AEIF Newsletter 4: Pathogenesis of AD (Meningoencephalitis)

February 1st, 2022

Determining the pathogenesis of any disease is critical in order to effectively develop a strategic treatment protocol. Pathogenesis is the process by which a disease or disorder develops. AD invades the brain via the nasal passage. The exposed and vulnerable olfactory mucosa and neuro-epithelium are the conduits into the olfactory tract traversing through the multiple holes in the cribriform plate of the skull.

Once intracranial, the olfactory bulb, in all medical probability, will harbor the offending vector(s). Overlying the olfactory bulb is the circulating cerebrospinal fluid which separates the bulb from the olfactory cortex. Increased production of major self-propagating detectable sticky proteins of beta-amyloid and tau in Alzheimer’s Disease. These biochemical by-products lead to a destructive cascade of pathological processes yet to be fully elucidated.

Figure 1. Comparison of Brains in Elderly and AD Patients

1.       2.              3.

PET scan of Beta-Amyloid and Tau Protein deposition comparisons in normal adult (1), older adult (2), and AD adult (3). 

Tau Protein deposition found in the medial temporal lobes. Beta-Amyloid concentration demonstrating possible infected areas via circulating CSF. 

Early in the course of this disease, minimal cognitive impairment, diminution of taste and smell have been implicated, as in COVID-19. It stands to reason that the pathogenesis of AD may be related to a viral or post-viral infection. 

 In AD, our theory proposes that: there exists an intranasal route of exposure with progression to chronic destruction meningoencephalitis. Meningoencephalitis is a combination of meningitis (infection of the CSF and brain covering) and encephalitis (infection of the brain). The meningitis; inflammation of the meninges and cerebrospinal fluid, is seen as a blotchy concentration over the surface of the brain (1).

Figure 2. Beta-Amyloid Pet CT

The vector(s) infiltrating the olfactory system leads to toxins penetrating into the brain and CSF, circulating over the entire surface area of the cerebral cortex,  and subsequently into the ventricular system. In the CSF, β-amyloid plaques and hyperphosphorylated tau have been implicated in AD pathogenesis.