A Paradigm shift in understanding

Alzheimer’s Disease and possible

treatment options

by Henry E. Aldorf MSc. , BSc. , MBA June, 2018

Fighting the physical lesions in the AD Brain has been today’s strategy

The current AD research spent billions on the reduction and elimination

of the two main physical manifestations and believed causes of AD
without real success

• Tau Entanglements (TE)

• B -Amyloid plaques (BAP)

Reason for failure: The source of the disease is not in

the brain and the “infectious agent” is the TE itself
What causes these entanglements and plaques?
• TE are caused by the miss folding of proteins also seen in other
neurological diseases and these proteins seem to display prion type
characteristics

• BAP seems to be a response by the brain fighting inflammation

caused by the TE prion formation. Similarly as seen in bacterial brain
infections.
Homeostasis in the Liver controls the Cat-ion balance and
hence protein Folding: “Cure the liver and one may cure
the brain”
• Protein folding is a complicated process involving certain critical Cat-ions (e.g. Cu,
Mo, Zn ,Mg , Fe).This process can be easily disturbed by imbalances in these Cat-
ions. Especially high copper concentrations in drinking water have been
implemented due to the extensive use of Copper tubing

• Miss-folding of the proteins can repeat and eventually increase the amount of
miss folded proteins through a prion mechanism not unlike a polymerisation
reaction.

• Not dissimilar to diseases like spongiform encephalitis( Creutzfeldt-Jakob) these

miss folded proteins have been identified as prions and have been shown to be
infectious and also play a role in Parkinson's disease

•
Source and possible treatments:
Miss-folding of Proteins –> The Homeostasis process in the Liver is the source of
the disease
Proposed Treatment
• In the Liver
• improve Homeostasis by measuring serum level of Cat-ions balance and supplement to get
balance (e.g. Cu/Mo and other Cat-ions ratio).
• Treating conditions leading to impaired Homeostasis
• fatty liver disease
• Diabetes
• Hepatitis
• Cirrhosis
• Hepatitis
• In the Brain
• Prevent the miss folding of Tau and treat miss folding Tau with low dose Doxycycline and
Rapamycin as in other prion diseases .
 Additional considerations
• Bacteria e.g SPIROCHETES may accelerate the BAP formation and intensify
neuro inflammation of the brain ,which could lead to ever more BAP
formation on top of the BAP formed by the brain due to TE
Treatment
• Classic Doxycycline treatment followed by periodical treatment to keep
the bacterial load down
• Gum disease treatment reduce opportunity for spirochetes to enter
• Strict mouth hygiene with daily Betadine mouth wash
• Reduce further the inflammation stress on the Brain reducing BAP
formation
*
Conclusions of the paradigm shift : Brain to Liver
• TE prions seem to cause the disease to progress ,which cause
inflammation within the brain, which in turn tries to combat this by BAP
formation
• The liver and homeostasis hold the key to treatment as it controls cat- ion
availability for correct Tau folding
• Bacterial infections can be an additional source of inflammation of the
brain and therefore additional BAP formation.
• Doxycycline and probably Rapamycin can combat both the TE prion and
the bacteria at low dose
• The same mechanism can be observed in Parkinson's disease only the
prion material is different
Treating the liver , the TE “prion” and the bacteria seem to be the best
cause of action as it can prevent further Tau miss folding and stop the
prion formation and stabilize over all BAP levels
literature
• Miklossy, Judith (2011-08-04). "Alzheimer's disease - a neurospirochetosis. Analysis of the
evidence following Koch's and Hill's criteria". Journal of Neuroinflammation. 8: 90. doi:10.1186/1742-
2094-8-90. ISSN 1742-2094. PMC 3171359 . PMID 21816039

• Doxycycline: bringing hope for early sporadic Creutzfeldt-Jakob disease patientsPosted on January 31,
2017 by Dr Jose Manuel Matamala, JNNP web editor.
• The antibiotic course has had its day02 August 2017 Detlef Degner associate Professor of Psychiatry,
assistant medical director Department of Psychiatry, Medical School of Georg-August University,
Goettingen D-37075 Göttingen, Germany
• Doxycycline counteracts neuroinflammation restoring memory in Alzheimer's disease mouse model
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RobertoViscomibMartenBeegcMarcoGobbicMarioSalmonacSimoneOttonellobGianluigiForlonia
Protein Folding and Metal Ions: Mechanisms, Biology and Disease
edited by Cláudio M. Gomes, Pernilla Wittung-Stafshede
**- Adv Neurobiol. 2017;18:199-216. doi: 10.1007/978-3-319-60189-2_10.
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• Am J Neurodegener Dis. 2013 Jun 21;2(2):46-56. Print 2013. Rosanna Squitti1,2 and Renato Polimanti3

• **Tau prions from Alzheimer’s disease and chronic traumatic encephalopathy patients propagate in cultured cells
Amanda L. Woerman, Atsushi Aoyagi, Smita Patel, Sabeen A. Kazmi, Iryna Lobach, Lea T. Grinberg, Ann C. McKee, William W.
Seeley, Steven H. Olson and Stanley B. Prusiner
• Structure-based drug design identifies polythiophenes as antiprion compounds
Science Translational Medicine 05 Aug 2015:
Uli S. Herrmann1, Uli S. Herrmann1, Anne K. Schütz2,*, Hamid Shirani3,*, Danzhi Huang4, Dino Saban1,†, Mario Nuvolo