Aluminum (Al) is one of the most extended metals in the Earth's crust. Its abundance, together with the widespread use by humans, makes Al-related toxicity particularly relevant for human health.Despite some factors influence individual bioavailability to this metal after oral, dermal, or inhalation exposures, humans are considered to be protected against Al toxicity because of its low absorption and efficient renal excretion. However, several factors can modify Al absorption and distribution through the body, which may in turn progressively contribute to the development of silent chronic exposures that may lately trigger undesirable consequences to health. For instance, Al has been recurrently shown to cause encephalopathy, anemia, and bone disease in dialyzed patients. On the other hand, it remains controversial whether low doses of this metal may contribute to developing Alzheimer's disease (AD), probably because of the multifactorial and highly variable presentation of the disease.This chapter primarily focuses on two key aspects related to Al neurotoxicity and AD, which are metabolic impairment and iron (Fe) alterations. We discuss sex and genetic differences as a plausible source of bias to assess risk assessment in human populations.

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Objective Rats were exposed to free‐choice diets (fat plus one of two different sugar solutions, glucose or sucrose), and the metabolic consequences and impact on locomotor activity and anxiety‐like behavior were explored. Methods For 3 weeks, 7‐week‐old male rats were offered either chow only or free‐choice high‐fat diets differing in their added sugar: no sugar, sucrose, or glucose. In a second experiment, after 2 weeks on the diets, rats were switched from high sucrose to high glucose for two additional weeks. Metabolic end points included body weight, food intake, food choice, glycemic control, metabolic hormones, fat pad weight, brown adipose tissue weight, and gene expression. Behavioral analysis included locomotor and anxiety‐like activity in the open field and elevated plus maze. Results Both sugar diets enhanced adiposity and induced hyperphagia, favoring unhealthier dietary selection above that of the control diets (chow or free‐choice high‐fat with no sugar). Despite isocaloric intake in the sugar‐containing diets, offering glucose instead of sucrose was associated with improved insulin sensitivity. The sugar‐containing diets reduced activity (but with movements of increased velocity) and induced an anxiety‐like phenotype. Conclusions Although free‐choice diets negatively impacted on metabolism and anxiety‐like behavior, replacing sucrose with glucose improved insulin sensitivity and may therefore be better for health.

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