New Alzheimer’s Study Aims to Delay or Prevent Symptoms

Summary: A new study will test a promising drug aimed at preventing or delaying Alzheimer’s symptoms.

Source: USC.

The international trial co-managed by USC will test a drug in people who show no symptoms of the disease.

USC researchers announced Tuesday they will test a promising drug aimed at preventing or delaying the symptoms of Alzheimer’s disease.

The international study, jointly managed by the USC Alzheimer’s Therapeutic Research Institute (ATRI) and Janssen Research & Development, will test Janssen’s BACE inhibitors in people who are currently showing no symptoms.

The investigational drug aims to block an enzyme involved in the generation of the amyloid peptide, a toxic molecule believed to play an essential role in causing Alzheimer’s.

“We are now looking at the stage of Alzheimer’s that precedes even mild symptoms,” said Paul Aisen, founding director of USC ATRI and professor of neurology at the Keck School of Medicine of USC. “It is our view that drugs such as BACE inhibitors may be most effective at the earliest stages of the disease.”

USC ATRI’s role in the study is funded by a new contract with Janssen. USC ATRI, located in San Diego, and Janssen will provide joint oversight for the study; in addition, ATRI will manage study activities at sites in the United States and Canada. Study sites in other countries will be managed by Quintiles.

“There is a lot of optimism that research may be ushering in a new era in Alzheimer’s drug development,” said Gary Romano, head of Alzheimer’s clinical development at Janssen. “We may be able to treat the disease using interventions before it becomes advanced, much like you treat high cholesterol to mitigate the risk of heart attacks.”

Trial details

This is a phase 2/3 randomized, double-blind, placebo-controlled, parallel group, multicenter study in people across North America, Europe, Japan and Australia who have evidence of brain amyloid accumulation but are asymptomatic.

Image shows amyloid deposits in the hippocampus.
In a person with Alzheimer’s, harmful amyloid beta clusters (red) build up among neurons (green) in a memory-related area of the brain. image is credited to Strittmatter Laboratory, Yale University.

The trial will recruit individuals who show no outward symptoms and are 60 or older. They will then be tested for amyloid accumulation in the brain and, if positive, will be invited to participate in the study. The study will assess cognitive performance, along with other measures related to Alzheimer’s, over time.

The study will employ a framework created by USC ATRI investigators for testing drugs at the earliest stages of the disease when treatment would be most effective by attacking the driving molecules before substantial damage to the brain has occurred.

It will enroll more than 1,600 people worldwide, including 660 participants at 75 sites in North America who have not experienced any clinical signs of Alzheimer’s. Aisen and Reisa Sperling, director of the Center for Alzheimer’s Research and Treatment at Harvard Medical School, will be the co-principal investigators of the research.

About this Alzheimer’s disease research article

Funding: The Janssen BACE inhibitor is licensed from Shionogi & Co. in Japan. More details about the study can be found at the National Institutes of Health’s Clinical Trials website.

Source: Eddie North-Hager – USC
Image Source: This image is credited to Strittmatter Laboratory, Yale University.

Cite This Article

[cbtabs][cbtab title=”MLA”]USC. “New Alzheimer’s Study Aims to Delay or Prevent Symptoms.” NeuroscienceNews. NeuroscienceNews, 17 June 2016.
<>.[/cbtab][cbtab title=”APA”]USC. (2016, June 17). New Alzheimer’s Study Aims to Delay or Prevent Symptoms. NeuroscienceNews. Retrieved June 17, 2016 from[/cbtab][cbtab title=”Chicago”]USC. “New Alzheimer’s Study Aims to Delay or Prevent Symptoms.” (accessed June 17, 2016).[/cbtab][/cbtabs]

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  1. As we can see in the references below, supported by research, the neurons glucose deprivation (neuroglycopenia) or  the brain energy deprivation (that by it self can leads to neurons apoptosis) are the brain disorders that starts , UPSTREAMS dozens years before to any betamyloid accumulation , and years later, perpetuates such accumulations of misfolded proteins. The brain energy disorders are related to peroxinitrites acccumulation , mitochondrial dysfunction, glication, heavy metal accumulation ,etc.,are some of the main disorders in most neurodegenerative diseases (as AD,PD,etc.)
    And between others neurons and astrocytes disorders, the BRAIN ENERGY DEPRIVATION , that is present too in the LASTS STEPS of AD , increases BACE levels , that can be one of the dozens triggers of betamyloid accumulation in AD.Professor Robert Vassar and colleagues reported that glucose deprivation (actually , brain energy deprivation) ,increases BACE1 levels and Aβ production in the brains of the Tg2576 transgenic APP mouse model of AD. 
    They identified the molecular mechanism of the BACE1 increase, showing that GLUCOSE (or ENERGY ) DEPRIVATION , induces phosphorylation of the translation initiation factor eIf2α, which in turn increases the translation of BACE1.Based on that logic ,IMPROVING BRAIN ENERGY can indirectly lower or control the overexpression of BACE1, Increasing brain energy with, for example, an association of drugs and supplements that control peroxinitrites accumulation, improves mitochondrial function,lowers glycation and works as an alternative fuel and enhances the glucose metabolization by the neurons, based on rational thinking , it can lower the excessive eIF2α phosphorylation that, in consequence, will lower the BACE1 levels in a more “physiological” and less toxic ,cheap and more safe way (without to need none BACE1 inhibitors).And improving brain energy , it improves the neurons functions , and helps to protects against neurons apoptosis caused by energy deprivation.Increasing brain energy with such supplements (that maybe can works as “precursor” substances to the development of drugs with a higher efficacy and effectiveness), we have the advantage to treat or prevent not only the BACE1 disorders (without to use None expensive BACE1 Inhibitors, that did Not Work in others trials), and we can also treat the others neuronal and astrocytes disorders, that are consequences of brains under energy deprivation. Then, there are some (still unexplored) ways of enhancing brain energy, such as giving alternative fuels and/or controlling factors that impair glucose metabolism in the brain. These could be substances that regulate the macrovascular and microvascular system; drugs and supplements that lower oxidative stress, peroxynitrite accumulation, and glycation and that are mild heavy metal chelators; or substances that enhance mitochondrial function.Supplements such as L-glucuronolactone, Acetyl-L-Carnitine (so called ALCAR), microdoses of Alpha Lipoic Acid, L-carnosine, glucosamine sulfate, and medium-chain triglycerides, might be worth investigating, and can be the “precursors” to the development of drugs with a higher efficacy to treat brain energy disorders in most neurodegenerative diseases.
    Note : It is important to stress that no matter how much sugar or glucose the patient eats or takes , it will NOT increase the brain energy, once the problem it is not the sugar or glucose levels, but the disorders in glucose metabolization, as mitochondrial dysfunction,etc., that leads to brain energy deprivation, no matter how much sugar, glucose or carbs the patient takes.
    As a metaphor, is like a car that the “fuel tank” (the body) is plenty of “gasoline” (glucose), but the “fuel pump” (the mitochondria) its “broken”, and can NOT pull the “gas” (the glucose) to the right places fo the “engine” works well.Then, to takes lots of glucose, sugar or carbs, that means, to try to put more “fuel”(glucose) in a “tank” (the body and the brain) that are absolutely plenty of “fuel” (glucose) , will NOT works, once the “fuel pump” (mitochondria, etc.) is “broken” , and more glucose, etc. , will Not works , and can be harmful.
    Velliquette RA, O’Connor T, Vassar R. Energy inhibition elevates beta-secretase levels and activity and is potentially amyloidogenic in APP transgenic mice: possible early events in Alzheimer’s disease pathogenesis. J Neurosci. 2005 Nov 23;25(47):10874-83. PubMed.
    O’Connor T, Sadleir KR, Maus E, Velliquette RA, Zhao J, Cole SL, Eimer WA, Hitt B, Bembinster LA, Lammich S, Lichtenthaler SF, Hébert SS, De Strooper B, Haass C, Bennett DA, Vassar R. Phosphorylation of the translation initiation factor eIF2alpha increases BACE1 levels and promotes amyloidogenesis. Neuron. 2008 Dec 26;60(6): 988-1009. PubMed.
    Vassar R. BACE1, the Alzheimer’s beta-secretase enzyme, in health and disease. Mol Neurodegener. 2012 Feb 7;7 Suppl 1:L3. PubMed.

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