AZ (Alzheimer's) protocol — experimental

Twice a day for several months—


HEPPS [aka, EPPS] — 1g (1/4 level teaspoon)

Taurine — 4g (1 level teaspoon)

Oleuropein — 200 mg

Vitamin C — 2g


Note: Oleuropein + taurine can lower BP substantially





EPPS reduces Aβ-aggregate-induced memory deficits in mice

Previously, we reported a series of small ionic molecules that could accelerate the formation of Aβ aggregates in vitro. Unexpectedly, in addition to the compounds facilitating Aβ aggregation, we identified six small molecules that inhibited the formation of Aβ oligomers and fibrils13. In the current study, we tested whether these molecules could affect AD-like cognitive impairments of rodents. For this purpose, we induced memory deficits in 8.5-week-old Imprinting Control Region (ICR) mice (male, n=9–10 per group) by injecting Aβ42 aggregates (Fig. 1a,b) into the intracerebroventricular region14. This Aβ-infusion model allowed us to control the onset of abnormal Aβ deposition before or after the administration of our compounds. Among the six orally administered molecules, only 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS) ameliorated AD-like phenotypes in our mouse model.


Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

We orally administered taurine via drinking water to adult APP/PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice.


Noncovalent Interaction Between Amyloid-β-Peptide (1-40) and Oleuropein Studied by Electrospray Ionization Mass Spectrometry


The successful detection of the noncovalent complex between Aβ and OE [Oleuropein] could be invaluable in a series of studies focused on screening the ability of several bioactive phytochemicals in terms of complexating Aβ and Aβox and “locking” them in a non-toxic conformation, thus acting as potential anti-amyloidogenic agents. This may offer an ideal protective alternative against Aβ toxicity.

Preventive and therapeutic potential of ascorbic acid in neurodegenerative diseases.

Ascorbic acid acts mainly by decreasing oxidative stress and reducing the formation of protein aggregates, which may contribute to the reduction of cognitive and/or motor impairments observed in neurodegenerative processes.