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Women older than 60 have a higher risk of dementia, aging-related cognitive decline, and Alzheimer's Disease (AD) than the rest of the population. The main reason is hormonal senescence after menopause, a period characterized by a decline in estrogen levels. Since the effectiveness of drugs currently approved for the treatment of AD is limited, it is necessary to seek the development of new therapeutic strategies. Vitamin D deficiency is prevalent in AD patients and individuals with dementia in general. The supplementation of this vitamin in dementia patients might be an interesting approach for increasing the effectiveness of pre-existing medications for dementia treatment. Thus, the present study aims to investigate the effect of vitamin D treatment associated with memantine and donepezil in female mice submitted to ovariectomy (OVX) for five months and subjected to a dementia animal model induced by intracerebroventricular injection of aggregated amyloid βeta (Aβ

The postmenopausal period is characterized by a decrease in the hormonal supply which is associated with Alzheimer's Disease (AD). Vitamin D is neuroprotective and can be used in combination with pre-existing medications to improve its effects. The objective was to evaluate the effect of vitamin D associated with memantine and donepezil in female mice submitted to ovariectomy (OVX) for 5 months and subjected to an AD-induced dementia model. Animals were divided into 5 groups who received 17 days of treatment and were subjected to behavioral tests. The animals underwent euthanasia at 18th day. OVX groups exhibit reduced levels of E2 and triple treatment group had high levels of vitamin D. The induction of dementia with OVX induced short- and long-term spatial and habituation memories damage. Also, induced reduction of BDNF and IL-4 levels in hippocampus, and increasing levels of TNFα in hippocampus and of IL-1β in hippocampus and frontal cortex of animals, as well as a significant increase on GFAP immunoreactivity. Triple-association treatment reversed the effects of long-term spatial and habituation memories damage, as well as reversed changes in TNFα, IL-1β, IL-4 and GFAP immunoreactivity levels in hippocampus of treated animals. Therapeutic association has beneficial effects on memory and inflammation parameters in female mice subjected to OVX and the AD animal model of dementia.

This study aimed to evaluate the effectiveness of acepromazine as an adjuvant to ketamine, midazolam and methadone in the chemical restraint and anesthesia of cats undergoing ovariohysterectomy. We allocated 14 cats in two groups: group ketamine (GK), premedicated with ketamine 8 mg/kg, midazolam 0.3 mg/kg and methadone 0.3 mg/kg and group acepromazine (GAK), premedicated with acepromazine 0.05 mg/kg in addition to the above-mentioned drugs. At baseline (T0) and every 5 mins up to 20 mins (T5, T10, T15 and T20) after premedication, the sedation score was evaluated at 0 to 24 points. The sedation score was significantly higher at T5, T10, T15 and T20 in both groups. There were no significant differences in extubation times (3.7 ± 1.3 mins in GK; 5.2 ± 2.6 mins in GAK) and the time to reach a score equal to 0 on the sedation scale (88 ± 63.9 mins in GK; 133 ± 39.7 mins in GAK); however, the time of anesthetic release was significantly higher in the GAK than in GK (19.7 ± 6.5 mins vs 11 ± 5.9 mins) (P = 0.023). Sedation was adequate in both groups. The results indicated that the administration of acepromazine did not contribute to sedation in the protocol and could delay the anesthetic release. El objetivo de este estudio fue evaluar el efecto de la acepromazina con adyuvante al protocolo de ketamina, midazolam y metadona sobre la contención química y la anestesia de gatos sometidos a ovariosalpingohisterectomía. Los animales fueron divididos en dos grupos: grupo ketamina (GK), premedicado con ketamina 8 mg/kg, midazolam 0,3 mg/kg y metadona 0,3 mg/kg, y el grupo acepromazina (GAK), premedicado con acepromazina 0,05 mg/kg asociado a los fármacos mencionados anteriormente. Al inicio (T0) y cada 5 minutos hasta 20 minutos (T5, T10, T15 y T20), después de la premedicación, se evaluó un puntaje de sedación de 0 a 24 puntos. La sedación fue significativamente mayor en T5, T10, T15 y T20 en ambos grupos. No hubo diferencias significativas en los tiempos de extubación (3,7 ± 1,3 minutos en GK; 5,2 ± 2,6 minutos en GAK); y a tiempo para lograr una puntuación igual a 0 en la escala de sedación (88 ± 63,9 minutos en GK; 133 ± 39,7 minutos en GAK); sin embargo, el tiempo de descarga anestésico era perceptiblemente más largo en GAK que en GK (19,7 ± 6,5 minutos contra 11 ± 5,9 minutos) (P = 0,023). La sedación fue adecuada en ambos grupos. La administración de acepromazina no contribuyó a la sedación y aumentó el tiempo de anestésico alto. O objetivo desse estudo foi avaliar o efeito da acepromazina com adjuvante ao protocolo de cetamina, midazolam e metadona na contenção química e anestesia de gatas submetidas a ovariosalpingohisterectomia. Os animais foram divididos em dois grupos: grupo cetamina (GK), premedicados com cetamina 8 mg/kg, midazolam 0,3 mg/kg e metadona 0,3 mg/kg, e o grupo acepromazina (GAK), premedicados com acepromazina 0,05 mg/kg associada aos fármacos citados anteriormente. No momento basal (T0) e a cada 5 minutos até 20 minutos (T5, T10, T15 e T20), após a premedicação, um escore de sedação foi avaliado de 0 a 24 pontos. A sedação foi significativamente maior nos T5, T10, T15 e T20 em ambos os grupos. Não teve diferença significativa nos tempos de extubação (3.7 ± 1.3 minutos no GK; 5.2 ± 2.6 minutos no GAK); e no tempo para alcançar escore igual a 0 na escala de sedação (88 ± 63.9 minutos no GK; 133 ± 39.7 minuto no GAK); entretanto, o tempo de alta anestésica foi significativamente maior no GAK do que no GK (19.7 ± 6.5 minutos contra 11 ± 5.9 minutos) (P = 0.023). A sedação foi adequada em ambos os grupos. A administração de acepromazina não contribuiu para a sedação e aumentou a o tempo de alta anestésica.