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Brewer G.J.,University of Michigan | Brewer G.J.,Arbor Pharmaceuticals
Journal of Trace Elements in Medicine and Biology | Year: 2012

In this review I present the hypothesis that a toxic substance, inorganic copper, ingested from drinking water and vitamin/mineral supplements containing inorganic copper, is at least partially causal of the epidemic of Alzheimer's disease (AD) we are seeing in developed countries. I set the stage for this hypothesis by pointing out that the epidemic is a new disease phenomenon coinciding temporally with the use of copper plumbing in developed countries. The evidence is good that AD was nonexistent or rare in the 1800s and early 1900s, and the arguments that elderly people did not exist in those times, or that AD was simply attributed to senility, are refuted. The web of evidence tying ingestion of inorganic copper as a causal factor in AD is strong, and includes AD animal model data where trace amounts of inorganic copper in the drinking water markedly worsened AD, human studies where ingestion of copper supplements, along with a high fat diet, is associated with a marked loss of cognition, human studies showing a markedly higher mortality in elderly women ingesting copper supplements, as well as other data. It is likely that a high fat diet works in conjunction with ingestion of inorganic copper to increase the risk of AD. It is clear that some factor toxic to the brain is present in the environment in developed countries, but not undeveloped countries, and is a major risk factor for AD. I believe that that toxic factor is ingestion of inorganic copper. © 2012 Elsevier GmbH. Source

Brewer G.J.,University of Michigan | Brewer G.J.,Arbor Pharmaceuticals
BioFactors | Year: 2012

In this special issue about biofactors causing cognitive impairment, we present evidence for and discuss two such biofactors. One is excess copper, causing neuronal toxicity. The other is zinc deficiency, causing neuronal damage. We present evidence that Alzheimer's disease (AD) has become an epidemic in developed, but not undeveloped, countries and that the epidemic is a new disease phenomenon, beginning in the early 1900s and exploding in the last 50 years. This leads to the conclusion that something in the developed environment is a major risk factor for AD. We hypothesize that the factor is inorganic copper, leached from the copper plumbing, the use of which coincides with the AD epidemic. We present a web of evidence supporting this hypothesis. Regarding zinc, we have shown that patients with AD are zinc deficient when compared with age-matched controls. Zinc has critical functions in the brain, and lack of zinc can cause neuronal death. A nonblinded study about 20 years ago showed considerable improvement in AD with zinc therapy, and a mouse AD model study also showed significant cognitive benefit from zinc supplementation. In a small blinded study we carried out, post hoc analysis revealed that 6 months of zinc therapy resulted in significant benefit relative to placebo controls in two cognitive measuring systems. These two factors may be linked in that zinc therapy significantly reduced free copper levels. Thus, zinc may act by lowering copper toxicity or by direct benefit on neuronal health, or both. © 2012 International Union of Biochemistry and Molecular Biology, Inc. Source

Brewer G.J.,University of Michigan | Brewer G.J.,Arbor Pharmaceuticals
Inorganica Chimica Acta | Year: 2012

It is clear that copper accumulation and toxicity is the cause of Wilson's disease. It is also well established that zinc therapy is effective in treating Wilson's disease by a mechanism of blocking intestinal copper absorption. An emerging hypothesis holds that ingestion of inorganic copper, such as from drinking water, plays a causal role in Alzheimer's disease. The evidence behind this theory is discussed. There is good preliminary evidence that zinc therapy slows cognition loss in Alzheimer's disease, either by repleting zinc in zinc deficient neurons, or by lowering the body's free copper levels. Finally, evidence is presented on a variety of animal models and one human disease (primary biliary cirrhosis) that by lowering copper levels using a drug called tetrathiomolybdate, inflammatory fibrotic, and immune-modulated disease processes are benefitted. © 2012 Elsevier B.V. All rights reserved. Source

Arbor Pharmaceuticals | Date: 2015-04-23


News Article | October 3, 2014
Site: www.fiercebiotech.com

Private drugmaker Arbor Pharmaceuticals is looking for a buyer, according to Reuters, going on the market with a price tag that could exceed $1 billion. The Atlanta-headquartered company has retained JPMorgan Chase to spread the word of its availability, Reuters' sources say, talking up the potential of its on-the-market cardiology and pediatric drugs plus its pipeline of proprietary products. The majority of Arbor's marketed products are generics, but the company has branched out into developing molecules of its own, including the neurology treatment AR02, a drug under FDA review on which the company expects a final decision by Oct. 23. Arbor is also at work on the late-stage cardio drug AR05, the Phase III hospital-care treatment AR10 and the Phase II pediatric psychiatry candidate AR08. Arbor's approach to specialty pharma involves spotlighting treatments that can be quickly brought to market, whether via internal development or in-licensing. Last year, the company struck a deal with Takeda that gave U.S. rights to two hypertension treatments, and Arbor paid undisclosed sum to Eisai the year before to market Gliadel Wafer, an in-hospital treatment used during brain cancer surgeries. The company's reported interest in a deal comes amid a surge of M&A in the biopharma world, as patent expiries and reimbursement woes have left large drugmakers hungry for buyouts, while soaring valuations have smaller outfits commanding record price tags. Related Articles: J&J makes a splash in hep C with a $1.75B deal for Alios Troubled AMAG snaps up fresh-from-bankruptcy Lumara in $1.25B deal Daiichi Sankyo bags leukemia drug in $410M Ambit buyout

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