Effects of levothyroxine on learning and memory deficits in a rat model of Alzheimer’s disease: the role of BDNF and oxidative stress

Abstract

The effect of levothyroxine (L-T4) on the learning and memory impairment induced by streptozotocin (STZ) and brain tissue oxidative damage in rats was evaluated. An animal model of the Alzheimer's disease (AD) was established by intracerebroventricular injection of STZ (3 mg/kg) in male Wistar rats (250 ± 50 g). After that, the rats were treated for 3 weeks with L-T4 (10, 100 μg/kg) or normal saline. Passive avoidance (PA) learning and spatial memory were evaluated using shuttle box and Morris water maze (MWM), respectively. Finally, the rats were euthanized, their blood samples were collected for further thyroxine assessment and their brains were removed after decapitation in order to measure the oxidative stress parameters and brain-derived neurotrophic factor (BDNF). In the MWM, latency (s) increased in the AD rats compared with the normal control group while it decreased in the 10 μg/kg L-T4 injected AD rats compared with the AD group. In the PA, the latency for entering the dark compartment was lower in the AD group than in the normal control group and it decreased in the 10 μg/kg L-T4 injected AD rats. The low dose of L-T4 (10 μg/kg) reduced malondialdehyde concentration but increased thiols concentration, superoxide dismutase, catalase activities and BDNF level in hippocampal tissues of the AD rats. Injection of L-T4 (10 μg/kg) alleviated memory deficits and also improved factors of oxidative stress and BDNF level in the STZ-induced AD rats.

L-Thyroxine improves vestibular compensation in a rat model of acute peripheral vestibulopathy

“…Whereas in intact mature neurons, BDNF downregulated KCC2 (39, 62, 63), in injured neurons BDNF upregulated KCC2 (8, 61, 62). Interestingly, TH have been shown to increase the expression of BDNF in lesioned slices of the hippocampus (18, 64) and other pathological models (15–17). We can then assume that an acute L-T4 treatment after UVN induces a local increase of BDNF in the deafferented VN, thus promoting cell proliferation as demonstrated in our previous study (8).…”

“…TH signalling governs many aspects of neurogenesis, including proliferation, survival, migration, differentiation and maturation of neuronal and glial cells (11)(12)(13)(14). Thyroxine (T4) or triiodothyronine (T3) injections have been shown to increase the expression of BDNF in different pathological models (stroke : (15,16), Alzheimer disease: (17), and axotomy (18)). In addition, several studies have demonstrated the protective role of TH and their ability to promote functional recovery through genomic and non-genomic actions (for review see (19,20)).…”

Effect of Sanguisorba Minor on Scopolamine-induced Memory Loss in Rat: Involvement of Oxidative Stress and Acetylcholinesterase

“…In these trails, the rats were placed in the light chamber and an entering delay of the rat to the dark chamber was then measured as the latency time. Additionally, the time spent by the animal in the dark and light compartments was recorded (Bavarsad et al 2020). Notably, in retention trails, the shock punishment was not applied.…”

“…Subsequently, the obtained mixture was heated in boiling water and after 40 min, the samples were cooled and the absorbance was spectrophotometrically measured at 412 nm. The following equation was used to calculate the concentration of MDA (Bavarsad et al 2020). Concentration (M) = Absorbance / 1.56 × 10 5 .…”

The effects of the combination ofCyperus rotundus,Crocus sativus,Piper nigrum,andBoswellia serrataon learning and memory deficit and oxidative damage in brain tissue of hypothyroid rats

“…The testing session was performed on 2, 24, and 48 hr after delivering the foot shock. In this session, the animals were placed back into the illuminated compartment and the time taken by the animals to enter the dark part, the entries made by the animals and the time spent in there during the 5 min of the test was recorded (Bavarsad et al, 2020).…”