Published Paper Details:

Aluminium (Al), the third most abundant element in the Earth's crust, is extensively used in industrial processes, consumer products, and certain pharmaceuticals. Despite its non-essential role in human physiology, increasing evidence associates chronic aluminium exposure with neurotoxic effects, including oxidative stress, neuroinflammation, mitochondrial dysfunction, and cognitive impairment. Aluminium can cross the blood-brain barrier through transferrin-mediated and citrate-complex transport, accumulating preferentially in brain regions responsible for memory and learning. Experimental studies in rodents demonstrate dose- and time-dependent behavioural deficits, neuropathological alterations, and cholinergic system disruption. Factors influencing aluminium toxicity include dose, chemical form, exposure route, age, and renal function. Public health concerns persist regarding occupational, environmental, and dietary exposure, yet causal relationships with human neurodegenerative diseases remain debated. This review consolidates current evidence on aluminium sources, exposure pathways, mechanisms of neurotoxicity, behavioural outcomes, and research gaps, aiming to guide future studies and inform regulatory policies.