If you enter the phrase Aluminum and Alzheimer’s disease into the Google search box, you will receive over 31,000 articles debating the link of the metal to the cause of the disease. Searching the scientific literature, on the other hand, reveals only 268 scientific studies on the topic. This discrepancy demonstrates that speculation about the health risk connecting aluminum to Alzheimer’s disease in the popular media is more than the scientific research that actually exists on this topic. Several key studies are worth exploring in greater detail to weigh in on this topic.
The suspicion of a possible link between aluminum in the etiology of Alzheimer’s disease most likely came about in the 1960s when a basic science study found that injecting aluminum salts in the brain or cerebrospinal fluid of rabbits induced neurofibrillary tangles that at the time were thought to be reminiscent of Alzheimer’s pathology. The excitement of the scientific community over aluminum as a risk factor diminished when more sophisticated imaging techniques revealed that the aluminum-induced tangles in the rabbits were very different in structure from the pathology observed in Alzheimer’s disease. It was also shown that aluminum tended to influence motor neurons rather than neurons involved in memory. This study suggested that aluminum, when injected into a rabbit’s brain, has the capacity to induce a lesion, but this pathology is very different from the plaques and tangles seen in Alzheimer’s.
A research paper published in NEUROLOGY in 1979 analyzed 274 brain samples from the frontal cortex of patients with Alzheimer’s and age-matched individuals with no neurological disorders. The researchers found no statistically significant differences in brain aluminum concentration between patients with Alzheimer’s disease and the controls.
In the May 1998 issue of JAMA NEUROLOGY, a series called “Controversies in Neurology” hosted perspective pieces from individuals with two different viewpoints weighing in on whether or not exposure to aluminum is a risk factor for Alzheimer’s disease. The scientists calling the aluminum hypothesis into question cited the flawed premise of the early study conducted in rabbits as a reason to be skeptical of the link between aluminum and Alzheimer’s. The scientists also pointed out that patients who consume antacids that contain aluminum do not demonstrate an increased risk of dementia even if they ingest several hundreds of times the amount of aluminum present in drinking water.
Aluminum intoxication has been reported in patients with chronic renal failure and the high doses of aluminum in these patients have provided crucial insights into the possibility of neurological syndromes associated with aluminum overload. Patients with chronic renal failure are at risk of developing dialysis encephalopathy syndrome which is characterized by speech disturbances and epileptic seizures – a clinical presentation that is very different from Alzheimer’s disease.
Aluminum intake in humans largely comes about from food, drinking water, and aluminum-containing drugs. Normally, the digestive tract serves as an effective barrier in preventing gastrointestinal absorption of aluminum. Due to a connection between aluminum-overloading and disruption of iron in the body, the World Health Organization recommends keeping aluminum concentrations in the drinking water below 0.1 mg/L.
While there exists a minority of researchers who are of the opinion that aluminum increases Alzheimer’s risk, this does not represent current mainstream thinking about Alzheimer’s. More evidence suggests the greater importance of adequate sleep, a brain-stimulating lifestyle, a healthy diet, engagement in physical activity, and the management of other illnesses or conditions like high blood pressure in reducing risk.