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3. Organotypic cultures from AD11 anti-NGF transgenic mice

Author

RIGHI M, CAPSONI, SIMONA, GIANNOTTA S, AVOSSA D, CATTANEO, ANTONINO, RIGHI M, CAPSONI S, GIANNOTTA S, AVOSSA D, CATTANEO A, Righi, M, Capsoni, Simona, Giannotta, S, Avossa, D, and Cattaneo, Antonino

Published
2004

10. Beta amyloid plaques in a model for sporadic Alzheimer's disease based on transgenic anti-nerve growth factor antibodies

Author

CAPSONI, SIMONA, GIANNOTTA S, CATTANEO, ANTONINO, Capsoni, Simona, Giannotta, S, and Cattaneo, Antonino

Subjects
mental disorders
Abstract

Cerebral deposition of beta-amyloid (Abeta) is an invariant event of Alzheimer's disease (AD). We recently described that the brain of aged transgenic mice expressing anti-nerve growth factor (NGF) antibodies (AD11 mice) show a dramatic neurodegenerative phenotype, reminiscent of AD, which includes neuronal loss, cholinergic deficit, and tau hyperphosphorylation, associated with neurofibrillary pathology. We now report that brains of aged transgenic mice contain large amounts of beta-amyloid plaques and describe their morphology by a variety of approaches. In conclusion, the chronic deprivation of NGF leads to the formation and deposition of Abeta in AD11 mice, suggesting a direct link between NGF signaling and abnormal processing of amyloid precursor protein.

Published
2002

11. Mismatch between BDNF mRNA and protein expression in the developing visual cortex: the role of visual experience

Author

Tropea, D., Simona Capsoni, Tongiorgi, E., Giannotta, S., Cattaneo, A., Domenici, L., Tropea, D, Capsoni, Simona, Tongiorgi, E, Giannotta, S, Cattaneo, Antonino, and Domenici, L.

Subjects
Postnatal development, genetic structures, nervous system, Visual experience, Brain-derived neurotrophic factor, Dark rearing, Neurotrophins, Synaptic plasticity, Socio-culturale, eye diseases
Abstract

Brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) expression in the rat visual cortex of young and postnatal day 90 (P90) animals is developmentally regulated and influenced by visual experience. In the present paper we compared the expression of BDNF mRNA to the actual changes of BDNF protein occurring during postnatal development and verified whether BDNF protein distribution is controlled by visual activity. To achieve this aim we analysed BDNF mRNA and/or BDNF protein cellular distribution in the rat visual cortex at different postnatal ages by using immunohistochemistry and highly sensitive in situ hybridization. We found that before eye opening (P13), in all cortical layers a large number of visual cortical neurons contain BDNF mRNA with no detectable amount of BDNF protein. At later ages (P23 and P90), the number of BDNF-immunostained cells increases; most neurons are double labelled for BDNF mRNA and protein, and a small group of neurons is labelled only for BDNF protein. The cellular increase of BDNF immunolabelling is blocked in animals deprived of visual experience from birth (dark rearing), with a large population of neurons containing BDNF mRNA but not BDNF protein. This is similar to what is observed before eye opening. Exposure of dark-reared rats to a brief period (2 h) of light restores a good match between BDNF mRNA and BDNF protein cellular expression. We propose that visual experience controls the neuronal content of BDNF mRNA and BDNF protein in developing visual cortex.

Published
2001

16. Genome screen in familial intracranial aneurysm

Author

Foroud, T, Sauerbeck, L, Brown, R, Anderson, C, Woo, D, Kleindorfer, D, Flaherty, ML, Deka, R, Hornung, R, Meissner, I, Bailey-Wilson, JE, Langefeld, C, Rouleau, G, Connolly, ES, Lai, D, Koller, DL, Huston, J, Broderick, JP, Fisher, W, Forson, H, Mee, E, Howe, C, Vos, S, Hankey, G, Knuckey, N, Laidlaw, J, Reilly, P, Dorsch, N, Morgan, M, Besser, M, Rosenfeld, J, Athanasiadis, K, Claxton, A, Dunne, V, Griffith, J, Davidson, J, Pope, S, Froelich, A, Day, A, Brach, R, Zuccarello, M, Ringer, A, Yeh, H, Franklin, K, Ramussen, P, Andrews-Hinders, D, Wheeler, T, Sacco, R, Lamonica, D, Lewis, SB, Royster, A, Payner, T, Miracle, N, Murphy, K, Kohler, B, Ogilvy, C, Buckley, D, Manansala, J, Ferguson, G, Mayer, C, Peacock, J, Desjarlais, A, Aldrich, EF, Aldrich, C, Byard, C, Brown, RD, Jaeger, L, Morgenstern, L, Concannon, M, Qureshi, AI, Harris-Lane, P, Batjer, H, Joven, G, Thompson, S, Richard, MT, Hopper, A, Kassam, AB, Lee, K, Johnston, C, Katsura, K, Giannotta, S, Fishback, D, Steinberg, G, Luu, D, Coburn, M, Malkoff, M, Wojner, A, Kassel, N, Worrall, B, Radakovic, G, Tirschwell, D, Tanzi, P, Derdeyn, C, Catanzaro, M, Kaufmann, A, Gladish, D, Foroud, T, Sauerbeck, L, Brown, R, Anderson, C, Woo, D, Kleindorfer, D, Flaherty, ML, Deka, R, Hornung, R, Meissner, I, Bailey-Wilson, JE, Langefeld, C, Rouleau, G, Connolly, ES, Lai, D, Koller, DL, Huston, J, Broderick, JP, Fisher, W, Forson, H, Mee, E, Howe, C, Vos, S, Hankey, G, Knuckey, N, Laidlaw, J, Reilly, P, Dorsch, N, Morgan, M, Besser, M, Rosenfeld, J, Athanasiadis, K, Claxton, A, Dunne, V, Griffith, J, Davidson, J, Pope, S, Froelich, A, Day, A, Brach, R, Zuccarello, M, Ringer, A, Yeh, H, Franklin, K, Ramussen, P, Andrews-Hinders, D, Wheeler, T, Sacco, R, Lamonica, D, Lewis, SB, Royster, A, Payner, T, Miracle, N, Murphy, K, Kohler, B, Ogilvy, C, Buckley, D, Manansala, J, Ferguson, G, Mayer, C, Peacock, J, Desjarlais, A, Aldrich, EF, Aldrich, C, Byard, C, Brown, RD, Jaeger, L, Morgenstern, L, Concannon, M, Qureshi, AI, Harris-Lane, P, Batjer, H, Joven, G, Thompson, S, Richard, MT, Hopper, A, Kassam, AB, Lee, K, Johnston, C, Katsura, K, Giannotta, S, Fishback, D, Steinberg, G, Luu, D, Coburn, M, Malkoff, M, Wojner, A, Kassel, N, Worrall, B, Radakovic, G, Tirschwell, D, Tanzi, P, Derdeyn, C, Catanzaro, M, Kaufmann, A, and Gladish, D

Abstract

Background: Individuals with 1st degree relatives harboring an intracranial aneurysm (IA) are at an increased risk of IA, suggesting genetic variation is an important risk factor. Methods: Families with multiple members having ruptured or unruptured IA were recruited and all available medical records and imaging data were reviewed to classify possible IA subjects as definite, probable or possible IA or not a case. A 6 K SNP genome screen was performed in 333 families, representing the largest linkage study of IA reported to date. A 'narrow' (n = 705 definite IA cases) and 'broad' (n = 866 definite or probable IA) disease definition were used in multipoint model-free linkage analysis and parametric linkage analysis, maximizing disease parameters. Ordered subset analysis (OSA) was used to detect gene × smoking interaction. Results: Model-free linkage analyses detected modest evidence of possible linkage (all LOD < 1.5). Parametric analyses yielded an unadjusted LOD score of 2.6 on chromosome 4q (162 cM) and 3.1 on chromosome 12p (50 cM). Significant evidence for a gene × smoking interaction was detected using both disease models on chromosome 7p (60 cM; p ≤ 0.01). Our study provides modest evidence of possible linkage to several chromosomes. Conclusion: These data suggest it is unlikely that there is a single common variant with a strong effect in the majority of the IA families. Rather, it is likely that multiple genetic and environmental risk factors contribute to the susceptibility for intracranial aneurysms.

Published
2009

17. Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention

Author

Wiebers, D., Whisnant, J., Forbes, G., Meissner, I., Brown, R., Piepgras, D., Huston, J., Nichols, D., O Fallon, W., Peacock, J., Jaeger, L., Kassell, N., Kongable-Beckman, G., Torner, J., Rajput, M., Drake, C., Kurtzke, J., Marler, J., Walker, M., Meyer, F., Atkinson, J., Marsh, W., Thielen, K., Ferguson, G., Barr, H., Lownie, S., Hachinski, V., Fox, A., Sahjpaul, R., Parrent, A., Mayer, C., Lindsay, K., Teasdale, E., Bone, I., Fatukasi, J., Lindsay, M., Cail, W., Sagher, O., Davis, M., Sengupta, R., Bates, D., Gholkar, A., Murdy, J., Wilson, S., Praharaj, S., Partridge, G., Reynolds, C., Hind, N., Ogilvy, C., Crowell, R., Gress, D., Schaefer, P., Choi, I., Buckley, D., Sloan, K., King, D., Giannotta, S., Ameriso, S., Teitelbaum, T., Thomson, E., Fishback, D., Vajda, J., Nyary, I., Czirjak, S., Horvath, M., Szikora, I., Pasztor, E., Varady, P., Erdos, A., Edner, G., Wahlgren, N., Lindqvist, M., Antonsson, A., Da Pian, R., Pasqualin, A., Chioffi, F., Beltramello, A., Zampieri, G., Benati, A., Rossi, G., Ronkainen, A., Hernesniemi, J., Vapalahti, M., Rinne, J., Luukkonen, M., Vihavainen, M., Savolainen, S., Koivisto, T., Leivo, S., Helin, K., Steinberg, G., Marks, M., Vanefsky, M., Norbash, A., Thompson, R., Bell, T., Marcellus, M., Meyer, A., Kerr, R., Adams, C., Molyneux, A., Vinden, S., Bacon, F., Shrimpton, J., Parker, S., Day, A., Nadeau, S., Stachniak, J., Friedman, W., Fessler, R., Peters, K., Jacob, R., Roper, S., Smith, A., Lafrentz, P., Howard, M., Loftus, C., Adams, H., Crosby, D., Rogers, M., Broderick, J., Tew, J., Brott, T., Loveren, H., Yeh, H., Zuccarello, M., Tomsick, T., Gaskill-Shipley, M., Minneci, L., Mcmahon, N., Castel, J., Orgogozo, J., Loiseau, H., Bourgeois, P., Berge, J., Dousset, V., Cuny, E., Richard, M., Agbi, C., Hugenholtz, H., Benoit, B., Morrish, W., Wee, R., Grahovac, S., Pratt, L., Mortensen, M., Andreoli, A., Testa, C., Comani, V., Trevisan, C., Limoni, P., Carlucci, F., Leonardi, M., Sturiale, C., Pendl, G., Eder, H., Klein, G., Eder, M., Leber, K., Horner, T., Leipzig, T., Payner, T., Denardo, A., Scott, J., Redelman, K., Fisher, W., Rosner, M., Vitek, G., Hand, M., Flack, Wf, Sichez, J., Pertuiset, B., Fohanno, D., Marsault, C., Casasco, A., Biondi, A., Capelle, L., Duffau, H., Winn, H., Grady, M., Newell, D., Longstreth, W., Thompson, P., Bybee, H., Jones, D., Findlay, J., Petruk, K., Steinke, D., Ashforth, R., Stenerson, P., Schindel, D., Vanderhoven, H., Neves, J., Zager, E., Flamm, E., Raps, E., Hurst, R., Parrott, S., Sellers, M., Torchia, M., Anderson, B., West, M., Fewer, D., Hill, N., Sutherland, G., Ross, I., Mcclarty, B., Brownstone, R., Williams, O., Narotam, P., Christane, L., Mcginn, G., Gladish, D., Kirkpatrick, P., Pickard, J., Antoun, N., Simpson, D., Higgins, N., Turner, C., Tebbs, S., Holness, R., Malloy, D., Phillips, S., Maloney, W., Molina-De-Orozco, V., Baxter, B., Connolly-Campbell, K., Macdougall, A., Gentili, F., Wallace, M., Ter Brugge, K., Willinsky, R., Tymianski, M., Rickards, L., Tucker, W., Lambert, C., Montanera, W., Rychlewski, C., Flood, C., Villani, R., Sganzerla, E., Tomei, G., Bettinelli, A., Ceccarelli, G., Righini, A., Bello, L., Marras, C., Nelson, R., Lewis, T., Renowden, C., Clarke, Y., Varian, L., Chyatte, D., Sila, C., Perl, J., Masaryk, T., Porterfield, R., Shaw, M., Foy, P., Nixon, T., Dunn, L., Clitheroe, N., Smith, T., Eldridge, P., Humphrey, P., Wiseman, J., Hawkins, K., Owen, L., Ost, K., Saminaden, S., Mohr, G., Schondorf, R., Carlton, J., Maleki, M., Just, N., Brien, S., Entis, S., Tampieri, D., Simons, N., Mooij, J., Metzemackers, J., Hew, J., Beks, J., Veen, A., Bosma, I., Sprengers, M., Rinkel, G., Gijn, J., Ramos, L., Tulleken, C., Greebe, P., Vliet, F., Borgesen, S., Jespersen, B., Boge-Rasmussen, T., Willumsen, L., Homer, D., Eller, T., Carpenter, J., Meyer, J., Munson, R., Small, B., Nussbaum, E., Heros, R., Latchaw, R., Camarata, P., Lundgren, J., Mattsen, N., Whittle, I., Sellar, R., O Sullivan, M., Steers, A., Statham, P., Malcolm, G., Price, R., Hoffman, B., Yonas, H., Wechsler, L., Thompson-Dobkin, J., Jungreis, C., Kassam, A., Kirby, L., Parent, A., Lewis, A., Azordegan, P., Smith, R., Alexander, L., Gordon, D., Russell, W., Benashvili, G., Perry, R., Scalzo, D., Mandybur, G., Morgan, C., Karanjia, P., Madden, K., Kelman, D., Gallant, T., Vanderspek, H., Choucair, A., Neal, J., Mancl, K., Saveland, H., Brandt, L., Holtas, S., Trulsson, B., Macdonald, R., Weir, B., Mojtahedi, S., Amidei, C., Vermeulen, M., Bosch, D., Hulsmans, F., Albrecht, K., Roos, Y., Vet, A., Gorissen, A., Mechielsen, M., Martin, N., Gobin, Y., Saver, J., Vinuela, F., Duckwiler, G., Kelly, D., Frazee, J., Da Graca, R., Gravori, T., Illingworth, R., Richards, P., Wade, J., Colquhoun, I., Bashir, E., Shortt, S., Weaver, J., Fisher, M., Stone, B., Chaturvedi, S., Davidson, R., Davidson, K., Giombini, S., Solero, C., Boiardi, A., Cimino, C., Valentini, S., Antonio Silvani, Alberts, M., Friedman, A., Gentry, A., Hoffman, K., Hughes, R., Lillihei, K., Earnest, M., Nichols, J., Kindt, G., Anderson, A., Levy, S., Breeze, R., Noonan, V., Dowd, C., Vanwestrop, J., Wilson, C., Berger, M., Hannegan, L., Marcos, J., Ugarte, L., Kitchen, N., Taylor, W., Kumar, M., Grieve, J., Durity, F., Boyd, M., Fairholm, D., Griesdale, D., Honey, C., Redekop, G., Toyota, B., Turnbull, I., Woodhurst, W., Zwimpfer, T., Teal, P., Grabe, D., Brevner, A., Piepgras, A., Schmiedek, P., Schwartz, A., Weber, T., Biller, J., Brem, S., Cybulski, G., Chadwick, L., Bronstein, K., Pietila, T., Brock, M., Krug, D., Krznaric, I., and Kivisaari, R.

Subjects
Adult, Male, medicine.medical_specialty, International Subarachnoid Aneurysm Trial, Adolescent, Rupture rate, Aneurysm, Ruptured, Risk Factors, Intervention (counseling), Unruptured cerebral aneurysm, Medicine, Humans, Prospective Studies, Aged, Probability, Retrospective Studies, Aged, 80 and over, Rupture, Spontaneous, business.industry, Age Factors, Intracranial Aneurysm, General Medicine, Middle Aged, Subarachnoid Hemorrhage, Emergency medicine, Female, business, Vascular Surgical Procedures
Abstract

The management of unruptured intracranial aneurysms requires knowledge of the natural history of these lesions and the risks of repairing them.A total of 2621 patients at 53 participating centers in the United States, Canada, and Europe were enrolled in the study, which had retrospective and prospective components. In the retrospective component, we assessed the natural history of unruptured intracranial aneurysms in 1449 patients with 1937 unruptured intracranial aneurysms; 727 of the patients had no history of subarachnoid hemorrhage from a different aneurysm (group 1), and 722 had a history of subarachnoid hemorrhage from a different aneurysm that had been repaired successfully (group 2). In the prospective component, we assessed treatment-related morbidity and mortality in 1172 patients with newly diagnosed unruptured intracranial aneurysms.In group 1, the cumulative rate of rupture of aneurysms that were less than 10 mm in diameter at diagnosis was less than 0.05 percent per year, and in group 2, the rate was approximately 11 times as high (0.5 percent per year). The rupture rate of aneurysms that were 10 mm or more in diameter was less than 1 percent per year in both groups, but in group 1, the rate was 6 percent the first year for giant aneurysms (or =25 mm in diameter). The size and location of the aneurysm were independent predictors of rupture. The overall rate of surgery-related morbidity and mortality was 17.5 percent in group 1 and 13.6 percent in group 2 at 30 days and was 15.7 percent and 13.1 percent, respectively, at 1 year. Age independently predicted surgical outcome.The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.

Published
1998

22. Cerebral vasospasm and concurrent left ventricular outflow tract obstruction: requirement for modification of hyperdynamic therapy regimen.

Author

Zada G, Terterov S, Russin J, Clavijo L, Giannotta S, Zada, Gabriel, Terterov, Sergei, Russin, Jonathan, Clavijo, Leonardo, and Giannotta, Steven

Abstract

Background: Medical treatment of arterial vasospasm following aneurysmal subarachnoid hemorrhage (SAH) generally consists of triple H therapy, which frequently relies on inotropic agents in order to increase cardiac output (CO). Patients with concurrent left ventricular outflow tract (LVOT) obstruction may have paradoxical decreases in CO following administration of inotropic pressors, placing them at significant risk for cerebral ischemia and stroke.Methods: The clinical courses of two patients with SAH-induced arterial vasospasm and underlying left ventricular outflow obstruction are reported. Both patients had hypotension and low cardiac output that were refractory to medical management with triple H therapy. Echocardiography in both patients demonstrated LVOT obstruction secondary to hypertrophic obstructive cardiomyopathy (HOCM).Results: Intervention in both patients included discontinuation of inotropic agents and maintenance of hypervolemia to a target pulmonary capillary wedge pressure range, resulting in improved cardiac output and mean arterial pressure.Conclusion: Medical treatment for cerebral vasospasm with inotropic pressor agents may result in paradoxical decreases in hemodynamic parameters and cerebral perfusion in patients with LVOT obstruction. While HOCM is the most likely structural abnormality to cause this phenomenon, it can be induced by several physiological conditions encountered in the neurocritical care setting. Modifications in triple H therapy regimens may be required in order to optimize cerebral perfusion and prevent cerebral ischemia and stroke in these patients. [ABSTRACT FROM AUTHOR]

Published
2010
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25. Ganstigmine and donepezil improve neurodegeneration in AD11 antinerve growth factor transgenic mice.

Author

Capsoni S, Giannotta S, Stebel M, Garcia AA, DeRosa R, Villetti G, Imbimbo BP, Pietra C, and Cattaneo A

Abstract

Ganstigmine (CHF2819) is an acetylcholinesterase inhibitor that increases acetylcholine in rat hippocampus and ameliorates scopolamine-induced amnesia. In this article, we examined whether and how ganstigmine might prevent or rescue the neurodegenerative phenotype in AD11 antinerve growth factor (anti-NGF) mice, a transgenic model for Alzheimer's disease. The effects of ganstigmine were compared with those obtained after administration of donepezil. Results demonstrate that intraperitoneal and oral administration of ganstigmine and donepezil can reverse the cholinergic and behavioral deficit in AD11 mice but not the amyloid and phosphotau accumulation, uncovering different mechanisms leading to neurodegeneration in AD11 mice. [ABSTRACT FROM AUTHOR]

Published
2004
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27. Carotid stenosis in a multiethnic population

Author

Wang, M.Y., Mimran, R., Mohit, A., Lavine, S.D., and Giannotta, S.

Abstract

Background: Carotid stenosis is an important, treatable cause of stroke. Several population-based studies have shown ethnic differences in the prevalence of carotid atherosclerosis. This study was performed at a large multiethnic hospital to clarify these differences. Methods: One thousand six carotid artery ultrasounds performed by the Department of Radiology at Los Angeles County General Hospital over a 4-year period were reviewed. Patients were classified as Caucasian (n=151), Hispanic (n=515), Black (n=173), or Asian (n=167) by self-declaration and birthplace. Carotid stenosis was defined as mild (1% to 39%), moderate (40% to 59%), severe (60% to 79%), critical (80% to 99%), or total (100%). Results: Twenty and one-half percent of Caucasian patients had greater than 59% stenosis compared with 10.1% of Hispanics, 8.7% of Blacks, and 10.7% of Asians (P<0.001). Nine and two-tenths percent of Caucasians had greater than 79% stenosis compared with 4.3% of Hispanics, 2.9% of Blacks, and 2.8% of Asians (P<0.001). There were no significant differences in age or gender representations between ethnic groups, and the indications for ordering carotid duplex sonography also did not vary by race. Caucasians and Blacks had a higher prevalence of cardiac disease, smoking, and heavy alcohol abuse. Hispanics had higher rates of diabetes. Conclusions: These results indicate that significant differences in the degree of carotid stenosis exist among ethnic groups. Caucasian patients in our series showed a statistically higher likelihood of having a severe or critical level of stenosis. These findings may have implications for the allocation of health care resources as ethnic minorities compose a greater proportion of the population

Published
2000
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30. Carotid-cavernous sinus fistulas and venous thrombosis

Author

Seeger, J F, Gabrielsen, T O, Giannotta, S L, and Lotz, P R

Subjects
Adult, Carotid Artery Diseases, Male, Fistula, Case Reports, Radiography, Sinus Thrombosis, Intracranial, Central Nervous System Diseases, Arteriovenous Fistula, otorhinolaryngologic diseases, Humans, Cavernous Sinus, Female, Dura Mater, Aged
Abstract

Radiographic signs of cavernous sinus thrombosis were found in eight consecutive patients with an angiographic diagnosis of carotid-cavernous sinus fistula; six were of the dural type and the ninth case was of a shunt from a cerebral hemisphere vascular malformation. Diagnostic features consisted of filling defects within the cavernous sinus and its tributaries, an abnormal shape of the cavernous sinus, an atypical pattern of venous drainage, and venous stasis. Progression of thrombosis was demonstrated in five patients who underwent follow-up angiography. Because of a high incidence of spontaneous resolution, patients with dural-cavernous sinus fistulas who show signs of venous thrombosis at angiography should be followed conservatively.

Published
1980

31. RETROGRADE CATHODE SPOT BEHAVIOR IN LOW DENSITY ARCS.

Author

AEROSPACE RESEARCH LABS WRIGHT-PATTERSON AFB OHIO, Giannotta,S. F., AEROSPACE RESEARCH LABS WRIGHT-PATTERSON AFB OHIO, and Giannotta,S. F.

Abstract

In a low pressure arc discharge, simultaneous cathode spots are observed on a cold-cathode, copper plate electrode. These spots circle the plate in the -I X B direction. The number of spots and the patterns of movement change as functions of the pressure and the applied magnetic field. Since multispots exist, corrections are applied to find the effective magnetic field acting on the ith spot. For observed spot sizes and separations, it is found that the self-magnetic field is of the same order of magnitude as the applied field. (Author), Reprinted from Proceedings of the International Conference on Phenomena in Ionized Gases (8th), Vienna, 1967.

Published
1967

32. Access to emergency care

Author

clarence watridge, Solomon, R. A., Grady, M. S., Popp, A. J., Quest, D. O., Kondziolka, D., and Giannotta, S. L.

41. Natural history of microprolactinomas

Author

Weiss, M H, primary, Teal, J, additional, Gott, P, additional, Wycoff, R, additional, Yadley, R, additional, Apuzzo, M L, additional, Giannotta, S L, additional, Kletzky, O, additional, and March, C, additional

Published
1983
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49. Nerve growth factor and galantamine ameliorate early signs of neurodegeneration in anti-nerve growth factor mice

Author

Sabina Giannotta, Simona Capsoni, Antonino Cattaneo, Capsoni, Simona, Giannotta, S, and Cattaneo, Antonino

Subjects
medicine.medical_specialty, Transgene, brain, Mice, Transgenic, tau Proteins, Cholinergic Agonists, Biology, Antibodies, Choline O-Acetyltransferase, NO, Amyloid beta-Protein Precursor, Mice, Internal medicine, Nerve Growth Factor, medicine, Galantamine, Animals, Entorhinal Cortex, Humans, Phosphorylation, Mice, Knockout, NGF, Amyloid beta-Peptides, Multidisciplinary, NGF, nicotinic acetylcholine receptors, Alzheimer disease, messenger RNA, retrograde transport, cholinergic neurons, spatial memory, brain, neurotrophin, messenger RNA, Neurodegeneration, neurotrophin, Biological Sciences, spatial memory, medicine.disease, Phenotype, Recombinant Proteins, retrograde transport, Disease Models, Animal, Endocrinology, Nerve growth factor, nervous system, Nerve Degeneration, Cholinergic, nicotinic acetylcholine receptors, cholinergic neurons, Alzheimer's disease, Alzheimer disease, medicine.drug
Abstract

Phenotypic knockout of nerve growth factor (NGF) activity in transgenic anti-NGF mice (AD11 mice) results in a progressive neurodegenerative phenotype resembling Alzheimer's disease. In this article, we examine whether and how the progressive neurodegenerative phenotype of AD11 mice could be prevented or ameliorated by pharmacological treatments with NGF or the cholinergic agonist galantamine, at a relatively early phase of Alzheimer's disease-like neurodegeneration. We demonstrate that the neurodegeneration induced by the expression of anti-NGF antibodies in AD11 mice can be largely reversed by NGF delivery through an olfactory route.

Published
2002

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