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Dr. D’Andrea
Breakthroughs
Alzheimer’s Discoveries

 

Actual Microscopic Images

Show How Excess Amyloid Aβ42 Destroys Neurons, Eventually Killing Them and Forming Amyloid Plaques, which causes Additional Damage, Inflammation, and Neuronal Death

ZNF – Best to Treat Here

Complexities Expand at These Later Stages

1.Normal production & secretion of amyloid

2. Brain vessel dysfunction; unregulated amyloid enters

3. Toxic accumulation of amyloid in a neuron

4. Eventually the neuron dies

5. Plaque forms of neuronal debris & inflammation begins

6. Inflammation forms glial scar, nearby neurons die

KEY BREAKTHROUGH

DIAGNOSE EARLY – FOR BLOOD BRAIN BARRIER LEAKING 

 

Treat Early To Preserves Neurons and Memory Before Neuronal Damage, Inflammation, and Plaques Become a Much More Complex Problem

 

Study 1 = Success

In Vitro Study Breakthrough

USING A RECEPTOR TARGETED BINDING COMPOUND ZNF SUCCESSFULLY  PREVENTED EXCESS AMYLOID FROM ENTERING HEALTHY NEURONS

Slide Shows Excess Amyloid Inside the Neuron

Slide Shows Amyloid Successfully Blocked from Entering Healthy Neurons

 

The presence of brown stained intracellular amyloid is shown by the arrows; as the this progresses certain neurons die and others are degenerating shown by the arrowheads.

 

Using a receptor targeted binding compound, ZNF successfully prevented excess amyloid from entering healthy neurons. Arrows show the presence of dividing cells.

 

Study 2 = Success

In Vivo Animal Study Breakthrough

Zachriel Neurosciences Confirmed How Excess Intracellular 

Abeta42 Amyloid Destroyed Healthy Neurons 

 

Mice received a tail injection of pertussis toxin to affect the Blood Brain Barrier (BBB) followed by vascular administration of AB42 (amyloid protein) in order to demonstrate how neuronal damage and neuronal death occurs from the excess absorption of the AB42 amyloid protein (leaked from blood vessels in the brain) by the neurons. This caused learning impairment and accumulation of immunoglobulins in the brain, formation of plaques, and synaptic decline. 

 

This was the first time these events were shown to occur in live animals, confirming ZN’s hypothesis for how vascular Abeta42 amyloid leaked from blood vessels in the brain, gets absorbed in excess amounts by healthy neurons until they are damaged, destroyed, and die; causing a host of further complications including inflammation, toxic neuronal debris fields, and plaque formation by damaged neurons. Must Diagnose Early and Treat Early.

       Pilot Program

Development of MD Brain and Longevity Clinics

Starts with you speaking with your Doctor about the ATN Profile Test: 484400 CPT:83520(x4) which tests for the following signs of  MCI and early-stage Alzheimer's:

  • Amyloid-tau-Neurodegeneration (ATN) Profile    

  • Beta Amyloid 42/40 Ratio, Plasma    

  • Neurofilament Light Chain ( NFfL), Plasma 

                                                                                                                                                         

  • Reduce or Stop the BBB Leaking

  • Block Aβ42 Amyloid from Entering Healthy Neurons

  • Reduce Inflammation caused by these activities 

Triple Combination Treatment

In healthy brains, neurons produce the right amount of Aβ42.

In the AD brain, Aβ42 from outside enters without regulation through breaches in the blood-brain vessels = "vascular Aβ42".

Neuron receptors bind and store this additional "vascular Aβ42" without control; engorging the neurons and causing them to burst and die; leaving behind insoluble Aβ42 plaques, tangles, and other neuronal matter, which can destroy additional surrounding neurons.

Plaques and tangles are the remains of bursting neurons, not the causes of dying neurons.

By Reducing or Stopping the BBB leaking, and blocking Excess Vascular Aβ42 from Entering and Over Accumulating in Neurons, while reducing the inflammation in the brain, we can prevent Neurons from dying and stop or prevent the progression of AD, Dementia, and MCI.

           

RECAP - PREVENTION IS THE OBJECTIVE

TEST EARLY - TREAT EARLY

 USING “REPURPOSED” EXISTING FDA APPROVED MEDICATIONS

Key ZN Discoveries and Breakthroughs on the Causes of Alzheimer’s

 

Unwelcomed amyloid enters the brain through a breach in the blood-brain vessels, which binds to neuronal receptors (proven in Study 2).

 

•Over time, neurons store toxic amounts of amyloid, which causes the neurons to die, disrupting learning, memories, and ultimately body functions (proven in Study 2).

 

•Zachriel Neurosciences has proven how to block amyloid from entering neurons (proven in Study 1).

The Triple Combination Treatment Therapy

For the prevention, inhibition, or delay of the onset of Alzheimer’s or other forms of Dementia, and Mild Cognitive Impairment, comprising of:

  • One or more receptor binding agents to reduce/prevent amyloid from over-accumulating in neurons;

  • One or more cardiovascular agents to minimizes BBB leakage;   

  • One or more anti-inflammatory agents to reduce neuroinflammation in the brain.

    

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