Search

Your search keyword '"Solfrizzi V."' showing total 30 results
Start Over Author "Solfrizzi V." Publication Type Magazines
30 results on '"Solfrizzi V."'

1. Additive Role of a Potentially Reversible Cognitive Frailty Model and Inflammatory State on the Risk of Disability: The Italian Longitudinal Study on Aging

Author

Solfrizzi, Vincenzo, Scafato, Emanuele, Lozupone, Madia, Seripa, Davide, Giannini, Michele, Sardone, Rodolfo, Bonfiglio, Caterina, Abbrescia, Daniela I., Galluzzo, Lucia, Gandin, Claudia, Baldereschi, Marzia, Di Carlo, Antonio, Inzitari, Domenico, Daniele, Antonio, Sabbà, Carlo, Logroscino, Giancarlo, Panza, Francesco, Scafato, E., Farchi, G., Galluzzo, L., Gandin, C., Capurso, A., Panza, F., Solfrizzi, V., Lepore, V., Livrea, P., Motta, L., Carnazzo, G., Motta, M., Bentivegna, P., Bonaiuto, S., Cruciani, G., Postacchini, D., Inzitari, D., Amaducci, L., Di Carlo, A., Baldereschi, M., Gandolfo, C., Conti, M., Canal, N., Franceschi, M., Scarlato, G., Candelise, L., Scapini, E., Rengo, F., Abete, P., Cacciatore, F., Enzi, G., Battistin, L., Sergi, G., Crepaldi, G., Maggi, S., Minicucci, N., Noale, M., Grigoletto, F., Perissinotto, E., and Carbonin, P.

Abstract

•Cognitive frailty described coexisting physical frailty and cognitive impairment in nondemented older subjects.•Two subtypes have been proposed: “potentially reversible” cognitive frailty [physical frailty plus mild cognitive impairment (MCI)] and “reversible” cognitive frailty (physical frailty plus pre-MCI subjective cognitive decline).•The prevalence of potentially reversible cognitive frailty was 1 %, with all groups associated to increased incident rate ratios of dementia, disability, and mortality.•A significant difference in disability rates existed between the MCI and non-MCI groups in frail individuals with high inflammation.•With inflammation, a potentially reversible cognitive frailty model may have an additional predictive effect on the disability risk than frailty or MCI alone.

Published
2017
Full Text
View/download PDF

2. Worldwide trends in diabetes since 1980: a pooled analysis of 751 population-based studies with 4·4 million participants

Author

Zhou, B, Lu, Y, Hajifathalian, K, Bentham, J, Di Cesare, M, Danaei, G, Bixby, H, Cowan, MJ, Ali, MK, Taddei, C, Lo, WC, Reis-Santos, B, Stevens, GA, Riley, LM, Miranda, JJ, Bjerregaard, P, Rivera, JA, Fouad, HM, Ma, G, Mbanya, JC, McGarvey, ST, Mohan, V, Onat, A, Pilav, A, Ramachandran, A, Romdhane, HB, Paciorek, CJ, Bennett, JE, Ezzati, M, Abdeen, ZA, Abdul Kadir, K, Abu-Rmeileh, NM, Acosta-Cazares, B, Adams, R, Aekplakorn, W, Aguilar-Salinas, CA, Agyemang, C, Ahmadvand, A, Al-Othman, AR, Alkerwi, A, Amouyel, P, Amuzu, A, Andersen, LB, Anderssen, SA, Anjana, RM, Aounallah-Skhiri, H, Aris, T, Arlappa, N, Arveiler, D, Assah, FK, Avdicová, M, Azizi, F, Balakrishna, N, Bandosz, P, Barbagallo, CM, Barceló, A, Batieha, AM, Baur, LA, Romdhane, HB, Benet, M, Bernabe-Ortiz, A, Bharadwaj, S, Bhargava, SK, Bi, Y, Bjerregaard, P, Bjertness, E, Bjertness, MB, Björkelund, C, Blokstra, A, Bo, S, Boehm, BO, Boissonnet, CP, Bovet, P, Brajkovich, I, Breckenkamp, J, Brenner, H, Brewster, LM, Brian, GR, Bruno, G, Bugge, A, Cabrera de León, A, Can, G, Cândido, AP, Capuano, V, Carlsson, AC, Carvalho, MJ, Casanueva, FF, Casas, JP, Caserta, CA, Castetbon, K, Chamukuttan, S, Chaturvedi, N, Chen, CJ, Chen, F, Chen, S, Cheng, CY, Chetrit, A, Chiou, ST, Cho, Y, Chudek, J, Cifkova, R, Claessens, F, Concin, H, Cooper, C, Cooper, R, Costanzo, S, Cottel, D, Cowell, C, Crujeiras, AB, D'Arrigo, G, Dallongeville, J, Dankner, R, Dauchet, L, de Gaetano, G, De Henauw, S, Deepa, M, Dehghan, A, Deschamps, V, Dhana, K, Di Castelnuovo, AF, Djalalinia, S, Doua, K, Drygas, W, Du, Y, Dzerve, V, Egbagbe, EE, Eggertsen, R, El Ati, J, Elosua, R, Erasmus, RT, Erem, C, Ergor, G, Eriksen, L, Escobedo-de la Peña, J, Fall, CH, Farzadfar, F, Felix-Redondo, FJ, Ferguson, TS, Fernández-Bergés, D, Ferrari, M, Ferreccio, C, Feskens, EJ, Finn, JD, Föger, B, Foo, LH, Forslund, AS, Fouad, HM, Francis, DK, Franco Mdo, C, Franco, OH, Frontera, G, Furusawa, T, Gaciong, Z, Garnett, SP, Gaspoz, JM, Gasull, M, Gates, L, Geleijnse, JM, Ghasemian, A, Ghimire, A, Giampaoli, S, Gianfagna, F, Giovannelli, J, Giwercman, A, Gross, MG, González Rivas, JP, Gorbea, MB, Gottrand, F, Grafnetter, D, Grodzicki, T, Grøntved, A, Gruden, G, Gu, D, Guan, OP, Guerrero, R, Guessous, I, Guimaraes, AL, Gutierrez, L, Hambleton, IR, Hardy, R, Hari Kumar, R, Hata, J, He, J, Heidemann, C, Herrala, S, Hihtaniemi, IT, Ho, SY, Ho, SC, Hofman, A, Hormiga, CM, Horta, BL, Houti, L, Howitt, C, Htay, TT, Htet, AS, Htike, MM, Hu, Y, Hussieni, AS, Huybrechts, I, Hwalla, N, Iacoviello, L, Iannone, AG, Ibrahim, MM, Ikeda, N, Ikram, MA, Irazola, VE, Islam, M, Iwasaki, M, Jacobs, JM, Jafar, T, Jamil, KM, Jasienska, G, Jiang, CQ, Jonas, JB, Joshi, P, Kafatos, A, Kalter-Leibovici, O, Kasaeian, A, Katz, J, Kaur, P, Kavousi, M, Keinänen-Kiukaanniemi, S, Kelishadi, R, Kengne, AP, Kersting, M, Khader, YS, Khalili, D, Khang, YH, Kiechl, S, Kim, J, Kolsteren, P, Korrovits, P, Kratzer, W, Kromhout, D, Kujala, UM, Kula, K, Kyobutungi, C, Laatikainen, T, Lachat, C, Laid, Y, Lam, TH, Landrove, O, Lanska, V, Lappas, G, Laxmaiah, A, Leclercq, C, Lee, J, Lee, J, Lehtimäki, T, Lekhraj, R, León-Muñoz, LM, Li, Y, Lim, WY, Lima-Costa, MF, Lin, HH, Lin, X, Lissner, L, Lorbeer, R, Lozano, JE, Luksiene, D, Lundqvist, A, Lytsy, P, Ma, G, Machado-Coelho, GL, Machi, S, Maggi, S, Magliano, DJ, Makdisse, M, Mallikharjuna Rao, K, Manios, Y, Manzato, E, Margozzini, P, Marques-Vidal, P, Martorell, R, Masoodi, SR, Mathiesen, EB, Matsha, TE, Mbanya, JC, McFarlane, SR, McGarvey, ST, McLachlan, S, McNulty, BA, Mediene-Benchekor, S, Meirhaeghe, A, Menezes, AM, Merat, S, Meshram, II, Mi, J, Miquel, JF, Miranda, JJ, Mohamed, MK, Mohammad, K, Mohammadifard, N, Mohan, V, Mohd Yusoff, MF, Møller, NC, Molnár, D, Mondo, CK, Morejon, A, Moreno, LA, Morgan, K, Moschonis, G, Mossakowska, M, Mostafa, A, Mota, J, Motta, J, Mu, TT, Muiesan, ML, Müller-Nurasyid, M, Mursu, J, Nagel, G, Námešná, J, Nang, EE, NangThetia, VB, Navarrete-Muñoz, EM, Ndiaye, NC, Nenko, I, Nervi, F, Nguyen, ND, Nguyen, QN, Nieto-Martínez, RE, Ning, G, Ninomiya, T, Noale, M, Noto, D, Nsour, MA, Ochoa-Avilés, AM, Oh, K, Onat, A, Ordunez, P, Osmond, C, Otero, JA, Owusu-Dabo, E, Pahomova, E, Palmieri, L, Panda-Jonas, S, Panza, F, Parsaeian, M, Peixoto, SV, Pelletier, C, Peltonen, M, Peters, A, Peykari, N, Pham, ST, Pilav, A, Pitakaka, F, Piwonska, A, Piwonski, J, Plans-Rubió, P, Porta, M, Portegies, ML, Poustchi, H, Pradeepa, R, Price, JF, Punab, M, Qasrawi, RF, Qorbani, M, Radisauskas, R, Rahman, M, Raitakari, O, Rao, SR, Ramachandran, A, Ramke, J, Ramos, R, Rampal, S, Rathmann, W, Redon, J, Reganit, PF, Rigo, F, Robinson, SM, Robitaille, C, Rodríguez-Artalejo, F, Rodriguez-Perez Mdel, C, Rodríguez-Villamizar, LA, Rojas-Martinez, R, Ronkainen, K, Rosengren, A, Rubinstein, A, Rui, O, Ruiz-Betancourt, BS, Russo Horimoto, RV, Rutkowski, M, Sabanayagam, C, Sachdev, HS, Saidi, O, Sakarya, S, Salanave, B, Salonen, JT, Salvetti, M, Sánchez-Abanto, J, Santos, D, dos Santos, RN, Santos, R, Saramies, JL, Sardinha, LB, Sarrafzadegan, N, Saum, KU, Scazufca, M, Schargrodsky, H, Scheidt-Nave, C, Sein, AA, Sharma, SK, Shaw, JE, Shibuya, K, Shin, Y, Shiri, R, Siantar, R, Sibai, AM, Simon, M, Simons, J, Simons, LA, Sjostrom, M, Slowikowska-Hilczer, J, Slusarczyk, P, Smeeth, L, Snijder, MB, So, HK, Sobngwi, E, Söderberg, S, Solfrizzi, V, Sonestedt, E, Soumare, A, Staessen, JA, Stathopoulou, MG, Steene-Johannessen, J, Stehle, P, Stein, AD, Stessman, J, Stöckl, D, Stokwiszewski, J, Stronks, K, Strufaldi, MW, Sun, CA, Sundström, J, Sung, YT, Suriyawongpaisal, P, Sy, RG, Tai, ES, Tamosiunas, A, Tang, L, Tarawneh, M, Tarqui-Mamani, CB, Taylor, A, Theobald, H, Thijs, L, Thuesen, BH, Tolonen, HK, Tolstrup, JS, Topbas, M, Torrent, M, Traissac, P, Trinh, OT, Tulloch-Reid, MK, Tuomainen, TP, Turley, ML, Tzourio, C, Ueda, P, Ukoli, FA, Ulmer, H, Uusitalo, HM, Valdivia, G, Valvi, D, van Rossem, L, van Valkengoed, IG, Vanderschueren, D, Vanuzzo, D, Vega, T, Velasquez-Melendez, G, Veronesi, G, Verschuren, WM, Verstraeten, R, Viet, L, Vioque, J, Virtanen, JK, Visvikis-Siest, S, Viswanathan, B, Vollenweider, P, Voutilainen, S, Vrijheid, M, Wade, AN, Wagner, A, Walton, J, Wan Mohamud, WN, Wang, F, Wang, MD, Wang, Q, Wang, YX, Wannamethee, SG, Weerasekera, D, Whincup, PH, Widhalm, K, Wiecek, A, Wijga, AH, Wilks, RJ, Willeit, J, Wilsgaard, T, Wojtyniak, B, Wong, TY, Woo, J, Woodward, M, Wu, FC, Wu, SL, Xu, H, Yan, W, Yang, X, Ye, X, Yoshihara, A, Younger-Coleman, NO, Zambon, S, Zargar, AH, Zdrojewski, T, Zhao, W, Zheng, Y, and Zuñiga Cisneros, J

Abstract

One of the global targets for non-communicable diseases is to halt, by 2025, the rise in the age-standardised adult prevalence of diabetes at its 2010 levels. We aimed to estimate worldwide trends in diabetes, how likely it is for countries to achieve the global target, and how changes in prevalence, together with population growth and ageing, are affecting the number of adults with diabetes.

Published
2016
Full Text
View/download PDF

3. Effects of diabetes definition on global surveillance of diabetes prevalence and diagnosis: a pooled analysis of 96 population-based studies with 331 288 participants

Author

Danaei, G, Fahimi, S, Lu, Y, Zhou, B, Hajifathalian, K, Di Cesare, M, Lo, WC, Reis-Santos, B, Cowan, MJ, Shaw, JE, Bentham, J, Lin, JK, Bixby, H, Magliano, D, Bovet, P, Miranda, JJ, Khang, YH, Stevens, GA, Riley, LM, Ali, MK, Ezzati, M, Abdeen, ZA, Kadir, KA, Abu-Rmeileh, M, Acosta-Cazares, B, Aekplakorn, W, Aguilar-Salinas, CA, Ahmadvand, A, Al Nsour, M, Alkerwi, A, Amouyel, P, Andersen, LB, Anderssen, SA, Andrade, DS, Anjana, RM, Aounallah-Skhiri, H, Aris, T, Arlappa, N, Arveiler, D, Assah, FK, Avdicová, M, Balakrishna, N, Bandosz, P, Barbagallo, CM, Barceló, A, Batieha, AM, Baur, LA, Ben Romdhane, H, Bernabe-Ortiz, A, Bhargava, SK, Bi, Y, Bjerregaard, P, Björkelund, C, Blake, M, Blokstra, A, Bo, S, Boehm, BO, Boissonnet, CP, Bovet, P, Brajkovich, I, Breckenkamp, J, Brewster, LM, Brian, GR, Bruno, G, Bugge, A, Cabrera de León, A, Can, G, Cândido, AP, Capuano, V, Carvalho, MJ, Casanueva, FF, Caserta, CA, Castetbon, K, Chamukuttan, S, Chaturvedi, N, Chen, CJ, Chen, F, Chen, S, Cheng, CY, Chetrit, A, Chiou, ST, Cho, Y, Chudek, J, Cifkova, R, Claessens, F, Concin, H, Cooper, C, Cooper, R, Costanzo, S, Cottel, D, Cowell, C, Crujeiras, AB, D'Arrigo, G, Dallongeville, J, Dankner, R, Dauchet, L, de Gaetano, G, De Henauw, S, Deepa, M, Dehghan, A, Dhana, K, Di Castelnuovo, AF, Djalalinia, S, Doua, K, Drygas, W, Du, Y, Egbagbe, EE, Eggertsen, R, El Ati, J, Elosua, R, Erasmus, RT, Erem, C, Ergor, G, Eriksen, L, Escobedo-de la Peña, J, Fall, CH, Farzadfar, F, Felix-Redondo, FJ, Ferguson, TS, Fernández-Bergés, D, Ferrari, M, Ferreccio, C, Finn, JD, Föger, B, Foo, LH, Fouad, HM, Francis, DK, Franco Mdo, C, Frontera, G, Furusawa, T, Gaciong, Z, Galbarczyk, A, Garnett, SP, Gaspoz, JM, Gasull, M, Gates, L, Geleijnse, JM, Ghasemain, A, Giampaoli, S, Gianfagna, F, Giovannelli, J, Gonzalez Gross, M, González Rivas, JP, Gorbea, MB, Gottrand, F, Grant, JF, Grodzicki, T, Grøntved, A, Gruden, G, Gu, D, Guan, OP, Guerrero, R, Guessous, I, Guimaraes, AL, Gutierrez, L, Hardy, R, Hari Kumar, R, Heidemann, C, Hihtaniemi, IT, Ho, SY, Ho, SC, Hofman, A, Horimoto, AR, Hormiga, CM, Horta, BL, Houti, L, Hussieni, AS, Huybrechts, I, Hwalla, N, Iacoviello, L, Iannone, AG, Ibrahim, MM, Ikeda, N, Ikram, MA, Irazola, VE, Islam, M, Iwasaki, M, Jacobs, JM, Jafar, T, Jasienska, G, Jiang, CQ, Jonas, JB, Joshi, P, Kafatos, A, Kalter-Leibovici, O, Kasaeian, A, Katz, J, Kaur, P, Kavousi, M, Kelishadi, R, Kengne, AP, Kersting, M, Khader, YS, Khang, YH, Kiechl, S, Kim, J, Kiyohara, Y, Kolsteren, P, Korrovits, P, Koskinen, S, Kratzer, W, Kromhout, D, Kula, K, Kurjata, P, Kyobutungi, C, Lachat, C, Laid, Y, Lam, TH, Lanska, V, Lappas, G, Laxmaiah, A, Leclercq, C, Lee, J, Lee, J, Lehtimäki, T, Lekhraj, R, León-Muñoz, LM, Li, Y, Lim, WY, Lima-Costa, MF, Lin, HH, Lin, X, Lissner, L, Lorbeer, R, Lozano, JE, Lundqvist, A, Lytsy, P, Ma, G, Machado-Coelho, GL, Machi, S, Maggi, S, Magliano, D, Makdisse, M, Mallikharjuna v, K, Manios, Y, Manzato, E, Margozzini, P, Marques-Vidal, P, Martorell, R, Masoodi, SR, Matsha, TE, Mbanya, JC, McFarlane, SR, McGarvey, ST, McLachlan, S, McNulty, BA, Mediene-Benchekor, S, Meirhaeghe, A, Menezes, AM, Merat, S, Meshram, II, Mi, J, Miquel, JF, Miranda, JJ, Mohamed, MK, Mohammad, K, Mohan, V, Mohd Yusoff, MF, Møller, NC, Molnar, D, Mondo, CK, Moreno, LA, Morgan, K, Moschonis, G, Mossakowska, M, Mostafa, A, Mota, J, Muiesan, ML, Müller-Nurasyid, M, Mursu, J, Nagel, G, Námešná, J, Nang, EE, Nangia, VB, Navarrete-Muñoz, EM, Ndiaye, NC, Nervi, F, Nguyen, ND, Nieto-Martínez, RE, Alvarado, L, Ning, G, Ninomiya, T, Noale, M, Noto, D, Ochoa-Avilés, M, Oh, K, Onat, A, Osmond, C, Otero, JA, Palmieri, L, Panda-Jonas, S, Panza, F, Parsaeian, M, Peixoto, SV, Pereira, AC, Peters, A, Peykari, N, Pilav, A, Pitakaka, F, Piwonska, A, Piwonski, J, Plans-Rubió, P, Porta, M, Portegies, ML, Poustchi, H, Pradeepa, R, Price, JF, Punab, M, Qasrawi, RF, Qorbani, M, Raitakari, O, Ramachandra Rao, S, Ramachandran, A, Ramos, R, Rampal, S, Rathmann, W, Redon, J, Reganit, PF, Rigo, F, Robinson, SM, Robitaille, C, Rodríguez, LA, Rodríguez-Artalejo, F, del Cristo Rodriguez-Perez, M, Rojas-Martinez, R, Romaguera, D, Rosengren, A, Rubinstein, A, Rui, O, Ruiz-Betancourt, BS, Rutkowski, M, Sabanayagam, C, Sachdev, HS, Saidi, O, Sakarya, S, Salanave, B, Salonen, JT, Salvetti, M, Sánchez-Abanto, J, Santos, RN, Santos, R, Sardinha, LB, Scazufca, M, Schargrodsky, H, Scheidt-Nave, C, Shaw, JE, Shibuya, K, Shin, Y, Shiri, R, Siantar, R, Sibai, AM, Simon, M, Simons, J, Simons, LA, Sjostrom, M, Slowikowska-Hilczer, J, Slusarczyk, P, Smeeth, L, Snijder, MB, Solfrizzi, V, Sonestedt, E, Soumare, A, Staessen, JA, Steene-Johannessen, J, Stehle, P, Stein, AD, Stessman, J, Stöckl, D, Stokwiszewski, J, Strufaldi, MW, Sun, CA, Sundström, J, Suriyawongpaisal, P, Sy, RG, Tai, ES, Tarawneh, M, Tarqui-Mamani, CB, Thijs, L, Tolstrup, JS, Topbas, M, Torrent, M, Traissac, P, Trinh, OT, Tulloch-Reid, MK, Tuomainen, TP, Turley, ML, Tzourio, C, Ueda, P, Ukoli, FM, Ulmer, H, Valdivia, G, van Valkengoed, IG, Vanderschueren, D, Vanuzzo, D, Vega, T, Velasquez-Melendez, G, Veronesi, G, Verschuren, M, Vioque, J, Virtanen, J, Visvikis-Siest, S, Viswanathan, B, Vollenweider, P, Voutilainen, S, Wade, AN, Wagner, A, Walton, J, Mohamud, WN, Wang, MD, Wang, YX, Wannamethee, SG, Weerasekera, D, Whincup, PH, Widhalm, K, Wiecek, A, Wilks, RJ, Willeit, J, Wojtyniak, B, Wong, TY, Woo, J, Woodward, M, Wu, AG, Wu, FC, Wu, SL, Xu, H, Yang, X, Ye, X, Yoshihara, A, Younger-Coleman, NO, Zambon, S, Zargar, AH, Zdrojewski, T, Zhao, W, and Zheng, Y

Abstract

Diabetes has been defined on the basis of different biomarkers, including fasting plasma glucose (FPG), 2-h plasma glucose in an oral glucose tolerance test (2hOGTT), and HbA1c. We assessed the effect of different diagnostic definitions on both the population prevalence of diabetes and the classification of previously undiagnosed individuals as having diabetes versus not having diabetes in a pooled analysis of data from population-based health examination surveys in different regions.

Published
2015
Full Text
View/download PDF

4. Interacting with γSecretase for Treating Alzheimers Disease: From Inhibition to Modulation

Author

Panza, F., Frisardi, V., Solfrizzi, V., P. Imbimbo, B., Logroscino, G., Santamato, A., Greco, A., Seripa, D., and Pilotto, A.

Abstract

Drugs currently used for the treatment of Alzheimers disease (AD) produce limited clinical benefits, and there is no diseasemodifying therapy yet available. Compounds that inhibit or modulate γ-secretase, the pivotal enzyme that generates -amyloid (A), are potential therapeutics for AD. This article briefly reviews the profile of γ-secretase inhibitors and modulators that have reached the clinic. Studies in both transgenic and non-transgenic animal models of AD have indicated that γsecretase inhibitors, administered by the oral route, are able to lower brain A concentrations. However, scanty data are available on the effects of these compounds on brain A deposition after prolonged administration. γ-Secretase inhibitors may cause abnormalities in the gastrointestinal tract, thymus, spleen, skin, and decrease in lymphocytes and alterations in hair color in experimental animals and in man, effects believed to be associated with the inhibition of the cleavage of Notch, a transmembrane receptor involved in regulating cell-fate decisions. Unfortunately, two large Phase III clinical trials of semagacestat in mild-to-moderate AD patients were prematurely interrupted because of the observation of a detrimental cognitive and functional effect of the drug. These detrimental effects were mainly ascribed to the inhibition of the processing of an unknown substrate of γ-secretase. It has been also hypothesized that the detrimental cognitive effects observed after semagacestat administration are due to the accumulation of the neurotoxic precursor of A (the carboxy-terminal fragment of amyloid precursor protein, APP, or CTF) resulting from the block of the γ-secretase cleavage activity on APP. Some non-steroidal anti-inflammatory drugs and other small organic molecules have been found to modulate γsecretase shifting its cleavage activity from longer to shorter A species without affecting Notch cleavage. However, two large Phase III studies in mild AD patients with tarenflurbil, a putative γ- secretase modulator, were also completely negative. The failure of tarenflurbil was ascribed to low potency and brain penetration. New more selective γ-secretase inhibitors and more potent, more brain penetrant γ-secretase modulators are being developed with the hope of overcoming the previous setbacks. Further understanding of the reasons of the failures of these γ-secretase-based drugs in AD may be important for the future research on effective treatments for this devastating disease.

Published
2011

5. Mediterranean Diet in Predementia and Dementia Syndromes

Author

Solfrizzi, V., Frisardi, V., Seripa, D., Logroscino, G., P. Imbimbo, B., DOnofrio, G., Addante, F., Sancarlo, D., Cascavilla, L., Pilotto, A., and Panza, F.

Abstract

There is a critical need to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. Only recently higher adherence to a Mediterranean-type diet was associated with decreased cognitive decline although the Mediterranean diet (MeDi) combines several foods, micro- and macronutrients already separately proposed as potential protective factors against dementia and predementia syndromes. In fact, elevated saturated fatty acids could have negative effects on age-related cognitive decline and mild cognitive impairment (MCI). Furthermore, at present, epidemiological evidence suggested a possible association among fish consumption, monounsaturated fatty acids and polyunsaturated fatty acids (PUFA) (particularly, n-3 PUFA) and reduced risk of cognitive decline and dementia. Light to moderate alcohol use may be associated with a reduced risk of incident dementia and Alzheimers disease (AD), while for vascular dementia, cognitive decline, and predementia syndromes the current evidence is only suggestive of a protective effect. Finally, the limited epidemiological evidence available on fruit and vegetable consumption and cognition generally supported a protective role of these macronutrients against cognitive decline, dementia, and AD. Moreover, recent prospective studies provided evidence that higher adherence to a Mediterranean-type diet could be associated with slower cognitive decline, reduced risk of progression from MCI to AD, reduced risk of AD, and decreased all-causes mortality in AD patients. These findings suggested that adherence to the MeDi may affect not only the risk for AD, but also for predementia syndromes and their progression to overt dementia. Nonetheless, at present, no definitive dietary recommendations are possible. However, high levels of consumption of fats from fish, vegetable oils, non-starchy vegetables, low glycemic fruits, and diet low in foods with added sugars and with moderate wine intake should be encouraged. In fact, this dietary advice is in accordance with recommendations for lowering the risk of cardiovascular disease, obesity, diabetes, and hypertension and might open new ways for the prevention and management of cognitive decline and dementia.

Published
2011

6. Metabolic Syndrome, Mild Cognitive Impairment and Dementia

Author

Panza, F., Frisardi, V., Seripa, D., P. Imbimbo, B., Sancarlo, D., DOnofrio, G., Addante, F., Paris, F., Pilotto, A., and Solfrizzi, V.

Abstract

At present, the search for preventive strategies for cognitive decline and dementia appears to be of crucial importance, given that the therapeutic options currently available have demonstrated limited efficacy. Cumulative epidemiological evidence suggested that vascular and vascular-related factors may be important for the development of agerelated cognitive decline (ARCD), mild cognitive impairment (MCI), and cognitive decline of degenerative (Alzheimers disease, AD) or vascular origin (vascular dementia, VaD). Among vascular-related factors, metabolic syndrome (MetS) has been associated with the increased risk of predementia syndromes (ARCD and MCI), overall dementia, and VaD, but contrasting findings also exist on the possible role of MetS in AD. In the next future, trials could then be undertaken to determine if modifications of these risks including inflammation, another factor probably related to MetS, could lower risk of developing cognitive decline. If MetS is associated with increased risk of developing cognitive impairment, then early identification and treatment of these individuals at risk might offer new avenues for disease course modification. Future research aimed at identifying mechanisms that underlie comorbid associations will not only provide important insights into the causes and interdependencies of predementia and dementia syndromes, but will also inspire novel strategies for treating and preventing these disorders. At present, vascular risk factor management could be decisive in delaying the onset of dementia syndromes or in preventing the progression of predementia syndromes.

Published
2011

7. Towards Disease-Modifying Treatment of Alzheimers Disease: Drugs Targeting -Amyloid

Author

Frisardi, V., Solfrizzi, V., Imbimbo, B., Capurso, C., DIntrono, A., Colacicco, A., Vendemiale, G., Seripa, D., Pilotto, A., and Capurso, A.

Abstract

Pathological, genetic, biochemical and pharmacological studies support the hypothesis that brain accumulation of oligomeric species of -amyloid (A) peptides may cause Alzheimers disease (AD). Drugs currently used for the treatment of AD produce limited clinical benefits and do not treat the underlying causes of the disease. In the last 10 years, new therapeutic approaches targeting A have been discovered and developed with the hope of modifying the natural history of the disease. Several active and passive immunotherapy approaches are under investigation in clinical trials with the aim of accelerating A clearance from the brain of the AD patients. The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-A monoclonal antibodies, that is being tested in two large late-stage trials. Compounds that interfere with proteases regulating A formation from amyloid precursor protein (APP) are also actively pursued. Unfortunately, the most biologically attractive of these proteases, -secretase, that regulates the first step of the amyloidogenic APP metabolism, was found to be particularly problematic to block and only one compound (CTS21166) has reached clinical testing so far. Conversely, several inhibitors of -secretase, the protease that regulates the last metabolic step generating A, have been identified, the most advanced being LY-450139 (semagacestat), presently in Phase III clinical development. Compounds that stimulate -secretase, the enzyme responsible for the nonamyloidogenic metabolism of APP, are also being developed one of them, EHT-0202, has recently started a Phase II study. Furthermore, brain penetrant inhibitors of A aggregation have been identified and one of such compounds, PBT-2, has produced encouraging neuropsychological results in a recently completed Phase II study. With all these anti-A approaches in clinical testing, we will know in few years if the Av hypothesis of AD is correct.

Published
2010

8. Towards Disease-Modifying Treatment of Alzheimer's Disease: Drugs Targeting β -Amyloid

Author

Frisardi, V., Solfrizzi, V., Imbimbo, B. P., Capurso, C., D'Introno, A., Colacicco, A. M., Vendemiale, G., Seripa, D., Pilotto, A., Capurso, A., and Panza, F.

Abstract

Pathological, genetic, biochemical and pharmacological studies support the hypothesis that brain accumulation of oligomeric species of β-amyloid (Aβ) peptides may cause Alzheimer's disease (AD). Drugs currently used for the treatment of AD produce limited clinical benefits and do not treat the underlying causes of the disease. In the last 10 years, new therapeutic approaches targeting Aβ have been discovered and developed with the hope of modifying the natural history of the disease. Several active and passive immunotherapy approaches are under investigation in clinical trials with the aim of accelerating Aβ clearance from the brain of the AD patients. The most advanced of these immunological approaches is bapineuzumab, composed of humanized anti-Aβ monoclonal antibodies, that is being tested in two large late-stage trials. Compounds that interfere with proteases regulating Aβ formation from amyloid precursor protein (APP) are also actively pursued. Unfortunately, the most biologically attractive of these proteases, β-secretase, that regulates the first step of the amyloidogenic APP metabolism, was found to be particularly problematic to block and only one compound (CTS21166) has reached clinical testing so far. Conversely, several inhibitors of β-secretase, the protease that regulates the last metabolic step generating Aβ, have been identified, the most advanced being LY-450139 (semagacestat), presently in Phase III clinical development. Compounds that stimulate β-secretase, the enzyme responsible for the nonamyloidogenic metabolism of APP, are also being developed one of them, EHT-0202, has recently started a Phase II study. Furthermore, brain penetrant inhibitors of Aβ aggregation have been identified and one of such compounds, PBT-2, has produced encouraging neuropsychological results in a recently completed Phase II study. With all these anti-Aβ approaches in clinical testing, we will know in few years if the Av hypothesis of AD is correct.

Published
2010

10. Vascular risk factors, incidence of MCI, and rates of progression to dementia

Author

Solfrizzi, V, Panza, F, Colacicco, A M., D’Introno, A, Capurso, C, Torres, F, Grigoletto, F, Maggi, S, Del Parigi, A, Reiman, E M., Caselli, R J., Scafato, E, Farchi, G, and Capurso, A

Abstract

To estimate prevalence, incidence, and rate of progression of mild cognitive impairment (MCI) to dementia and correlated vascular risk factors with incident MCI and its progression to dementia.

Published
2004
Full Text
View/download PDF

11. Lipoprotein(a), apolipoprotein E genotype, and risk of Alzheimer's disease

Author

Solfrizzi, V., Panza, F., D'Introno, A., Colacicco, A.M., Capurso, C., Basile, A.M., and Capurso, A.

Abstract

OBJECTIVES: To explore the possible role of serum lipoprotein(a) (Lp(a)), apolipoprotein E polymorphism, and total cholesterol (TC) serum concentrations in Alzheimer's disease (AD). METHODS: Lp(a) serum concentrations, apolipoprotein E genotypes, and TC serum concentrations were determined in 61 patients with a diagnosis of probable AD and in 63 healthy unrelated age matched controls. Genomic DNA was obtained and amplified by polymerase chain reaction and apolipoprotein E genotypes were defined following a previously described procedure. RESULTS: Lp(a) serum concentrations were significantly associated in a non-linear relation with an increased risk for AD, independently of apolipoprotein E genotypes and sex and dependent on age (truth association) and TC serum concentrations (spurious association). The effect of age adjusted for TC on the odds of having AD increased non-linearly with increasing Lp(a) serum concentrations, with a plateau between 70 and 355 mg/l (odds ratio 11.33). For Lp(a) serum concentrations ≥ 360 mg/l, the effect of age (≥ 72 years) was associated with a reduction in odds of having AD (odds ratio 0.15). CONCLUSION: It is suggested that increased Lp(a) serum concentrations, by increasing the risk for cerebrovascular disease, may have a role in determining clinical AD.

Published
2002

16. Increased bile acid excretion and reduction of serum cholesterol after crenotherapy with salt-rich mineral water

Author

Capurso, A., Solfrizzi, V., Panza, F., Mastroianni, F., Torres, F., Parigi, A., Colacicco, A., Capurso, C., Nicoletti, G., Veneziani, B., Cellamare, S., and Scalabrino, A.

Abstract

The effect of a spring mineral water from Montecatini (Italy) on bile acid excretion, and lipid and apolipoprotein serum levels was evaluated. The study was conducted in subjects with serum total cholesterol (TC) level >240 mg/dL and LDL cholesterol (LDL-C) >170 mg/dL, over a 9-week period, with 3 weeks of dietary stabilization, 3 weeks of active treatment, and 3 weeks of tap-water treatment as a control period. Serum lipids and apolipoproteins, total and fractionated bile acid excretion, gallbladder motility, and safety parameters were evaluated. Active treatment with mineral water significantly reduced serum TC by 7.5%, LDL-C by 12.5%, TC/HDL-cholesterol ratio by 6.3%, and apolipoprotein B by 6.3%; total fecal bile acid excretion was increased by 98.9%, and gallbladder volume was reduced by 40%. The reduction in serum and LDL-cholesterol levels observed during the active treatment period ran parallel to the increased excretion of bile acids in the stools. We suggest that salt-rich spring water treatment reduces serum and LDL-cholesterol levels in subjects with mild hypercholesterolemia through a mechanism of increased excretion of fecal bile acid sterols.

Published
1999
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results