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(Oct. 1, 2023) — Aluminum is a ubiquitous element found in the Earth’s crust, where it was bound to silica for nearly all of the 3.8 billion years of organic evolution on this planet. Since the late 1800’s, has found its way into various aspects of human life, from cookware to vaccines. While it is generally considered safe for most applications, it is not: emerging evidence shows that have neurotoxic effects, particularly in the context of neurodegenerative diseases like Alzheimer’s. Here we explore the mechanisms through which aluminum exposure leads to brain injury.

Mechanisms of Aluminum Neurotoxicity

Oxidative Stress

Aluminum has been identified as a neurotoxic agent that results in oxidative damage to cellular biomarkers. Oxidative stress is a well-known factor in the pathogenesis of neurodegenerative diseases, and aluminum’s role in exacerbating this cannot be ignored.

“Aluminum is an environmentally abundant potential neurotoxic agent that may result in oxidative damage to a range of cellular biomarkers.” (REVIEW)

Neuronal Apoptosis

Aluminum has been shown to induce neuronal apoptosis both in vivo and in vitro. Apoptosis, or programmed cell death, is a critical mechanism in the development of neurodegenerative diseases.

“Aluminum induces neuronal apoptosis in vivo as well as in vitro, either by endoplasmic stress from the unfolded protein response, by mitochondrial dysfunction, or a combination of them.” (REVIEW with 167 citations therein)

Tau Protein and Amyloid-beta Accumulation

Aluminum exposure has been linked to the accumulation of tau protein and Amyloid-beta (Aβ) in the brain, both of which are hallmark features of Alzheimer’s disease.

“Aluminum causes the accumulation of tau protein and Aβ protein in the brain of experimental animals.” (REVIEW)

Evidence

Historical Context

The earliest evidence of aluminum’s potential involvement in Alzheimer’s disease dates back to the 1960s, from independent laboratories in the United States and Canada.

“The first successful attempt to obtain purified aluminum metal was accomplished by the Danish physicist and chemist Hans Christian Orsted in 1824, however it was not until about ~140 years later that aluminum’s capacity for neurological disruption and neurotoxicity was convincingly established.” (LINK)

Animal Models

An aluminum-based rat model for Alzheimer’s disease exhibited oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration, providing compelling evidence for aluminum’s neurotoxic effects.

“An aluminum-based rat model for Alzheimer’s disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration.” (STUDY)

Aluminum injections in mice cause motor deficits and motor neuron degneration (STUDY).

Sheep injected with aluminum adjuvants develop autoimmune diseases (STUDY).

Hormesis

The argument often made in favor of aluminum safety is that the doses used in medical interventions are low. Non-linear dose/response curves reflect hormesis, in which, paradoxically, low doses can have an increased risk of toxicity. With aluminum adjuvants, low-dose exposures over time can still lead to accumulation and associated risks. Moreover, the ‘low-dose’ argument does not consider the potential for repeated exposures through multiple vaccinations or other medical treatments. The concept of hormesis, where low-dose exposures could have non-linear toxic effects, is evidenced by the study by G. Crépeaux et al. on selective low-dose neurotoxicity[LINK].

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