It’s Never Too Early or Too Late—End the Epidemic of Alzheimer’s by Preventing or Reversing Causation From Pre-birth to Death

Abstract

The path to sporadic Alzheimer’s is a tragic journey beginning prior to birth and ending in the most dreaded disease of society. Along the disease path are a myriad of clues that portend AD, many of which are complaints of seemingly unrelated conditions from chronic migraines, mood disorders, eye diseases, metabolic syndromes, periodontal diseases, hormonal and autoimmune diseases. Properly treating, not just managing, these diseases, prior to onset of dementia, may significantly reduce dementia incidences. Current high levels of health complaints reflect a state of generalized poor health and compromised immunity. During the mid-Victorian era, people were long-lived yet healthy, suffering from chronic diseases at one tenth the rate of peoples today. It’s our poor health, at any age that increases susceptibility to chronic diseases and Alzheimer’s. Infection is involved in many cases of Alzheimer’s and other neurodegenerative diseases but is also implicated in many chronic conditions. Scientists looking for causation recognize that Alzheimer’ is multifactorial and systemic—not “brain only.” To slow, stop and reverse the AD epidemic, identification and reversal of causal factors must occur across the entire life spectrum of humans. This approach simply gives consideration to enhancing immune status of our bodies and brain, and controlling inflammation and infection, throughout the entire age spectrum. Infection is a causal factor, but the root cause is multi-factorial and immune health related. Pasteur stated it best when acknowledging the work of Bernard in 19th Century France, “The seed is nothing, the soil is everything.”

Hyperbaric oxygen therapy for Alzheimer’s dementia with positron emission tomography imaging: A case report

“…AD is a debilitating, costly, rapidly increasing neurological disorder for which there is no effective treatment 123. Etiology is multifactorial, systemic, and immune health-related from insults that occur across the spectrum of life,13 resulting in reductions of brain regional metabolism 14. Causes include infection,13 diabetes mellitus,13 metabolic disorders,7 and vascular factors 1516.…”

“…Etiology is multifactorial, systemic, and immune health-related from insults that occur across the spectrum of life,13 resulting in reductions of brain regional metabolism 14. Causes include infection,13 diabetes mellitus,13 metabolic disorders,7 and vascular factors 1516. Four pathological processes have been identified17: vascular hypoperfusion of the brain (and disturbed microcirculation)18 with associated mitochondrial dysfunction,6 2) destructive protein inclusions (intracellular neurofibrillary tangles--phosphorylated and aggregated tau protein), and extracellular amyloid plaques,7 3) uncontrolled oxidative stress, and 4) proinflammatory immune processes1319 secondary to microglial and astrocytic dysfunction in the brain.…”

The Role of Inflammation and Infection in Age-Related Neurodegenerative Diseases: Lessons From Bacterial Meningitis Applied to Alzheimer Disease and Age-Related Macular Degeneration

“…defense mechanism to eliminate infectious agents (Soscia et al, 2010). Numerous reviews are proposing the alternative theory of microbiological pathogenesis in AD, with overlapping and distinct perspectives (Fulop et al, 2018;Moir et al, 2018;Morris et al, 2018;Trempe and Lewis, 2018;Ashraf et al, 2019;Moir and Tanzi, 2019;Komaroff, 2020). Itzhaki and colleagues, and Komaroff, recently enunciated their viewpoints on the infectious aetiology of AD (Itzhaki et al, 2020;Komaroff, 2020).…”

“…This is backed by several lines of evidence, including detection of microbial components in AD biospecimens and empirical demonstration of the antimicrobial properties of Aβ, which is consistent with its production as part of a host defense mechanism to eliminate infectious agents (Soscia et al, 2010 ). Numerous reviews are proposing the alternative theory of microbiological pathogenesis in AD, with overlapping and distinct perspectives (Fulop et al, 2018 ; Moir et al, 2018 ; Morris et al, 2018 ; Trempe and Lewis, 2018 ; Ashraf et al, 2019 ; Moir and Tanzi, 2019 ; Komaroff, 2020 ). Itzhaki and colleagues, and Komaroff, recently enunciated their viewpoints on the infectious aetiology of AD (Itzhaki et al, 2020 ; Komaroff, 2020 ).…”

“…This mini literature review begins by providing a succinct overview of the role of infections in AD, focussing on the latest developments without extensively covering material that has been reviewed elsewhere by other authors (Fulop et al, 2018 ; Moir et al, 2018 ; Morris et al, 2018 ; Trempe and Lewis, 2018 ; Ashraf et al, 2019 ; Moir and Tanzi, 2019 ; Komaroff, 2020 ). Since, AD and AMD share common risk factors, e.g., aging and smoking, and pathologic features, e.g., the presence of extracellular deposits and complement system activation (Kaarniranta et al, 2011 ), this mini-review article also integrates recent evidence that suggests a contribution of parainfection in the aetiology of AMD.…”