AEIF Newsletter 5: Progressive Brain Atrophy in AD

February 15th, 2022

During the downward spiral of inflicted persons with Alzheimer’s Disease (AD), progressive atrophy of the cerebral cortex and inner layer of the ventricles has been well documented and represented below per the Alzheimer’s Society’s publication. 

Figure 1: Comparison of the Healthy Brain and the Progressive Deterioration of the Alzheimer’s Brain

AD is attributed to unknown harmful pathogen(s), particularly those promoting the increasing self propagating proteins Beta-amyloid and tau quantitatively identified in those CSF (cerebral spinal fluid). The offending pathogen(s) infiltrate via inhalation and relatively easily migrate through the holes in the skull (the cribriform plate). These pathogens adversely compromise  the exposed olfactory epithelium inhibiting the sense of taste and smell. In COVID-19, we’ve witnessed this inhalation process which led medical experts to recommend masking as a means of prevention. 

Visual Representation of this Inhalation Process of Pathogens Invading the Olfactory nerve, CSF and Brain Tissue

Beta-Amyloid Pet CT Present within CSF (1) and Attaching to Brain Tissue: A. Olfactory Cortex (2) and B. Anterior Commissure (3)

This  process consequently and continuously propagates production of CSF beta-amyloid and tau proteins.

Other pathogens, i.e. aluminum found exclusively in the neurofibrillary tangles associated with beta-amyloid in the memory centers of the temporal lobe,  can readily diffuse across the covering of these nerves, called the perineurium, and then into the  intra-axonal spaces. This increased permeability in turn leads to a chronic inflammation of the brain. The invasion Adjacent to the neuro-elements leads to the loss  of taste and smell, as demonstrated in our pictorial above. The existence of Aluminum particles has been identified in the neurofibrillary tangles. These Aluminum particles are found in the memory centers of the amygdala and hippocampus and no other locations during AD brain autopsies. The nature of this heavy metal’s infiltration has yet to be clearly understood. 

Because aluminum is found exclusively in the temporal lobes, it is reasonable to propose a hypothesis that this heavy metal is penetrating the nasal passage and diffusing along the olfactory epithelium. Eventually, the aluminum is found in the beta-amyloid related neurofibrillary tangles (NFTS). These NFTs are forming a plaque wall, which is observed as a specific pathological process in AD victims.

Progressive severe cortical atrophy of the brain and enlargement of the ventricles is the accepted process leading to death in AD.  In conclusion, the circulation of the CSF on the surface of the brain (as shown in Figure 1) and within the ventricle is the only possible mechanism for this progressive process of cell death in AD.