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John Marrone was in a car accident in 1989 on an icy road in which he suffered a spinal cord injury that left him paralyzed from the neck down. He went through therapy and, according to wife Penny, “a miracle happened because he had a great recovery and was able to walk with a cane when we got married in 1991.”

Things took a turn for the worse in 2014, though, when John was diagnosed with superficial siderosis, a rare condition in which blood enters the brain and spinal cord from a weak blood vessel, a tumor, or because of a previous head or spine injury. The breakdown of the blood leads to a buildup of iron in the brain. The toxic mix interferes with brain function.

The Marrones found E.Q. Sylvester of Hinsdale when Penny was searching online for how John could possibly golf in retirement.

The couple and son Joe drove from their home in Niagara, Ontario, to take part in the June 9 annual outing for the Freedom Golf Association, an organization Sylvester founded that helps people with disabilities golf.

John, who played many sports before the accident, is able to chip and putt from a single-rider golf cart, but he doesn’t have the shoulder strength to take a full swing.



What makes these articles about Alzheimer research interesting? They describe how researchers will soon be starting a study in removing brain iron using Deferiprone (Ferriprox) from Alzheimer’s patients using an ApoPharma provided special formulation of the drug.

The question we should be asking? Has ApoPharma manufactured a version of Ferriorox that is intended to target hemosiderin after crossing the blood-brain barrier? If so is this formulation experimental? Is it only being offered for studies in Australia or can Superficial Siderosis patients already prescribed Ferriprox be also allowed to test its efficacy?

Patients with more iron in their brains deteriorate first and fastest, and those with low iron seem to have slower or delayed progression of the disease, Ayton and colleagues showed in a seven-year study published in Nature Communications in 2015.

They hypothesized that a drug called a chelator that binds to iron, enabling it to be lured from tissues, could lower levels in the brain, possibly delaying the onset of Alzheimer’s by up to three years in people experiencing mild cognitive impairment, the early stages of the disease. Deferiprone, an oral iron chelator, is sold by Canada’s ApoPharma Inc. under the brand name Ferriprox for patients with thalassemia, an inherited blood disorder.


The researchers now plan to test anti-iron drug Deferiprone on a cohort of Alzheimer’s patients. Deferiprone is known to reach the brain and there is early clinical evidence that it is effective in slowing Parkinson’s, a neurological disease that leads to movement disorders and is also associated with brain iron.

“These results for Deferiprone in Parkinson’s are what have really encouraged us to test the same drug on Alzheimer’s,” says Dr Ayton.

Provided are compounds of Formula I which are derivatives of 3-Hydroxypyridin-4-ones. The compounds may be used in treatment of a medical condition related to a toxic concentration of iron. The medical condition related to a toxic concentration of iron may be selected from the group consisting of: cancer, pulmonary disease, progressive kidney disease and Friedreich’s ataxia.

The occurrence of in vivo iron toxicity in the human body can be categorized into iron overload and non-iron overload conditions. Iron overload conditions are common in thalassemia patients through chronic blood transfusions and in hereditary hemochromatosis patients. Non-iron overloaded conditions include anthracycline mediated cardiotoxicity, viral infections, neurodegenerative diseases, photo induced damage, and proliferative conditions.

”… At present, there are several iron chelator drugs that have reached the market. Examples of those include deferiprone (Ferriprox™), ICL670 (ExJade™), dexrazoxane hydrochloride (Zinecard™) and desferrioxamine mesylate (Desferal™). However, only two of these compounds, namely deferiprone and ICL670, are orally active for the removal of iron in iron-overloaded diseases…”

In designing 3-hydroxypyridin-4-one that will lead to improved brain exposure, one approach is to increase the lipophilicity of the chelator via the introduction of a trifluoroethyl group at the C2 or C5 or C6 position of the 3-hydroxypyridin-4-one (US20080242706). This invention is based in part on compounds with a trifluoroethyl group at the N1 position, or a 2-difluoroethyl group at the C2 position of the 3-hydroxypyridin-4-one skeleton. The use of low molecular weight substituents is also considered in the design of new bidentate 3-hydroxypyridin-4-one ligands (L). A MLn complex is formed upon complexation with a metal (M), for example FeL3.

Amines are known to have favorable interaction with predominately negatively charged phospholipids head groups at the BBB (blood brain barrier)….


  • A Leak in His Brain, Troubling Symptoms, and Finally an Elusive Fix

grinstead mayo clinic

Steve Grinstead was eager to resolve a medical condition causing troubling symptoms. Physicians around the country turned him down for surgery. His team at Mayo Clinic found a solution that put him on the road to recovery.

By SharingMayoClinic
May 25th, 2017

Steve Grinstead knows how to handle dangerous situations. For more than 20 years, the Winnabow, North Carolina, resident has led crime prevention seminars through a nonprofit organization he founded. So when he was facing a different type of threat — a health scare that left him with a constellation of troubling symptoms — it’s no surprise that he confronted it head on.

“First, I lost my sense of smell. Then, my sense of taste,” Steve says of the symptoms that surfaced in 2012.

His hearing and balance were the next to be affected. The symptoms got progressively worse and would eventually lead him to a local neurologist, then to a specialist at a nearby university health system, where he was diagnosed with superficial siderosis. The rare, complex condition is caused by iron deposits in the brain and spinal cord. In Steve’s case, doctors suspected the iron deposits were a result of a cerebrospinal fluid leak.

“I had a hole in my dura,” he explains, referring to one of the membranes surrounding the brain and spinal cord. “Spinal fluid was leaking out and blood was leaking in.”