Straumann implants with Al2O3, Alzheimer's disease, relative insufficiency of Magnesium (Mg) in the brain and decrease in Ca2+ level

We know that the surface of Straumann implants contains particles of aluminum oxide.

https://www.hindawi.com/journals/ijbm/2019/6318429/

if you read the two articles below, it turns out that particles of aluminum oxide break when screwed in and get into the bloodstream

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4420732/

al2o3 induce degenerative changes in the brain including a decrease in Ca2 +, a decrease in Mg ion content, oxidative stress, and neuronal damage.

All these contribute to dementia and Alzheimer's disease in humans.

ALUMINIUM OXIDE NANOPARTICLES COMPROMISE SPATIAL LEARNING AND MEMORY PERFORMANCE IN RATS Effect of four Al2O3-NP injections on rats.

https://www.researchgate.net/publication/323410364_Aluminium_oxide_nanoparticles_compromise_spatial_learning_and_memory_performance_in_rats

The purpose of this study was to examine the effects of Al2O3-NPs on spatial learning, memory, oxidative response, and bio-distri-bution of Al and other minerals in the rat hip-pocampus. The hippocampus is the site in the brain responsible for memory and learning. The spatial learning capacities of rats were evaluated in the Morris water maze test. The Al2O3-NP-treated rats had a lower spatial performance than the control rats did, which was revealed by the probe test results. Additionally, the rats did not learn to accurately locate the escape point in the maze. Our findings showed an increased Al concentration in the hippo-campi of the rats. We believe that NPs are absorbed in the brain in their ionic form. Al is a neur otoxin that is implicated in some neurodegenerative diseases such as Alz-heimer’s disease (Abdel-Aal et al., 2011; Gauthier et al., 2000). Accumulation of Al in the hippocampus can partially contribute to the toxicity of Al2O3-NPs. Al can dam-age neurons and lead to depletion in AChE level. Moreover, Al alters the BBB and pro-duces changes in noradrenergic and choliner-gic neurotransmissions (Yokel, 2000). Al and Al2O3-NPs can alter ion homoeostasis, in-cluding Ca2+ homoeostasis, and decrease the release of ACh, which results in decreased AChE levels. This was confirmed in the pre-sent study by the significant decrease in Ca2+ levels in the hippocampi of rats. 

Oxidative stress is the most common mechanism through which toxicity occurs fol-lowing exposure to NPs (Yang et al., 2009). Our results showed that, MDA levels in-creased significantly while SOD activity de-creased in the hippocampi of the Al2O3-NP-treated rats. Sethi et al. (2008) reported simi-lar findings after administering oral Al to rats. Inhibition of SOD activity leads in part to in-crease in lipid peroxidation (Kumar et al., 2009). Furthermore, it disturbs Fe homoeosta-sis, which results in excessive levels of free Fe ions, which causes oxidative damage by the Fenton reaction and further leads to neu-rodegeneration. No differences were ob-served between the two groups with regards to thiol group levels and the activities of CAT and GPx. In addition, our results showed that Al2O3-NPs can disrupt the metabolism of mineral elements that are necessary for anti-oxidant enzyme synthesis in the rat brain. Flora et al. (2008) reported that the production of reactive oxygen species is related to de-crease in the levels of some antioxidant en-zyme cofactors such as Fe, Zn, Mg, and Cu. 

Moreover, the Al2O3-NPs might have induced free radical generation that further initiated li-pid peroxidation and damaged cellular com-ponents. Previous studies have shown that Al can induce lipid peroxidation in the brain and cause neurodegeneration (Kumar et al., 2009; Tripathi et al., 2009), which can be confirmed by increased MDA levels and inhibition of SOD activity in the brain (Morsy et al., 2013). Furthermore, Al can cause neuronal inflam-mation, which leads to a decline in visoper-ception and attention, and impairment in working and semantic memories (Platt et al., 2001). Our data revealed no difference in hip-pocampus structure between the control and treated groups. Al-NPs can alter the neural membrane by reducing its lipoprotein integrity (Banks et al., 2006). This induces partial damage to the BBB, which leads to Al accumulation in the brain. It has been reported by Rebai and Djebli (2008) that increase in Al levels in the hippocampus and cortex causes damages, such as neurofibrillary degeneration, to these regions. Many studies have attributed NP-in-duced toxicities to oxidative stress and in-flammatory reactions (Adamcakova-Dodd et al., 2014; Ma et al., 2010). In conclusion, our findings suggest that short-term systemic exposure to Al2O3-NPs induces oxidative stress in the hippocampus. We also found that the latter possibly results from Al accumulation in the hippocampus and leads to changes in metabolic activity, thereby affecting learning and memory in rats.  

Dementias: the role of magnesium deficiency and an hypothesis concerning the pathogenesis of Alzheimer's disease

Evidence is presented indicating that dementias are associated with a relative insufficiency of Magnesium (Mg) in the brain. Such insufficiency may be attributable to low intake or retention of Mg; high intake of a neurotoxic metal, such as aluminum (Al), which inhibits activity of Mg-requiring enzymes; or impaired transport of Mg and/or enhanced transport of the neurotoxic metal into brain tissue. It is proposed that Alzheimer's disease (AD) involves a defective transport process, characterized by both an abnormally high incorporation of Al and an abnormally low incorporation of Mg into brain neurons. The hypothesis is advanced that an altered serum protein contributes to the progression of AD by having a greater affinity for Al than for Mg, in contrast to the normal protein, which binds Mg better than Al. The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate Al uptake and impede Mg uptake. Evidence suggests that albumin is the serum protein that is altered.

https://pubmed.ncbi.nlm.nih.gov/2092675/