Aim: Several reports have shown environmental neuron toxins such as aluminium to accumulate in the brain, potentially triggering neurodegenerative disorders. Adansonia digitata (Baobab) has been reported to possess beneficial properties. This study, assessed the neuroprotective properties of aqueous fruit pulp extract of Adansonia digitata (AEAD) on aluminum chloride (AlCl3) – induced memory dysfunctions and hippocampal changes in Wistar rats. The neuroprotective effects of AEAD were assessed with the Morris water maze for learning and memory, oxidative stress biomarkers glutathione (GSH), superoxide dismutase (SOD), and Malondialdehyde (MDA), and histopathological changes on the hippocampal CA3 region using histological techniques. Materials and Methods: Thirty male Wistar rats (110 and 150 g) were divided into six groups at random (n=5). The Control group, the animals in Group 1 received 2 ml/ kg distilled water. Group 2 received 100 mg/kg of AlCl3. Ascorbic acid at a dose of 595 mg/kg was given to Group 3. 100 mg/kg AlCl3 and different concentrations of the AEAD (500 mg/kg and 1500 mg/kg, respectively) were given to groups 4 and 5. Group 6 received 595 mg/kg of ascorbic acid and 100 mg/kg of AlCl3. Results: The latency time spent to locate the escape platform in the Morris water maze test was observed with remarkable (P<0.05) improvement in the AEAD treatments compared with the AlCl3- treated group. There was a notable increase in MDA levels and a reduction in SOD and GSH activities in the AlCl3-treated group in relation to the AEAD-treated groups. Histopathological examination of the CA3 hippocampal region treated with AlCl3 revealed neurodegenerative changes, whereas, administration of AEAD ameliorated AlCl3-induced neuronal damages in rats at doses 500mg/kg and 1500mg/kg when compared with the AlCl3-treated group. Conclusion: Aqueous fruit pulp extract of Adansonia digitata demonstrated a possible neuroprotection against aluminium chloride-induced memory deficit and CA3 hippocampal neurotoxicity.

Aim: Lack of sleep has been linked in studies to increased beta-amyloid levels, oxidative stress, and memory impairments. Furthermore, sleep is known to help clear toxins that accumulate in the brain. This study investigated the restorative potentials of recovery sleep on total sleep deprivationinduced memory impairment, oxidative stress, stress response and changes in beta amyloid plaques in the hippocampus of adult male Wistar rats. Materials and Methods: Twenty-four male Wistar rats weighing between 150 and 200 g were divided into four groups. Group I remained in their home cages, while Groups II, III, and IV underwent sleep deprivation for 5 days. Groups III and IV then had recovery periods of 7 and 21 days, respectively. Spatial learning and memory was measured using the Novel Object Recognition test. The rats were euthanized with ketamine, oxidative stress was analyzed using hippocampal tissue homogenate and beta-amyloid plaques in the CA1 and CA3 regions using Congo red stain. Results: Comparing the sleep-deprived group to the sleep-recovered group, the discrimination ratio increased significantly (p < 0.0001). Sleep recovery also decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malonaldehyde (MDA) and corticosterone (p < 0.01). Additionally, extracellular amyloid-beta expression in the CA1 and CA3 regions of the sleep recovery groups was significantly reduced (p < 0.0001 and p < 0.01). Conclusion: Recovery sleep was found to improve memory and decrease beta amyloid expression and oxidative stress in the CA1 and CA3 areas of the hippocampus. 

Background: Lead acetate (Pb) exposure during frontal cortex development is associated with developmental
toxicity later in life, causing both morphological and functional alterations. Curcuma longa,
however, has been suggested to possess neuroprotective qualities that could lessen these adverse effects.
Objective: Assessed the frontal cortex following treatment with Curcuma longa. Materials and Methods:
Twenty adult female Wistar rats and ten adult male Wistar rats were matched during the proestrous phase
of the estrous cycle in order to mate and create five groups of six (n=6) in a 4:2 (4 females to 2 males)
ratio. Gestational day 0 was marked as the confirmation of pregnancy based on if sperm is present and a
vaginal plug in the vaginal smear. Four (n=4) pregnant Wistar rats were put together. Group 1 (control) rats
were given 2 milliliters per kilogram of distilled water. Pb was given at a dose of 120 mg/kg to Group 2.
Group 3 rats were given 120 mg/kg of lead and 100 mg/kg of vitamin C. The animals in Group 4 received
750 mg/kg of Curcuma longa and 120 mg/kg of Pb. The animals in Group 5 rats were given 1500 mg/kg
of Curcuma longa and 120 mg/kg of Pb. From gestational day 7 to day 21 (14 days), the medication was
administered orally. The animals were allowed to litter naturally. At postnatal day (PND) 1, some pups
were euthanized using chloroform inhalation and their brains were harvested for Oxidative stress markers,
histology, histochemical assessments. While some pups were kept for Cliff avoidance test at PND 4-7.
Results: The study found that lead acetate (Pb) exposure during gestation significantly decreased the mean
turning latency in the cliff avoidance test and increased lipid peroxidation (MDA) levels, while decreasing
antioxidant enzyme levels (SOD, CAT, GSH) compared to the control group. These neurological and oxidative
changes were mitigated by co-administration of Curcuma longa, with a notable improvement in the
cliff avoidance test performance and restoration of the altered histological and histochemical markers. The
results suggest that Curcuma longa, a natural antioxidant, has neuroprotective properties that can counteract
the adverse effects of lead toxicity during gestational development. Conclusion: N-Butanol Fraction
of Curcuma Longa ameliorated lead-induced neurotoxicity in rat pups.

Background: Epilepsy is a neurological illness that disturbs the central nervous system and is
characterized by regular convulsions. Over 70 million people worldwide are thought to have
epilepsy, with the prevalence rate estimated to be around 1%. Aims: The objective of this study
was to assess antiepileptic activities and histological changes after Mentat administration in the
hippocampus of pentylenetetrazole (PTZ)‑induced seizure mice. Materials and Methods: Twenty
Swiss albino mice (18–28 g) were divided into four groups (n = 5) and were given the following
intraperitoneally, 2 ml/kg distilled water and 50 mg/kg PTZ to Groups 1 and 2 animals, respectively.
Groups 3 and 4 animals were given 200 mg/kg and 400 mg/kg of Mentat, respectively, 1 h before
the administration of PTZ and were observed for 300 s. After the experiment, all surviving animals
in the various groups were humanely sacrificed and the brains were harvested and preserved in
10% buffered formalin. The brain tissues were processed using routine histological procedures
and stained with hematoxylin and eosin. Results: Results of this revealed that Mentat was able to
delay the onset time of seizure and offered quantal protection to the animals. Mentat also showed
a dose‑dependent ameliorative effect against histological changes following PTZ administration in
mice. Conclusion: Mentat attenuates PTZ‑induced seizure in mice.

Recent years have seen a surge in psychiatric diseases, which has resulted in considerable disease
distress and considerably decreased living conditions. Many considerable synthetic medications have
been used to treat these illnesses throughout the years, but they have been found to have limited
effects and substantial recurrence risks in many individuals. Mental illnesses such as depression
and anxiety are persistently on the rise around the world, posing serious challenges to the affected
person’s and their family members’ personal lives. There is mounting evidence that suggests the gut–
brain axis (GBA) contributes to the genesis and development of psychiatric diseases. This review
focuses on contemporary dietary therapies such as Mediterranean diets and dietary supplements
and emphasizes nutrition’s critical role in psychiatric care through the GBA. Several research have
indicated that dietary quality affects mental health because it controls metabolic processes, has
anti‑inflammatory and antiapoptotic characteristics, and promotes neurogenesis and synaptogenesis.
This study demonstrates many dietary components, their relationships to depression, and how they
work. The use of dietary recommendations to support mental health appears to be a novel, affordable,
useful, nonpharmacological intervention for people with mental problems.

Background: Tramadol has a high potential for misuse resulting in cognitive impairment.
Zingiber officinale, however, possesses neuroprotective qualities. Objective: Microscopically
assessed hippocampal CA1 and CA3 following Z. officinale and tramadol treatment.
Materials and Methods: Two milliliters/kilogram of distilled water was given to Group 1,
Groups 2–5 were administered 50 mg/kg of tramadol while Group 3 was also administered 12.5 mg/
kg of naltrexone, and Groups 4 and 5 were also administered 500, and 1000 mg/kg ethanol extract of
Z. officinale (EEZO), respectively, orally for 21 days. The rats were euthanized and their brains were
collected, fixed in 10% formal saline, and processed routinely using crystal fast violet (CFV) stain for
the demonstration of Nissl substance, glial fibrillary acidic protein (GFAP) for the demonstration of
astrocytes, and Hematoxylin and Eosin for general histoarchitecture and estimation of cell number and
volume using physical dissector and Cavalieri estimator, respectively. Results: CFV stain revealed
alterations in regions of CA1 and CA3 of the hippocampus presenting as indistinct staining intensity
and peripheral Nissl substance accumulation in the tramadol‑treated group. GFAP revealed numerous
reactive astrocyte processes. The area of reactive astrocytes remarkably increased (P < 0.05) and
the intensity of the Nissl substance remarkably reduced in the tramadol-exposed group. When
compared to the control, the tramadol-exposed group’s hippocampal volume considerably (P < 0.05)
decreased (coefficient of error [CE] =0.050). The tramadol treatment group (CE = 0.090) relative to
the control group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal
cells in the CA3 region. The tramadol treatment group (CE = 0.090) compared to the control
group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal cells in the
CA3 region. Tramadol toxicity was attenuated in the groups treated with EEZO in a dose-dependent
manner. Conclusion: Z. officinale possesses a potential neuroprotective effect against tramadol‑induced
neurotoxicity.