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Despite early criticism of the aluminum hypothesis, numerous biochemical, toxicological, cell biological and genetic studies have supported the notion that aluminium-induced Alzheimer-like pathological changes are primarily associated with accumulations of amyloid-beta plaques  and tau protein (NFT). Moreover, recent immunohistochemical imaging has shown that aluminum is highly enriched in the brains of donors with familial Alzheimer’s disease who share a single mutation that causes elevated levels of amyloid-beta, early disease onset, and aggressive disease etiology .
Aluminum neurotoxicity impairs long-term potentiation (LTP), a form of synaptic memory storage well-known for its role in learning and memory, inhibits voltage-gated calcium channels and disrupts signaling through GTP-binding proteins including neurotransmitter receptors, induces apoptotic cell death, influences emotional reactivity and spatial memory deficit, increases pro-BDNF expression via advanced glycation end products (AGEs), and promotes tau hyperphosphorylation in neurons.
Our study confirms that oral exposure to alumina nanoparticles leads to cognitive impairment in rats by increasing spatial memory performance and decreasing hippocampal LTP, revealing a direct relationship between the aluminum-induced amyloid-beta accumulation and hippocampal LTP deficit. In addition, aluminaNPs induced impaired spatial memory consolidation by decreasing proximity score in the probe test, suggesting that they may interfere with memory consolidation through modulating the activity of fast-spiking interneurons. Moreover, aluminaNPs significantly decreased the firing rate of pyramidal neurons in the hippocampus during the probe test, indicating that they impair spatial memory by lowering neuronal correlate. Interestingly, however, this effect was not seen in the memory retrieval test and the control group did not exhibit any change in the firing rate of pyramidal neurons during the probe test or in the basal frequency during the memory consolidation test.