amtashar, F., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., D'Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Kasuga, K., Kawarabayashi, T., Klunk, W., koeppe, R., Kuder-Buletta, E., Laske, C., Levin, J., Marcus, D., Martins, R., Mason, N.S., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., and Xu, X.

Abstract

Parietal cortex RNA-sequencing (RNA-seq) data were generated from individuals with and without Alzheimer disease (AD; ncontrol = 13; nAD = 83) from the Knight Alzheimer Disease Research Center (Knight ADRC). Using this and an independent (Mount Sinai Brain Bank (MSBB)) AD RNA-seq dataset, cortical circular RNA (circRNA) expression was quantified in the context of AD. Significant associations were identified between circRNA expression and AD diagnosis, clinical dementia severity and neuropathological severity. It was demonstrated that most circRNA–AD associations are independent of changes in cognate linear messenger RNA expression or estimated brain cell-type proportions. Evidence was provided for circRNA expression changes occurring early in presymptomatic AD and in autosomal dominant AD. It was also observed that AD-associated circRNAs co-expressed with known AD genes. Finally, potential microRNA-binding sites were identified in AD-associated circRNAs for miRNAs predicted to target AD genes. Together, these results highlight the importance of analyzing non-linear RNAs and support future studies exploring the potential roles of circRNAs in AD pathogenesis.

Published
2019

11. Alzheimer's Disease: A Journey from Amyloid Peptides and Oxidative Stress, to Biomarker Technologies and Disease Prevention Strategies-Gains from AIBL and DIAN Cohort Studies

Author

Martins, R., Villemagne, V., Sohrabi, H., Chatterjee, P., Shah, T., Verdile, Giuseppe, Fraser, P., Taddei, K., Gupta, V., Rainey-Smith, S., Hone, E., Pedrini, S., Lim, W., Martins, I., Frost, S., Gupta, S., O'Bryant, S., Rembach, A., Ames, D., Ellis, K., Fuller, S., Brown, B., Gardener, S., Fernando, B., Bharadwaj, Prashant, Burnham, S., Laws, S., Barron, A., Goozee, K., Wahjoepramono, E., Asih, P., Doecke, J., Salvado, O., Bush, A., Rowe, C., Gandy, S., Masters, C., Martins, R., Villemagne, V., Sohrabi, H., Chatterjee, P., Shah, T., Verdile, Giuseppe, Fraser, P., Taddei, K., Gupta, V., Rainey-Smith, S., Hone, E., Pedrini, S., Lim, W., Martins, I., Frost, S., Gupta, S., O'Bryant, S., Rembach, A., Ames, D., Ellis, K., Fuller, S., Brown, B., Gardener, S., Fernando, B., Bharadwaj, Prashant, Burnham, S., Laws, S., Barron, A., Goozee, K., Wahjoepramono, E., Asih, P., Doecke, J., Salvado, O., Bush, A., Rowe, C., Gandy, S., and Masters, C.

Abstract

© 2018-IOS Press and the authors. All rights reserved. Worldwide there are over 46 million people living with dementia, and this number is expected to double every 20 years reaching about 131 million by 2050. The cost to the community and government health systems, as well as the stress on families and carers is incalculable. Over three decades of research into this disease have been undertaken by several research groups in Australia, including work by our original research group in Western Australia which was involved in the discovery and sequencing of the amyloid-β peptide (also known as Aβ or A4 peptide) extracted from cerebral amyloid plaques. This review discusses the journey from the discovery of the Aβ peptide in Alzheimer's disease (AD) brain to the establishment of pre-clinical AD using PET amyloid tracers, a method now serving as the gold standard for developing peripheral diagnostic approaches in the blood and the eye. The latter developments for early diagnosis have been largely achieved through the establishment of the Australian Imaging Biomarker and Lifestyle research group that has followed 1,100 Australians for 11 years. AIBL has also been instrumental in providing insight into the role of the major genetic risk factor apolipoprotein E ϵ4, as well as better understanding the role of lifestyle factors particularly diet, physical activity and sleep to cognitive decline and the accumulation of cerebral Aβ.

Published
2018

13. A blood-based biomarker panel indicates IL-10 and IL-12/23p40 are jointly associated as predictors of β-amyloid load in an AD cohort

Author

Pedrini, Steve, Gupta, Veer B, Hone, Eugene, Doecke, James, O'Bryant, Sid, James, Ian, Bush, Ashley I, Rowe, Christopher C, Villemagne, Victor L, Ames, David, Masters, Colin L, Martins, Ralph N, Savage, G, Wilson, B, Bourgeat, P, Fripp, J, Gibson, S, Leroux, H, McBride, S, Salvado, O, Fenech, M, Francois, M, Barnes, M, Baker, J, Barnham, K, Bellingham, S, Bomke, J, Pejoska, SB, Buckley, R, Cheng, L, Collins, S, Cooke, I, Cyarto, E, Darby, D, Dore, V, El-Sheikh, D, Faux, N, Fowler, C, Harrington, K, Hill, A, Horne, M, Jones, G, Kamer, A, Killeen, N, Korrel, H, Lamb, F, Lautenschlager, N, Lennon, K, Li, QX, Lim, YY, Louey, A, Macaulay, L, Mackintosh, L, Maruff, P, McIlroy, A, Nigro, J, Perez, K, Pertile, K, Restrepo, C, Rita Cardoso, Barbara, Rembach, A, Roberts, B, Robertson, J, Rumble, R, Ryan, T, Sach, J, Silbert, B, Thai, C, Trounson, B, Volitakis, I, Vovos, M, Ward, L, Watt, A, Williams, R, Woodward, M, Yates, P, Ugarte, FY, Zhang, P, Bird, S, Brown, B, Burnham, S, Chatterjee, P, Cox, K, Fernandez, S, Fernando, B, Gardener, S, Laws, S, Lim, F, Lim, L, Tegg, M, Lucas, K, Martins, G, Pedrini, Steve, Gupta, Veer B, Hone, Eugene, Doecke, James, O'Bryant, Sid, James, Ian, Bush, Ashley I, Rowe, Christopher C, Villemagne, Victor L, Ames, David, Masters, Colin L, Martins, Ralph N, Savage, G, Wilson, B, Bourgeat, P, Fripp, J, Gibson, S, Leroux, H, McBride, S, Salvado, O, Fenech, M, Francois, M, Barnes, M, Baker, J, Barnham, K, Bellingham, S, Bomke, J, Pejoska, SB, Buckley, R, Cheng, L, Collins, S, Cooke, I, Cyarto, E, Darby, D, Dore, V, El-Sheikh, D, Faux, N, Fowler, C, Harrington, K, Hill, A, Horne, M, Jones, G, Kamer, A, Killeen, N, Korrel, H, Lamb, F, Lautenschlager, N, Lennon, K, Li, QX, Lim, YY, Louey, A, Macaulay, L, Mackintosh, L, Maruff, P, McIlroy, A, Nigro, J, Perez, K, Pertile, K, Restrepo, C, Rita Cardoso, Barbara, Rembach, A, Roberts, B, Robertson, J, Rumble, R, Ryan, T, Sach, J, Silbert, B, Thai, C, Trounson, B, Volitakis, I, Vovos, M, Ward, L, Watt, A, Williams, R, Woodward, M, Yates, P, Ugarte, FY, Zhang, P, Bird, S, Brown, B, Burnham, S, Chatterjee, P, Cox, K, Fernandez, S, Fernando, B, Gardener, S, Laws, S, Lim, F, Lim, L, Tegg, M, Lucas, K, and Martins, G

Abstract

Alzheimer's Disease (AD) is the most common form of dementia, characterised by extracellular amyloid deposition as plaques and intracellular neurofibrillary tangles of tau protein. As no current clinical test can diagnose individuals at risk of developing AD, the aim of this project is to evaluate a blood-based biomarker panel to identify individuals who carry this risk. We analysed the levels of 22 biomarkers in clinically classified healthy controls (HC), mild cognitive impairment (MCI) and Alzheimer's participants from the well characterised Australian Imaging, Biomarker and Lifestyle (AIBL) study of aging. High levels of IL-10 and IL-12/23p40 were significantly associated with amyloid deposition in HC, suggesting that these two biomarkers might be used to detect at risk individuals. Additionally, other biomarkers (Eotaxin-3, Leptin, PYY) exhibited altered levels in AD participants possessing the APOE ϵ4 allele. This suggests that the physiology of some potential biomarkers may be altered in AD due to the APOE ϵ4 allele, a major risk factor for AD. Taken together, these data highlight several potential biomarkers that can be used in a blood-based panel to allow earlier identification of individuals at risk of developing AD and/or early stage AD for which current therapies may be more beneficial.

Published
2017

14. Increased Carbohydrate Intake is Associated with Poorer Performance in Verbal Memory and Attention in an APOE Genotype-Dependent Manner

Author

Gardener, S., Rainey-Smith, S., Sohrabi, H., Weinborn, M., Verdile, Giuseppe, Fernando, W., Lim, Y., Harrington, K., Burnham, S., Taddei, K., Masters, C., Macaulay, S., Rowe, C., Ames, D., Maruff, P., Martins, R., Gardener, S., Rainey-Smith, S., Sohrabi, H., Weinborn, M., Verdile, Giuseppe, Fernando, W., Lim, Y., Harrington, K., Burnham, S., Taddei, K., Masters, C., Macaulay, S., Rowe, C., Ames, D., Maruff, P., and Martins, R.

Abstract

Evidence suggests that a diet low in carbohydrates can impact on cognitive performance among those with Alzheimer's disease (AD). However, there is a lack of data assessing this relationship among cognitively normal (CN) older adults at increased future risk of developing AD due to carriage of the apolipoprotein E (APOE) ?4 allele. We assessed the cross-sectional association between carbohydrate intake, cognitive performance, and cerebral amyloid-ß (Aß) load in CN older adults, genotyped for APOE ?4 allele carrier status. Greater carbohydrate intake was associated with poorer performance in verbal memory in APOE ?4 allele non-carriers, and poorer performance in attention in APOE ?4 allele carriers. There were no associations between carbohydrate intake and cerebral Aß load. These results provide support to the idea that decreasing carbohydrate intake may offer neurocognitive benefits, with specific cognitive domains affected in an APOE genotype-dependent manner. These findings warrant further investigation utilizing a longitudinal study design.

Published
2017

15. High content, multi-parameter analyses in buccal cells to identify Alzheimer's disease

Author

François, M., Fenech, M., Thomas, P., Hor, M., Rembach, A., Martins, R.N., Rainey-Smith, S.R., Masters, C.L., Ames, D., Rowe, C.C., Macaulay, S.L., Hill, A.F., Leifert, W.R., Appannah, A., Barnes, M., Barnham, K., Bedo, J., Bellingham, S., Bon, L., Bourgeat, P., Brown, B., Buckley, R., Burnham, S., Bush, A., Chandler, G., Chen, K., Clarnette, R., Collins, S., Cooke, I., Cowie, T., Cox, K., Cuningham, E., Cyarto, E., Dang, P.A.V., Darby, D., Desmond, P., Doecke, J., Dore, V., Downing, H., Dridan, B., Duesing, K., Fahey, M., Farrow, M., Faux, N., Fernandez, S., Fernando, B., Fowler, C., Fripp, J., Frost, S., Gardener, S., Gibson, S., Graham, P., Gupta, V., Hansen, D., Harrington, K., Hone, E., Horne, M., Huckstepp, B., Jones, A., Jones, G., Kamer, A., Kanagasingam, Y., Keam, L., Kowalczyk, A., Krivdic, B., Lam, C.P., Lamb, F., Lautenschlager, N., Laws, S., Lenzo, N., Leroux, H., Lftikhar, F., Li, Q-X, Lim, F., Lim, L., Lockett, L., Lucas, K., Mano, M., Marczak, C., Martins, G., Matsumoto, Y., Bird, S., McBride, S., McKay, R., Mulligan, R., Nash, T., Nigro, J., O'Keefe, G., Ong, K., Parker, B., Pedrini, S., Peiffer, J., Pejoska, S., Penny, L., Perez, K., Pertile, K., Phal, P., Porter, T., Raniga, P., Restrepo, C., Riley, M., Roberts, B., Robertson, J., Rodrigues, M., Rooney, A., Rumble, R., Ryan, T., Salvado, O., Samuel, M., Saunders, I., Savage, G., Silbert, B., Sohrabi, H.R., Syrette, J., Szoeke, C., Taddei, K., Taddei, T., Tan, S., Tegg, M., Trivedi, D., Trounson, B., Veljanovski, R., Verdile, G., Villemagne, V., Volitakis, I., Vockler, C., Vovos, M., Vrantsidis, F., Walker, S., Watt, A., Weinborn, M., Wilson, B., Woodward, M., Yastrubetskaya, O., Yates, P., Zhang, P., Chatterjee, P., Creegan, R., De Ruyck, K., Ding, H., Groth, D., Head, R., Krause, D., Lachovitzki, R., Lim, Y.Y., Lintern, T., Mondal, A., Nuttall, S., O'Callaghan, N., Osborne, L., Pang, C., Patten, G., Tuckfield, A., Varghese, J., Wilson, A., Zhang, Q., François, M., Fenech, M., Thomas, P., Hor, M., Rembach, A., Martins, R.N., Rainey-Smith, S.R., Masters, C.L., Ames, D., Rowe, C.C., Macaulay, S.L., Hill, A.F., Leifert, W.R., Appannah, A., Barnes, M., Barnham, K., Bedo, J., Bellingham, S., Bon, L., Bourgeat, P., Brown, B., Buckley, R., Burnham, S., Bush, A., Chandler, G., Chen, K., Clarnette, R., Collins, S., Cooke, I., Cowie, T., Cox, K., Cuningham, E., Cyarto, E., Dang, P.A.V., Darby, D., Desmond, P., Doecke, J., Dore, V., Downing, H., Dridan, B., Duesing, K., Fahey, M., Farrow, M., Faux, N., Fernandez, S., Fernando, B., Fowler, C., Fripp, J., Frost, S., Gardener, S., Gibson, S., Graham, P., Gupta, V., Hansen, D., Harrington, K., Hone, E., Horne, M., Huckstepp, B., Jones, A., Jones, G., Kamer, A., Kanagasingam, Y., Keam, L., Kowalczyk, A., Krivdic, B., Lam, C.P., Lamb, F., Lautenschlager, N., Laws, S., Lenzo, N., Leroux, H., Lftikhar, F., Li, Q-X, Lim, F., Lim, L., Lockett, L., Lucas, K., Mano, M., Marczak, C., Martins, G., Matsumoto, Y., Bird, S., McBride, S., McKay, R., Mulligan, R., Nash, T., Nigro, J., O'Keefe, G., Ong, K., Parker, B., Pedrini, S., Peiffer, J., Pejoska, S., Penny, L., Perez, K., Pertile, K., Phal, P., Porter, T., Raniga, P., Restrepo, C., Riley, M., Roberts, B., Robertson, J., Rodrigues, M., Rooney, A., Rumble, R., Ryan, T., Salvado, O., Samuel, M., Saunders, I., Savage, G., Silbert, B., Sohrabi, H.R., Syrette, J., Szoeke, C., Taddei, K., Taddei, T., Tan, S., Tegg, M., Trivedi, D., Trounson, B., Veljanovski, R., Verdile, G., Villemagne, V., Volitakis, I., Vockler, C., Vovos, M., Vrantsidis, F., Walker, S., Watt, A., Weinborn, M., Wilson, B., Woodward, M., Yastrubetskaya, O., Yates, P., Zhang, P., Chatterjee, P., Creegan, R., De Ruyck, K., Ding, H., Groth, D., Head, R., Krause, D., Lachovitzki, R., Lim, Y.Y., Lintern, T., Mondal, A., Nuttall, S., O'Callaghan, N., Osborne, L., Pang, C., Patten, G., Tuckfield, A., Varghese, J., Wilson, A., and Zhang, Q.

Abstract

Alzheimer’s disease (AD) is a degenerative brain disorder and is the most common form of dementia. Minimally invasive approaches are required that combine biomarkers to identify individuals who are at risk of developing mild cognitive impairment (MCI) and AD, to appropriately target clinical trials for therapeutic discovery as well as lifestyle strategies aimed at prevention. Buccal mucosa cells from the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing cohort (n=60) were investigated for cytological markers that could be used to identify both MCI and AD individuals. Visual scoring of the buccal cytome demonstrated a significantly lower frequency of basal and karyorrhectic cells in the MCI group compared with controls. A high content, automated assay was developed using laser scanning cytometry to simultaneously measure cell types, nuclear DNA content and aneuploidy, neutral lipid content, putative Tau and amyloid-β (Aβ) in buccal cells. DNA content, aneuploidy, neutral lipids and Tau were similar in all groups. However, there was significantly lower Tau protein in both basal and karyolytic buccal cell types compared with differentiated buccal cells. Aβ, as measured by frequency of cells containing Aβ signal, as well as area and integral of Aβ signal, was significantly higher in the AD group compared with the control group. Buccal cell Aβ was correlated with mini-mental state examination (MMSE) scores (r = -0.436, P=0.001) and several blood-based biomarkers. Combining newly identified biomarkers from buccal cells with those already established may offer a potential route for more specific biomarker panels which may substantially increase the likelihood of better predictive markers for earlier diagnosis of AD.

Published
2016

16. O2-02-05: APOE genotype-dependent effects of diet and physical activity on cognition and alzeimer's-related pathology: Data from the AIPL study of ageing

Author

Rainey-Smith, S.R., Brown, B., Gardener, S., Peiffer, J., Bourgeat, P., Laws, S.M., Barnes, M., Taddei, K., Sohrabi, H.R., Weinborn, M., Rembach, A., Burnham, S., Villemagne, V.L., Ellis, K.A., Macaulay, L., Masters, C.L., Rowe, C.C., Ames, D., Martins, R., Rainey-Smith, S.R., Brown, B., Gardener, S., Peiffer, J., Bourgeat, P., Laws, S.M., Barnes, M., Taddei, K., Sohrabi, H.R., Weinborn, M., Rembach, A., Burnham, S., Villemagne, V.L., Ellis, K.A., Macaulay, L., Masters, C.L., Rowe, C.C., Ames, D., and Martins, R.

Abstract

Oral presentation

Published
2014

17. Adherence to a Mediterranean diet and Alzheimer’s disease risk in an Australian population

Author

Gardener, S., Gu, Y., Rainey-Smith, S.R., Keogh, J.B., Clifton, P.M., Mathieson, S.L., Taddei, K., Mondal, A., Ward, V.K., Scarmeas, N., Barnes, M., Ellis, K.A., Head, R., Masters, C.L., Ames, D., Macaulay, S.L., Rowe, C.C., Szoeke, C., Martins, R.N., Gardener, S., Gu, Y., Rainey-Smith, S.R., Keogh, J.B., Clifton, P.M., Mathieson, S.L., Taddei, K., Mondal, A., Ward, V.K., Scarmeas, N., Barnes, M., Ellis, K.A., Head, R., Masters, C.L., Ames, D., Macaulay, S.L., Rowe, C.C., Szoeke, C., and Martins, R.N.

Abstract

The Mediterranean diet (MeDi), due to its correlation with a low morbidity and mortality for many chronic diseases, has been widely recognised as a healthy eating model. We aimed to investigate, in a cross-sectional study, the association between adherence to a MeDi and risk for Alzheimer’s disease (AD) and mild cognitive impairment (MCI) in a large, elderly, Australian cohort. Subjects in the Australian Imaging, Biomarkers and Lifestyle Study of Ageing cohort (723 healthy controls (HC), 98 MCI and 149 AD participants) completed the Cancer Council of Victoria Food Frequency Questionnaire. Adherence to the MeDi (0- to 9-point scale with higher scores indicating higher adherence) was the main predictor of AD and MCI status in multinominal logistic regression models that were adjusted for cohort age, sex, country of birth, education, apolipoprotein E genotype, total caloric intake, current smoking status, body mass index, history of diabetes, hypertension, angina, heart attack and stroke. There was a significant difference in adherence to the MeDi between HC and AD subjects (P<0.001), and in adherence between HC and MCI subjects (P<0.05). MeDi is associated with change in Mini-Mental State Examination score over an 18-month time period (P<0.05) in HCs. We conclude that in this Australian cohort, AD and MCI participants had a lower adherence to the MeDi than HC participants.

Published
2012

18. Dietary Patterns Associated with Alzheimer?s Disease and Related Chronic Disease Risk: A Review

Author

Gardener, S., Rainey-Smith, S.R., Keogh, J.B., Mathieson, S.L., Martins, R.N., Gardener, S., Rainey-Smith, S.R., Keogh, J.B., Mathieson, S.L., and Martins, R.N.

Abstract

The world’s population is growing older due to improved healthcare and nutrition. As a result, Alzheimer’s disease (AD) prevalence is rapidly increasing. The focus of the current research climate is shifting from understanding AD pathology and diagnosis to primary prevention and intervention strategies. Diet represents one potential intervention strategy accessible to all. Accumulating evidence suggests diet plays a major role in risk and development of AD and AD-related chronic diseases of the periphery like cardiovascular disease (CVD) and diabetes. This paper reviews studies that have explored the relationship between “a priori” dietary patterns, AD and AD-related chronic disease risk. The dietary patterns we will review are the healthy eating index, healthy diet indicator, recommended food score, and the Mediterranean diet (MeDi). Our review of the literature suggests a generally positive association between healthy diet patterns, AD and AD-related chronic disease risk; however the magnitude of the protective effect is modest in many studies. Consequently, we can only confidently conclude that the MeDi is associated with reduced AD risk, and further studies on the remaining indices need to be carried out. It is our opinion that a combination of dietary scores could predict overall dietary quality and chronic disease risk to a greater extent than one score individually. Analysis in multi-ethnic cohorts, investigating combinations of scores must be completed before firm conclusions can be reached on the ideal combination of scores. Obtaining further insight into the association between dietary patterns, AD and AD-related chronic disease risk may help in prioritizing public health efforts and provide a stronger basis for recommendations to improve dietary patterns.

Published
2012

19. Adherence to a Mediterranean diet and Alzheimer's disease risk in an Australian population

Author

Gardener, S, Gu, Y, Rainey-Smith, SR, Keogh, JB, Clifton, PM, Mathieson, SL, Taddei, K, Mondal, A, Ward, VK, Scarmeas, N, Barnes, M, Ellis, KA, Head, R, Masters, CL, Ames, D, Macaulay, SL, Rowe, CC, Szoeke, C, Martins, RN, Gardener, S, Gu, Y, Rainey-Smith, SR, Keogh, JB, Clifton, PM, Mathieson, SL, Taddei, K, Mondal, A, Ward, VK, Scarmeas, N, Barnes, M, Ellis, KA, Head, R, Masters, CL, Ames, D, Macaulay, SL, Rowe, CC, Szoeke, C, and Martins, RN

Abstract

The Mediterranean diet (MeDi), due to its correlation with a low morbidity and mortality for many chronic diseases, has been widely recognised as a healthy eating model. We aimed to investigate, in a cross-sectional study, the association between adherence to a MeDi and risk for Alzheimer's disease (AD) and mild cognitive impairment (MCI) in a large, elderly, Australian cohort. Subjects in the Australian Imaging, Biomarkers and Lifestyle Study of Ageing cohort (723 healthy controls (HC), 98 MCI and 149 AD participants) completed the Cancer Council of Victoria Food Frequency Questionnaire. Adherence to the MeDi (0- to 9-point scale with higher scores indicating higher adherence) was the main predictor of AD and MCI status in multinominal logistic regression models that were adjusted for cohort age, sex, country of birth, education, apolipoprotein E genotype, total caloric intake, current smoking status, body mass index, history of diabetes, hypertension, angina, heart attack and stroke. There was a significant difference in adherence to the MeDi between HC and AD subjects (P < 0.001), and in adherence between HC and MCI subjects (P < 0.05). MeDi is associated with change in Mini-Mental State Examination score over an 18-month time period (P < 0.05) in HCs. We conclude that in this Australian cohort, AD and MCI participants had a lower adherence to the MeDi than HC participants.

Published
2012

20. Vav is a regulator of cytoskeletal reorganization mediated by the T-cell receptor

Author

Fischer, K-D., primary, Kong, Y-Y., additional, Nishina, H., additional, Tedford, K., additional, Marengère, L.E.M., additional, Kozieradzki, I., additional, Sasaki, T., additional, Starr, M., additional, Chan, G., additional, Gardener, S., additional, Nghiem, M.P., additional, Bouchard, D., additional, Barbacid, M., additional, Bernstein, A., additional, and Penninger, J.M., additional

Published
1998
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26. High content, multi-parameter analyses in buccal cells to identify alzheimer’s disease

Author

François, M., Fenech, M. F., Thomas, P., Hor, M., Rembach, A., Martins, R. N., Rainey-Smith, S. R., Masters, C. L., Ames, D., Rowe, C. C., Lance Macaulay, S., Hill, A. F., Leifert, W. R., Appannah, A., Barnes, M., Barnham, K., Bedo, J., Bellingham, S., Bon, L., Bourgeat, P., Brown, B., Buckley, R., Burnham, S., Bush, A., Chandler, G., Chen, K., Clarnette, R., Collins, S., Cooke, I., Cowie, T., Cox, K., Cuningham, E., Cyarto, E., Dang, P. A. V., Darby, D., Desmond, P., Doecke, J., Dore, V., Downing, H., Dridan, B., Duesing, K., Fahey, M., Farrow, M., Faux, N., Fenech, M., Fernandez, S., Fernando, B., Fowler, C., Francois, M., Fripp, J., Frost, S., Gardener, S., Gibson, S., Graham, P., Gupta, V., Hansen, D., Harrington, K., Hill, A., Hone, E., Horne, M., Huckstepp, B., Jones, A., Jones, G., Kamer, A., Kanagasingam, Y., Keam, L., Kowalczyk, A., Krivdic, B., Lam, C. P., Lamb, F., Lautenschlager, N., Laws, S., Leifert, W., Lenzo, N., Leroux, H., Lftikhar, F., Li, Q. -X, Lim, F., Lim, L., Lockett, L., Lucas, K., Mano, M., Marczak, C., Martins, G., Maruff, P., Matsumoto, Y., Bird, S., Mcbride, S., Mckay, R., Mulligan, R., Nash, T., Nigro, J., O Keefe, G., Ong, K., Parker, B., Pedrini, S., Peiffer, J., Pejoska, S., Penny, L., Perez, K., Pertile, K., Phal, P., Porter, T., Rainey-Smith, S., Raniga, P., Restrepo, C., Riley, M., Roberts, B., Robertson, J., Rodrigues, M., Rooney, A., Rumble, R., Ryan, T., Salvado, O., Samuel, M., Saunders, I., Savage, G., Silbert, B., Sohrabi, H., Syrette, J., Cassandra Szoeke, Taddei, K., Taddei, T., Tan, S., Tegg, M., Trivedi, D., Trounson, B., Veljanovski, R., Verdile, G., Villemagne, V., Volitakis, I., Vockler, C., Vovos, M., Vrantsidis, F., Walker, S., Watt, A., Weinborn, M., Wilson, B., Woodward, M., Yastrubetskaya, O., Yates, P., Zhang, P., Chatterjee, P., Creegan, R., Ruyck, K., Ding, H., Groth, D., Head, R., Krause, D., Lachovitzki, R., Lim, Y. Y., Lintern, T., Mondal, A., Nuttall, S., O Callaghan, N., Osborne, L., Pang, C., Patten, G., Tuckfield, A., Varghese, J., Wilson, A., and Zhang, Q.

30. Analysis of Mammalian ras Effector Function

Author

Hall, A., primary, Cales, C., additional, Hancock, J.F., additional, Lloyd, A., additional, Self, A., additional, Gardener, S., additional, Houslay, M.D., additional, Wakelam, M.J.O., additional, and Marshall, C.J., additional

Published
1988
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36. Dietary patterns associated with Alzheimer's disease and related chronic disease risk: a review

Author

Gabriela Chiosis, Wenjie Lou, Sarah Kishinevsky, Aaron J. Carman, John Koren, Gardener, S, Rainey-Smith, SR, Keogh, JB, Mathieson, SL, and Martins, RN

Subjects
medicine.medical_specialty, education.field_of_study, Mediterranean diet, business.industry, Public health, Population, healthcare, Disease, Alzheimer's disease, medicine.disease, Omics, Obesity, nutrition, Diabetes mellitus, Environmental health, Health care, medicine, business, education, diet, chronic disease
Abstract

The world’s population is growing older due to improved healthcare and nutrition. As a result, Alzheimer’s disease (AD) prevalence is rapidly increasing. The focus of the current research climate is shifting from understanding AD pathology and diagnosis to primary prevention and intervention strategies. Diet represents one potential intervention strategy accessible to all. Accumulating evidence suggests diet plays a major role in risk and development of AD and AD-related chronic diseases of the periphery like cardiovascular disease (CVD) and diabetes. This paper reviews studies that have explored the relationship between “a priori” dietary patterns, AD and AD-related chronic disease risk. The dietary patterns we will review are the healthy eating index, healthy diet indicator, recommended food score, and the Mediterranean diet (MeDi). Our review of the literature suggests a generally positive association between healthy diet patterns, AD and AD-related chronic disease risk; however the magnitude of the protective effect is modest in many studies. Consequently, we can only confidently conclude that the MeDi is associated with reduced AD risk, and further studies on the remaining indices need to be carried out. It is our opinion that a combination of dietary scores could predict overall dietary quality and chronic disease risk to a greater extent than one score individually. Analysis in multi-ethnic cohorts, investigating combinations of scores must be completed before firm conclusions can be reached on the ideal combination of scores. Obtaining further insight into the association between dietary patterns, AD and AD-related chronic disease risk may help in prioritizing public health efforts and provide a stronger basis for recommendations to improve dietary patterns. Refereed/Peer-reviewed

Published
2013

37. Adherence to a Mediterranean diet and Alzheimer's disease risk in an Australian population

Author

Christopher C. Rowe, Peter M. Clifton, Cassandra Szoeke, Vanessa Ward, Samantha L. Gardener, David Ames, Richard Head, Yian Gu, Nikolaos Scarmeas, Stephanie R. Rainey-Smith, Kathryn A. Ellis, Jennifer B Keogh, Ralph N. Martins, Colin L. Masters, Alinda Mondal, Margaret Barnes, S L Macaulay, Kevin Taddei, S. L. Mathieson, Gardener, S, Gu, Y, Rainey-Smith, SR, Keogh, JB, Clifton, PM, Mathieson, SL, Taddei, K, Mondal, A, Ward, VK, Scarmeas, N, Barnes, M, Ellis, KA, Head, R, Masters, CL, Ames, D, Macaulay, SL, Rowe, CC, Szoeke, C, Martins, RN, and AIBL Research Group

Subjects
Male, Gerontology, medicine.medical_specialty, Mediterranean diet, Cross-sectional study, Neuropsychological Tests, AIBL, Diet, Mediterranean, Cohort Studies, Cellular and Molecular Neuroscience, Alzheimer Disease, Risk Factors, Surveys and Questionnaires, Internal medicine, Diabetes mellitus, Humans, Medicine, Dementia, Cognitive Dysfunction, Geriatric Assessment, Stroke, Biological Psychiatry, Aged, business.industry, Australia, Alzheimer's disease, medicine.disease, MCI, Psychiatry and Mental health, Cross-Sectional Studies, Cohort, Patient Compliance, Original Article, Female, business, Body mass index, Alzheimer’s disease, Follow-Up Studies, Cohort study
Abstract

The Mediterranean diet (MeDi), due to its correlation with a low morbidity and mortality for many chronic diseases, has been widely recognised as a healthy eating model. We aimed to investigate, in a cross-sectional study, the association between adherence to a MeDi and risk for Alzheimer's disease (AD) and mild cognitive impairment (MCI) in a large, elderly, Australian cohort. Subjects in the Australian Imaging, Biomarkers and Lifestyle Study of Ageing cohort (723 healthy controls (HC), 98 MCI and 149 AD participants) completed the Cancer Council of Victoria Food Frequency Questionnaire. Adherence to the MeDi (0- to 9-point scale with higher scores indicating higher adherence) was the main predictor of AD and MCI status in multinominal logistic regression models that were adjusted for cohort age, sex, country of birth, education, apolipoprotein E genotype, total caloric intake, current smoking status, body mass index, history of diabetes, hypertension, angina, heart attack and stroke. There was a significant difference in adherence to the MeDi between HC and AD subjects (P

Published
2012

38. Fluid biomarkers in cerebral amyloid angiopathy.

Author

Savar SM, Ma B, Hone E, Jahan F, Markovic S, Pedrini S, Shemehsavar S, Easwaran V, Taddei K, Gardener S, Chhatwal JP, van Etten ES, van Osch MJP, Clarke D, Gnjec A, van Buchem MA, Wermer MJH, Hankey GJ, Greenberg SM, Martins RN, and Sohrabi HR

Abstract

Cerebral amyloid angiopathy (CAA) is a type of cerebrovascular disorder characterised by the accumulation of amyloid within the leptomeninges and small/medium-sized cerebral blood vessels. Typically, cerebral haemorrhages are one of the first clinical manifestations of CAA, posing a considerable challenge to the timely diagnosis of CAA as the bleedings only occur during the later disease stages. Fluid biomarkers may change prior to imaging biomarkers, and therefore, they could be the future of CAA diagnosis. Additionally, they can be used as primary outcome markers in prospective clinical trials. Among fluid biomarkers, blood-based biomarkers offer a distinct advantage over cerebrospinal fluid biomarkers as they do not require a procedure as invasive as a lumbar puncture. This article aimed to provide an overview of the present clinical data concerning fluid biomarkers associated with CAA and point out the direction of future studies. Among all the biomarkers discussed, amyloid β, neurofilament light chain, matrix metalloproteinases, complement 3, uric acid, and lactadherin demonstrated the most promising evidence. However, the field of fluid biomarkers for CAA is an under-researched area, and in most cases, there are only one or two studies on each of the biomarkers mentioned in this review. Additionally, a small sample size is a common limitation of the discussed studies. Hence, it is hard to reach a solid conclusion on the clinical significance of each biomarker at different stages of the disease or in various subpopulations of CAA. In order to overcome this issue, larger longitudinal and multicentered studies are needed., Competing Interests: The authors declare that while some of their CAA research projects have been supported by commercial funding from Biogen Inc. and Alnylam Pharmaceuticals, this specific manuscript did not receive any funding and the funders of our research were not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Savar, Ma, Hone, Jahan, Markovic, Pedrini, Shemehsavar, Easwaran, Taddei, Gardener, Chhatwal, van Etten, van Osch, Clarke, Gnjec, van Buchem, Wermer, Hankey, Greenberg, Martins and Sohrabi.)

Published
2024
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39. Plasma Amyloid-Beta Levels in a Pre-Symptomatic Dutch-Type Hereditary Cerebral Amyloid Angiopathy Pedigree: A Cross-Sectional and Longitudinal Investigation.

Author

Chatterjee P, Tegg M, Pedrini S, Fagan AM, Xiong C, Singh AK, Taddei K, Gardener S, Masters CL, Schofield PR, Multhaup G, Benzinger TLS, Morris JC, Bateman RJ, Greenberg SM, van Buchem MA, Stoops E, Vanderstichele H, Teunissen CE, Hankey GJ, Wermer MJH, Sohrabi HR, Martins RN, and The Dominantly Inherited Alzheimer Network

Subjects
Adult, Amyloid beta-Peptides blood, Amyloid beta-Protein Precursor blood, Asymptomatic Diseases, Biomarkers blood, Cerebral Amyloid Angiopathy, Familial blood, Cerebral Amyloid Angiopathy, Familial diagnosis, Cerebral Amyloid Angiopathy, Familial pathology, Disease Progression, Female, Gene Expression, Genes, Dominant, Heterozygote, Humans, Longitudinal Studies, Male, Middle Aged, Mutation, Neuropsychological Tests, Pedigree, Peptide Fragments blood, Amyloid beta-Peptides genetics, Amyloid beta-Protein Precursor genetics, Cerebral Amyloid Angiopathy, Familial genetics, Peptide Fragments genetics
Abstract

Plasma amyloid-beta (Aβ) has long been investigated as a blood biomarker candidate for Cerebral Amyloid Angiopathy (CAA), however previous findings have been inconsistent which could be attributed to the use of less sensitive assays. This study investigates plasma Aβ alterations between pre-symptomatic Dutch-type hereditary CAA (D-CAA) mutation-carriers (MC) and non-carriers (NC) using two Aβ measurement platforms. Seventeen pre-symptomatic members of a D-CAA pedigree were assembled and followed up 3-4 years later (NC = 8; MC = 9). Plasma Aβ1-40 and Aβ1-42 were cross-sectionally and longitudinally analysed at baseline (T1) and follow-up (T2) and were found to be lower in MCs compared to NCs, cross-sectionally after adjusting for covariates, at both T1(Aβ1-40: p = 0.001; Aβ1-42: p = 0.0004) and T2 (Aβ1-40: p = 0.001; Aβ1-42: p = 0.016) employing the Single Molecule Array (Simoa) platform, however no significant differences were observed using the xMAP platform. Further, pairwise longitudinal analyses of plasma Aβ1-40 revealed decreased levels in MCs using data from the Simoa platform ( p = 0.041) and pairwise longitudinal analyses of plasma Aβ1-42 revealed decreased levels in MCs using data from the xMAP platform ( p = 0.041). Findings from the Simoa platform suggest that plasma Aβ may add value to a panel of biomarkers for the diagnosis of pre-symptomatic CAA, however, further validation studies in larger sample sets are required.

Published
2021
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40. Adherence to a Mediterranean diet and Alzheimer's disease risk in an Australian population.

Author

Gardener S, Gu Y, Rainey-Smith SR, Keogh JB, Clifton PM, Mathieson SL, Taddei K, Mondal A, Ward VK, Scarmeas N, Barnes M, Ellis KA, Head R, Masters CL, Ames D, Macaulay SL, Rowe CC, Szoeke C, and Martins RN

Subjects
Aged, Alzheimer Disease prevention & control, Australia epidemiology, Cognitive Dysfunction epidemiology, Cognitive Dysfunction prevention & control, Cohort Studies, Cross-Sectional Studies, Female, Follow-Up Studies, Geriatric Assessment methods, Geriatric Assessment statistics & numerical data, Humans, Male, Neuropsychological Tests statistics & numerical data, Risk Factors, Surveys and Questionnaires, Alzheimer Disease epidemiology, Diet, Mediterranean statistics & numerical data, Patient Compliance statistics & numerical data
Abstract

The Mediterranean diet (MeDi), due to its correlation with a low morbidity and mortality for many chronic diseases, has been widely recognised as a healthy eating model. We aimed to investigate, in a cross-sectional study, the association between adherence to a MeDi and risk for Alzheimer's disease (AD) and mild cognitive impairment (MCI) in a large, elderly, Australian cohort. Subjects in the Australian Imaging, Biomarkers and Lifestyle Study of Ageing cohort (723 healthy controls (HC), 98 MCI and 149 AD participants) completed the Cancer Council of Victoria Food Frequency Questionnaire. Adherence to the MeDi (0- to 9-point scale with higher scores indicating higher adherence) was the main predictor of AD and MCI status in multinominal logistic regression models that were adjusted for cohort age, sex, country of birth, education, apolipoprotein E genotype, total caloric intake, current smoking status, body mass index, history of diabetes, hypertension, angina, heart attack and stroke. There was a significant difference in adherence to the MeDi between HC and AD subjects (P < 0.001), and in adherence between HC and MCI subjects (P < 0.05). MeDi is associated with change in Mini-Mental State Examination score over an 18-month time period (P < 0.05) in HCs. We conclude that in this Australian cohort, AD and MCI participants had a lower adherence to the MeDi than HC participants.

Published
2012
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41. Mood and somatic symptoms during pregnancy.

Author

Lubin B, Gardener SH, and Roth A

Subjects
Abortion, Spontaneous, Abortion, Therapeutic, Adult, Age Factors, Educational Status, Female, Fetal Death, Humans, Indiana, Menstruation Disturbances complications, Parity, Pregnancy, Pregnancy Trimester, First, Pregnancy Trimester, Second, Pregnancy Trimester, Third, Social Class, Test Anxiety Scale, Anxiety, Depression epidemiology, Pregnancy Complications, Psychophysiologic Disorders epidemiology
Abstract

A predominantly white, middle class sample of pregnant women (N = 93) completed the AACL (Anxiety), the DACL (Depressive Mood), the SCL (Somatic Symptoms) and the IPAT Anxiety Questionnaire at the second, fifth and eighth months of pregnancy. A menstrual history questionnaire was administered on the first testing occasion. Analyses revealed that anxiety varied significantly as a function of trimester and that previous pregnancy history interacted significantly with trimester. Depressive mood was not significantly affected by any of the sources of variation. Correlational analysis (average correlations over trimesters) indicated significant relationships between somatic symptoms and anxiety, but not between somatic symptoms and depressive mood; a small but significant relationship between history of menstrual complaint and somatic symptoms; and a significant negative correlation between education and overt anxiety.

Published
1975
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