According to the literature low body temperature is considered a risk factor for Alzheimer’s disorder (AD) and may contribute to a significant worsening of its histological pathology. Less is known about the alteration of the thermoregulation in AD subjects. Therefore, our aim was to identify it in the popular triple transgenic mouse model (3xTg-AD) of AD.In addition to continuous telemetric monitoring of circadian temperature changes, we used cold and warm stimulations as well as an NK3 agonist (senktide)-induced drop in core body temperature modelling post-menopausal heat waves. Six-month-old female animals are compared to wild-type (WT). As the important thermoregulatory centrum, the medial preoptic area is rich in oestrogen-sensitive cells, the stimuli were used also after ovariectomy (OVX).No difference was found after cold stimulation (neither in the forced swim test in cold water), while there was a significant difference between genotypes after warm stimulation. The senktide was effective (drop in temperature) in WT animals, but not in 3xTg-AD animals. OVX did not have significant impact on the outcome.Our results confirm that the 3xTg-AD animals have disturbed thermoregulation, which was more sensitive to external heat (both warm stimulus and senktide-induced increase in tail temperature). The one week OVX does not seem to be long enough to substantially influence the thermoregulation. The ineffectiveness of senktide in 3xTg-AD animals might have a potential as new biomarker for AD, however, further studies needed in this aspect.