Background: This study aims to examine the potential neuroprotective effects of flaxseed oil (FSO) on the brain activity of rat pups sired by females intoxicated with aluminum (Al). The brain is known to be particularly vulnerable to the deleterious effects of aluminum, which promotes oxidative stress and neuroinflammation. FSO is a rich source of omega-3 (ω-3) fatty acids (FA), essential components of neuronal membranes and neurotransmission. Methods: After collecting 36 offspring aged three weeks from a control group and an intoxicated female group that received an intraperitoneal injection of aluminum chloride (AlCl3) (75 mg/kg body weight, twice a week) in the morning for 30 days. Six subgroups of pup rats for each group (n = 6) were used, with control groups having free access to food and water and two experimental groups receiving low and high doses of FSO administered by gavage (0.5 and 2 mL/kg b.wt.). An intoxicated group was also tested with rats receiving low and high FSO concentrations and free access to water. The study appears to focus on the effect of omega-3 in the FSO on the brains development of young rats a neurobehavioral study was carried out, followed by estimation of prooxidant parameters and neurotransmitter activity of the brain, and a lipid composition was carried out on the brain membrane by gas chromatography-mass spectrometry (GC-MS) analysis. Results: The FA profile of FSO revealed domination by ω-3 type (86.9%). The 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging capability was found at half maximal inhibitory concentration (IC₅₀) values of 18.12 g/mL. Neurobehavioral experiments showed significant hyperactivity and memory loss in intoxicated young rats, with decreased levels of lipid peroxidation (LPO) and nitric oxide (NO) and a significant increase in acetylcholinesterase (AChE) activity in the brain. However, ameliorative results were found in both concentrations of FSO administration when compared with intoxicated groups. GC-MS analysis of the brain membrane FA profile revealed the presence of elaidic acid in both the AL and AL+FSO. Neurobehavioral experiments showed significant hyperactivity and memory loss in intoxicated young rats, with decreased levels of lipid peroxidation (LPO) and nitric oxide (NO) and a significant increase in acetylcholinesterase (AChE) activity in the brain. However, ameliorative results were found in both concentrations of FSO administration when compared with intoxicated groups. GC-MS analysis of the brain membrane FA profile revealed the presence of elaidic acid in both the AL and AL+FSO” groups. In contrast, only the AL+FSO group had eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) areas. Conclusions: Our results suggest that FSO supplementation at low concentrations has neuroprotective effects on developing rat brains, correcting and ameliorating the abnormalities brought on by embryo/fetal aluminum chloride toxicity.