Acute toxicity refers to harmful effects caused by high concentrations of aluminium. Descriptions are available particularly www.selleckchem.com/products/bmn-673.html with regard to dementia: The first description of the aluminium-related dementias can be traced back into the 1970s [23] and [24] and most studies report a positive link between aluminium accumulation and cognitive impairments. However, some study designs are highly variable and their quality is questionable. More recently, evidence has demonstrated that high aluminium exposure from, i.e., drinking water can trigger acute episodes of dementia in patients with renal insufficiency, providing strong evidence for the causal relationship with aluminium [25]. The use of silicic

acid has also been suggested to have a protective affect against the development of dementia [26], [27] and [28]. As previously mentioned, the bioavailability of aluminium in drinking water is, for instance, co-dependent on its silica content: large amounts of silicic acid in drinking water reduce the uptake of aluminium and vice versa [6] and [10]. Exley and co-workers [26] have demonstrated that

regular consumption of silicon-rich mineral waters reduce gastrointestinal uptake of aluminium and removal of systemic aluminium from the body. As a result, this ROCK inhibitor may provide the basis of a non-invasive means for a therapy to treat the symptoms of Alzheimer’s disease, in an attempt to reduce their body burden of aluminium. However, in-depth follow up studies involved in identifying clinical improvement of symptoms are at an early stage. In the 1940s, inhalation of aluminium was propagated as prophylaxis against silicosis in mine workers [29]. Examinations of these mine workers conducted in the study revealed the neurotoxic Tryptophan synthase effects of this aluminium

exposure [30]. In 1988, the drinking water of the Camelford community in Cornwall, UK, was accidentally contaminated with 20 t of aluminium sulphate. Follow-up examination in the affected population demonstrated the consecutive neurotoxic effects of aluminium [31]. In another study, a neuropathological examination of an exposed individual who died from an unspecified neurological condition was performed. High aluminium levels were measured in affected regions of the cortex, where a rare form of β amyloid angiopathy was identified [32]. Chronic toxicity refers to the harmful effects of protracted low-dose contamination. Increased concentrations of aluminium have been demonstrated in senile plaques in the brains of Alzheimer patients. The property of aluminium to produce amyloid-beta and cause damage to neurons, as well as epidemiologic connections, have been indicative of a relationship between aluminium and Alzheimer’s disease for decades. Current reviews cite respective, but sometimes contradictory, studies [33]. To summarise the current state of knowledge, Bondy et al.