The Science

Alzheimer’s disease is one of the most significant global health threats we face today, It is an ailment that, as our population ages, is forecasted to become a worldwide epidemic. However, we now understand that Alzheimer’s disease is not a genetic destiny. With the ReCODE and the Bredesen Protocol, a partnership between Apollo Health and vanguard Alzheimer’s researcher Dr. Dale Bredesen, program participants exhibiting early signs of cognitive decline are finally able to take their brain health back into their own hands. A real reversal of this debilitating condition is possible.

ReCODE, and The Bredesen Protocol are based on research that uncovered the biochemical mechanism behind the erosion of memory associated with Alzheimer’s disease. ReCODE and The Bredesen Protocol have opened the door to new approaches to treating Alzheimer’s disease.

This approach challenges the idea that memory loss, cognitive decline, and Alzheimer’s disease are foregone conclusions. Science tells us that these mental health ailments are not just treatable, but preventable.

ReCODE and the Bredesen Protocol

ReCODE and the Bredesen Protocol provide a comprehensive, personalized program designed to improve cognition and reverse the cognitive decline of subjective cognitive impairment (SCI), Mild Cognitive Impairment (MCI), and early Alzheimer’s disease. Continued research and testing by Dr. Bredesen began by evolving Metabolic Enhancement for Neurodegeneration (MEND) into the ReCODE program—and his continued research and testing has identified new and previously unrecognized causes of Alzheimer’s disease.

ReCODE is the optimal starting point and road map for you and your trained practitioner to reverse your symptoms by referencing your unique genetic information and Dr. Bredesen’s cutting-edge research, along with hormonal support and individualized nutritional advice.


million out of 318 million currently living Americans will develop Alzheimer’s disease.

The Bredesen Protocol

Ready to take control of your brain’s destiny? Dr. Bredesen’s research has fundamentally altered everything we knew about Alzheimer’s disease. Take a look at the science underlying the groundbreaking Bredesen Protocol and ReCODE.

Reversal of Cognitive Decline

Dr. Bredesen presents a plan for nutritional intervention and reducing environmental risk factors can be implemented as part of an individualized plan for treating depression and reversing the effects of Alzheimer’s disease.

Reversing Alzheimer’s

In this wide-ranging discussion with Dr. Mark Hyman, Dr. Bredesen discusses his “radical approach to rethinking Alzheimer’s.”

The Science of ReCODE 

Dr. Dale Bredesen

Reversal of Cognitive Decline: 100 Patients

The first examples of reversal of cognitive decline in Alzheimer’s disease and pre-Alzheimer’s conditions published by Dr. Dale Bredesen in 2018 were Mild Cognitive Impairment (MCI), and Subjective Cognitive Impairment (SCI). These two research studies describe patients showing sustained subjective and objective improvement in cognition, using a comprehensive, precision medicine approach that involves determining the potential contributors to the cognitive decline (e.g., activation of the innate immune system by pathogens or intestinal permeability, reduction in trophic or hormonal support, specific toxin exposure, or other contributors).

The studies leveraged a computer-based algorithm to determine a participant’s subtype and then addressed each contributor using a personalized, targeted, multi-factorial approach dubbed ReCODE for the reversal of cognitive decline. 

The ReCODE Report, along with Dr. Bredesen’s research, provides further support for a randomized, controlled clinical trial of the Bredesen Protocol and the overall approach to reversing cognitive decline. 

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Reversal of cognitive decline in Alzheimer’s disease

Alzheimer’s disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer’s disease or its precursors, MCI, and SCI, were published. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Participants who had been forced to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co‐workers all reported clear improvements. 

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Transcriptional Effects of ApoE4: Relevance to Alzheimer’s Disease

The major genetic risk factor for sporadic Alzheimer’s disease (AD) is the lipid binding and transporting carrier protein apolipoprotein E, epsilon 4 allele (ApoE4). One of the complex mysteries of AD is how the presence of ApoE4 elicits this age-associated (thought to be incurable) neurodegenerative disease. Recently, we showed that ApoE4 acts as a transcription factor and binds to the promoters of genes involved in a range of processes linked to aging and AD disease pathogenesis. 

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Downregulation of protein phosphatase 2A by apolipoprotein E: Implications for Alzheimer’s disease.

The apolipoprotein E ε4 allele is the single most important genetic risk factor associated with Alzheimer’s disease (AD). Tau phosphorylation and hyperphosphorylation is an underlying feature of AD and is regulated by specific kinases and phosphatases. Among phosphatases, protein phosphatase 2A (PP2A) is the principal tau-dephosphorylating enzyme in the brain. Several abnormalities of PP2A have been reported in AD, including among others decreased protein levels of PP2A, decreased mRNA and protein levels of the catalytic subunit PP2AC and variable regulatory B subunits and reduced methylation of the catalytic subunit, all of which results in disruption of the PP2A phosphatase activity. 

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Dr. Cyrus Raji

Uncovering the Long-term Neurological Ramifications of COVID-19

The COVID-19 virus targets the brain in ways that are just now starting to be understood. Patients with COVID-19 can present with a wide range of neurological manifestations that can be due to the injury to central and peripheral nervous system via a cytokine storm, blood clots, direct damage by SARS-CoV-2, and/or molecular mimicry. Apollo Health’s Chief Neuroimaging Science Advisor, Dr. Cyrus Raji, has written a review of what is currently known about this virus and the related clinical neurology which represents the foundation of what will eventually become a separate active field of research.

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Neurobiology of COVID-19 Abstract

Anosmia, stroke, paralysis, cranial nerve deficits, encephalopathy, delirium, meningitis, and seizures are some of the neurological complications in patients with coronavirus disease-19 (COVID-19) which is caused by acute respiratory syndrome coronavirus 2 (SARS-CoV-2). There remains a challenge to determine the extent to which neurological abnormalities in COVID-19 are caused by SARS-CoV-2 itself, the exaggerated cytokine response it triggers, and/or the resulting hypercoagulapathy and formation of blood clots in blood vessels throughout the body and the brain. In this article, we review the reports that address neurological manifestations in patients with COVID-19, who may present with acute neurological symptoms (e.g., stroke), even without typical respiratory symptoms such as fever, cough, or shortness of breath. Next, we discuss the different neurobiological processes and mechanisms that may underlie the link between SARS-CoV-2 and COVID-19 in the brain, cranial nerves, peripheral nerves, and muscles. Finally, we propose a basic “NeuroCovid” classification scheme that integrates these concepts and highlights some of the short-term challenges for the practice of neurology today and the long-term sequalae of COVID-19 such as depression, OCD, insomnia, cognitive decline, accelerated aging, Parkinson’s disease, or Alzheimer’s disease in the future. In doing so, we intend to provide a basis from which to build on future hypotheses and investigations regarding SARS-CoV-2 and the nervous system.

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Overview of MR Imaging Volumetric Quantification in Neurocognitive Disorders.

This review article provides a general overview of the various methodologies for quantifying brain structure on magnetic resonance images of the human brain. This overview is followed by examples of applications for AD and mild cognitive impairment. Other examples will include traumatic brain injury and other neurodegenerative dementias.

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MRI Volumetric Quantification in Persons with a History of Traumatic Brain Injury and Cognitive Impairment.

While traumatic brain injury (TBI) is recognized as a risk factor for dementia, there is a lack of clinical tools to identify brain changes that may confer such vulnerability. Brain MRI volumetric quantification can sensitively identify brain atrophy. The objective of this study is to characterize regional brain volume loss in persons with TBI presenting with cognitive impairment.

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