Caballero-Bleda, M.

Link to this page

Authority KeyName Variants
30b59dc2-1c3b-4a4a-ad35-21a7ca5c998f
  • Caballero-Bleda, M. (4)
Projects
No records found.

Author's Bibliography

Cold restraint-induced gastric lesions in individual-and group-stressed rats in an experimental model of Alzheimer's disease

Popović, M.; Popović, N.; Caballero-Bleda, M.

(Taylor & Francis Ltd, Abingdon, 1998)

TY  - JOUR
AU  - Popović, M.
AU  - Popović, N.
AU  - Caballero-Bleda, M.
PY  - 1998
UR  - http://intor.torlakinstitut.com/handle/123456789/101
AB  - Ten days after bilateral electrolytic lesions of the nucleus basalis magnocellularis (NBM) (an experimental model of Alzheimer's disease), adult male Wistar rats were exposed to cold restraint stress in individual and social condition. Therefore, rats were placed into individual or group restraint boxes (composed of six single boxes) and exposed during 2 hr to the cold (4 degrees C). The results showed that: 1) there were no differences in type and intensity of stress-induced gastric lesions between single-stressed intact control (IC), sham-operated (SO) and NBM-lesioned rats, 2) the incidence, number and length of gastric erosions were significantly higher in group-stressed NBM-lesioned rats than in IC and SO rats, 3) the individual-stressed IC and SO rats have significantly higher incidence, number and length of gastric erosions as well as ulcer index than IC and SO group-stressed rats, and 4) there were no significant differences in intensity and type of acute gastric lesions between single- and group-stressed NBM-lesioned rats. Ir could be concluded that NBM lesions induce significant changes in social behavior in rats.
PB  - Taylor & Francis Ltd, Abingdon
T2  - International Journal of Neuroscience
T1  - Cold restraint-induced gastric lesions in individual-and group-stressed rats in an experimental model of Alzheimer's disease
EP  - 257
IS  - 3-4
SP  - 251
VL  - 94
DO  - 10.3109/00207459808986450
ER  - 
@article{
author = "Popović, M. and Popović, N. and Caballero-Bleda, M.",
year = "1998",
abstract = "Ten days after bilateral electrolytic lesions of the nucleus basalis magnocellularis (NBM) (an experimental model of Alzheimer's disease), adult male Wistar rats were exposed to cold restraint stress in individual and social condition. Therefore, rats were placed into individual or group restraint boxes (composed of six single boxes) and exposed during 2 hr to the cold (4 degrees C). The results showed that: 1) there were no differences in type and intensity of stress-induced gastric lesions between single-stressed intact control (IC), sham-operated (SO) and NBM-lesioned rats, 2) the incidence, number and length of gastric erosions were significantly higher in group-stressed NBM-lesioned rats than in IC and SO rats, 3) the individual-stressed IC and SO rats have significantly higher incidence, number and length of gastric erosions as well as ulcer index than IC and SO group-stressed rats, and 4) there were no significant differences in intensity and type of acute gastric lesions between single- and group-stressed NBM-lesioned rats. Ir could be concluded that NBM lesions induce significant changes in social behavior in rats.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "International Journal of Neuroscience",
title = "Cold restraint-induced gastric lesions in individual-and group-stressed rats in an experimental model of Alzheimer's disease",
pages = "257-251",
number = "3-4",
volume = "94",
doi = "10.3109/00207459808986450"
}
Popović, M., Popović, N.,& Caballero-Bleda, M.. (1998). Cold restraint-induced gastric lesions in individual-and group-stressed rats in an experimental model of Alzheimer's disease. in International Journal of Neuroscience
Taylor & Francis Ltd, Abingdon., 94(3-4), 251-257.
https://doi.org/10.3109/00207459808986450
Popović M, Popović N, Caballero-Bleda M. Cold restraint-induced gastric lesions in individual-and group-stressed rats in an experimental model of Alzheimer's disease. in International Journal of Neuroscience. 1998;94(3-4):251-257.
doi:10.3109/00207459808986450 .
Popović, M., Popović, N., Caballero-Bleda, M., "Cold restraint-induced gastric lesions in individual-and group-stressed rats in an experimental model of Alzheimer's disease" in International Journal of Neuroscience, 94, no. 3-4 (1998):251-257,
https://doi.org/10.3109/00207459808986450 . .
1
2
2

Importance of immunological and inflammatory processes in the pathogenesis and therapy of Alzheimer's disease

Popović, M.; Caballero-Bleda, M.; Puelles, L.; Popović, N.; Popović, N.

(Taylor & Francis Ltd, Abingdon, 1998)

TY  - JOUR
AU  - Popović, M.
AU  - Caballero-Bleda, M.
AU  - Puelles, L.
AU  - Popović, N.
AU  - Popović, N.
PY  - 1998
UR  - http://intor.torlakinstitut.com/handle/123456789/85
AB  - The contribution of autoimmune processes or inflammatory components in the etiology and pathogenesis of Alzheimer's disease (AD) has been suspected for many years. The presence of antigen-presenting, HLA-DR-positive and other immunoregulatory cells, components of complement, inflammatory cytokines and acute phase reactants have been established in tissue of AD neuropathology. Although these data do not confirm the immune response as a primary cause of AD, they indicate involvement of immune processes at least as a secondary or tertiary reaction to the preexisting pathogen and point out its driving-force role in AD pathogenesis. These processes may contribute to systemic immune response. Thus, experimental and clinical studies indicate impairments in both humoral and cellular immunity in an animal model of AD as well as in AD patients. On the other hand, anti-inflammatory drugs applied for the treatment of some chronic inflammatory diseases have been shown to reduce risk of AD in these patients. Therefore, it seems that anti-inflammatory drugs and other substances which can control the activity of immunocompetent cells and the level of endogenous immune response can be valuable in the treatment of AD patients.
PB  - Taylor & Francis Ltd, Abingdon
T2  - International Journal of Neuroscience
T1  - Importance of immunological and inflammatory processes in the pathogenesis and therapy of Alzheimer's disease
EP  - 236
IS  - 3-4
SP  - 203
VL  - 95
DO  - 10.3109/00207459809003341
ER  - 
@article{
author = "Popović, M. and Caballero-Bleda, M. and Puelles, L. and Popović, N. and Popović, N.",
year = "1998",
abstract = "The contribution of autoimmune processes or inflammatory components in the etiology and pathogenesis of Alzheimer's disease (AD) has been suspected for many years. The presence of antigen-presenting, HLA-DR-positive and other immunoregulatory cells, components of complement, inflammatory cytokines and acute phase reactants have been established in tissue of AD neuropathology. Although these data do not confirm the immune response as a primary cause of AD, they indicate involvement of immune processes at least as a secondary or tertiary reaction to the preexisting pathogen and point out its driving-force role in AD pathogenesis. These processes may contribute to systemic immune response. Thus, experimental and clinical studies indicate impairments in both humoral and cellular immunity in an animal model of AD as well as in AD patients. On the other hand, anti-inflammatory drugs applied for the treatment of some chronic inflammatory diseases have been shown to reduce risk of AD in these patients. Therefore, it seems that anti-inflammatory drugs and other substances which can control the activity of immunocompetent cells and the level of endogenous immune response can be valuable in the treatment of AD patients.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "International Journal of Neuroscience",
title = "Importance of immunological and inflammatory processes in the pathogenesis and therapy of Alzheimer's disease",
pages = "236-203",
number = "3-4",
volume = "95",
doi = "10.3109/00207459809003341"
}
Popović, M., Caballero-Bleda, M., Puelles, L., Popović, N.,& Popović, N.. (1998). Importance of immunological and inflammatory processes in the pathogenesis and therapy of Alzheimer's disease. in International Journal of Neuroscience
Taylor & Francis Ltd, Abingdon., 95(3-4), 203-236.
https://doi.org/10.3109/00207459809003341
Popović M, Caballero-Bleda M, Puelles L, Popović N, Popović N. Importance of immunological and inflammatory processes in the pathogenesis and therapy of Alzheimer's disease. in International Journal of Neuroscience. 1998;95(3-4):203-236.
doi:10.3109/00207459809003341 .
Popović, M., Caballero-Bleda, M., Puelles, L., Popović, N., Popović, N., "Importance of immunological and inflammatory processes in the pathogenesis and therapy of Alzheimer's disease" in International Journal of Neuroscience, 95, no. 3-4 (1998):203-236,
https://doi.org/10.3109/00207459809003341 . .
43
34
37

Effect of acute verapamil treatment on body temperature in nucleus basalis magnocellularis-lesioned rats

Popović, M.; Popović, N.; Caballero-Bleda, M.; Puelles, L.

(Wiley, Hoboken, 1998)

TY  - JOUR
AU  - Popović, M.
AU  - Popović, N.
AU  - Caballero-Bleda, M.
AU  - Puelles, L.
PY  - 1998
UR  - http://intor.torlakinstitut.com/handle/123456789/84
AB  - Our recent studies suggest that lesions of the nucleus basalis magnocellularis (nbm) in rats induce a significant decrease of core body temperature in standard laboratory conditions. Considering the importance of calcium homeostasis in thermoregulation, as well as in the pathogenesis of neurodegeneration, the aim of the present study was to investigate the effect of acute verapamil treatment on body temperature in nbm-lesioned rats. The body temperature was registered before and 30 min after verapamil was subcutaneously administered (1.0, 2.5, 5.0 and 10.0 mg/kg). Verapamil did not change body temperature in control animals. However, verapamil in doses of 2.5 and 5.0 mg/kg significantly increased the core body temperature in nbm-lesioned rats nearly up to the temperature of control animals. Findings that verapamil in doses of 1.0 and 10.0 mg/kg did not change body temperature in nbm-lesioned suggest the existence of an inverted U-shape curve in its effect.
PB  - Wiley, Hoboken
T2  - Neuroscience Research Communications
T1  - Effect of acute verapamil treatment on body temperature in nucleus basalis magnocellularis-lesioned rats
EP  - 187
IS  - 3
SP  - 181
VL  - 23
DO  - 10.1002/(SICI)1520-6769(199811/12)23:3181::AID-NRC63.0.CO;2-E
ER  - 
@article{
author = "Popović, M. and Popović, N. and Caballero-Bleda, M. and Puelles, L.",
year = "1998",
abstract = "Our recent studies suggest that lesions of the nucleus basalis magnocellularis (nbm) in rats induce a significant decrease of core body temperature in standard laboratory conditions. Considering the importance of calcium homeostasis in thermoregulation, as well as in the pathogenesis of neurodegeneration, the aim of the present study was to investigate the effect of acute verapamil treatment on body temperature in nbm-lesioned rats. The body temperature was registered before and 30 min after verapamil was subcutaneously administered (1.0, 2.5, 5.0 and 10.0 mg/kg). Verapamil did not change body temperature in control animals. However, verapamil in doses of 2.5 and 5.0 mg/kg significantly increased the core body temperature in nbm-lesioned rats nearly up to the temperature of control animals. Findings that verapamil in doses of 1.0 and 10.0 mg/kg did not change body temperature in nbm-lesioned suggest the existence of an inverted U-shape curve in its effect.",
publisher = "Wiley, Hoboken",
journal = "Neuroscience Research Communications",
title = "Effect of acute verapamil treatment on body temperature in nucleus basalis magnocellularis-lesioned rats",
pages = "187-181",
number = "3",
volume = "23",
doi = "10.1002/(SICI)1520-6769(199811/12)23:3181::AID-NRC63.0.CO;2-E"
}
Popović, M., Popović, N., Caballero-Bleda, M.,& Puelles, L.. (1998). Effect of acute verapamil treatment on body temperature in nucleus basalis magnocellularis-lesioned rats. in Neuroscience Research Communications
Wiley, Hoboken., 23(3), 181-187.
https://doi.org/10.1002/(SICI)1520-6769(199811/12)23:3181::AID-NRC63.0.CO;2-E
Popović M, Popović N, Caballero-Bleda M, Puelles L. Effect of acute verapamil treatment on body temperature in nucleus basalis magnocellularis-lesioned rats. in Neuroscience Research Communications. 1998;23(3):181-187.
doi:10.1002/(SICI)1520-6769(199811/12)23:3181::AID-NRC63.0.CO;2-E .
Popović, M., Popović, N., Caballero-Bleda, M., Puelles, L., "Effect of acute verapamil treatment on body temperature in nucleus basalis magnocellularis-lesioned rats" in Neuroscience Research Communications, 23, no. 3 (1998):181-187,
https://doi.org/10.1002/(SICI)1520-6769(199811/12)23:3181::AID-NRC63.0.CO;2-E . .
2
3

Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental Alzheimer's disease in rats

Popović, M.; Caballero-Bleda, M.; Popović, N.; Bokonjić, D.; Dobrić, Silva

(Taylor & Francis Ltd, Abingdon, 1997)

TY  - JOUR
AU  - Popović, M.
AU  - Caballero-Bleda, M.
AU  - Popović, N.
AU  - Bokonjić, D.
AU  - Dobrić, Silva
PY  - 1997
UR  - http://intor.torlakinstitut.com/handle/123456789/74
AB  - It is well known that disturbance of calcium homeostasis has a significant role in the development of neurodegenerative disorders, such as Alzheimer's disease (AD). Our recent data suggest that acute treatment with the calcium antagonist verapamil can improve some behavioral deficits in an experimental model of AD. Therefore, the present study was done to establish the effect of chronically administered verapamil on cognitive and noncognitive behavior of rats with bilateral electrolytical lesions of nucleus basalis manocellularis (NBM) - an animal model of AD. The NBM lesions produce a deficit in performance of diverse behavior tests: active avoidance (AA), low level of fear (the open field test) as well as aggressive (the test of foot-shock induced aggression) and depressive (the learned helplessness test) behavior. Verapamil (1.0, 2.5, 5.0 and 10.0 mg/kg i.p.) or saline solution (1 ml/kg i.p.) were injected 24 hr after the lesion of NBM and then repeatedly administered during the next 8 days (twice a day). Performance of the two-way active avoidance test, the open field test, the foot shock-induced aggression test and the learned helplessness test were done on day 4 after the last verapamil or saline treatment (day 13 after the lesion). Verapamil in doses of 2.5 and 5.0 mg/kg significantly ameliorated the deficit in the performance of AA, the open field behavior, and the depression, but not the aggressive behavior. The obtained beneficial effect of chronic administered verapamil suggests that the regulation of calcium homeostasis during the early period after NBM lesions might be a reasonable way to prevent the behavioral deficits in an experimental model of AD.
PB  - Taylor & Francis Ltd, Abingdon
T2  - International Journal of Neuroscience
T1  - Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental Alzheimer's disease in rats
EP  - 93
IS  - 1-2
SP  - 79
VL  - 92
DO  - 10.3109/00207459708986392
ER  - 
@article{
author = "Popović, M. and Caballero-Bleda, M. and Popović, N. and Bokonjić, D. and Dobrić, Silva",
year = "1997",
abstract = "It is well known that disturbance of calcium homeostasis has a significant role in the development of neurodegenerative disorders, such as Alzheimer's disease (AD). Our recent data suggest that acute treatment with the calcium antagonist verapamil can improve some behavioral deficits in an experimental model of AD. Therefore, the present study was done to establish the effect of chronically administered verapamil on cognitive and noncognitive behavior of rats with bilateral electrolytical lesions of nucleus basalis manocellularis (NBM) - an animal model of AD. The NBM lesions produce a deficit in performance of diverse behavior tests: active avoidance (AA), low level of fear (the open field test) as well as aggressive (the test of foot-shock induced aggression) and depressive (the learned helplessness test) behavior. Verapamil (1.0, 2.5, 5.0 and 10.0 mg/kg i.p.) or saline solution (1 ml/kg i.p.) were injected 24 hr after the lesion of NBM and then repeatedly administered during the next 8 days (twice a day). Performance of the two-way active avoidance test, the open field test, the foot shock-induced aggression test and the learned helplessness test were done on day 4 after the last verapamil or saline treatment (day 13 after the lesion). Verapamil in doses of 2.5 and 5.0 mg/kg significantly ameliorated the deficit in the performance of AA, the open field behavior, and the depression, but not the aggressive behavior. The obtained beneficial effect of chronic administered verapamil suggests that the regulation of calcium homeostasis during the early period after NBM lesions might be a reasonable way to prevent the behavioral deficits in an experimental model of AD.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "International Journal of Neuroscience",
title = "Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental Alzheimer's disease in rats",
pages = "93-79",
number = "1-2",
volume = "92",
doi = "10.3109/00207459708986392"
}
Popović, M., Caballero-Bleda, M., Popović, N., Bokonjić, D.,& Dobrić, S.. (1997). Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental Alzheimer's disease in rats. in International Journal of Neuroscience
Taylor & Francis Ltd, Abingdon., 92(1-2), 79-93.
https://doi.org/10.3109/00207459708986392
Popović M, Caballero-Bleda M, Popović N, Bokonjić D, Dobrić S. Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental Alzheimer's disease in rats. in International Journal of Neuroscience. 1997;92(1-2):79-93.
doi:10.3109/00207459708986392 .
Popović, M., Caballero-Bleda, M., Popović, N., Bokonjić, D., Dobrić, Silva, "Neuroprotective effect of chronic verapamil treatment on cognitive and noncognitive deficits in an experimental Alzheimer's disease in rats" in International Journal of Neuroscience, 92, no. 1-2 (1997):79-93,
https://doi.org/10.3109/00207459708986392 . .
26
23
29