A CURE FOR ALZHEIMER’S

What is Alzheimer's disease?

Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Alzheimer’s disease is the most common cause of dementia among older adults.

In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems and unpredictable behavior. After she died, he examined her brain and found many abnormal clumps (now called amyloid plaques) and tangled bundles of fibers (now called neurofibrillary, or tau tangles).

What happens to the brain in Alzheimer's disease?

Scientists continue to unravel the complex brain changes involved in the onset and progression of Alzheimer’s disease. It seems likely that damage to the brain starts a decade or more before memory and other cognitive problems become evident. During this preclinical stage of Alzheimer’s disease, people seem to be symptom-free, but toxic changes are taking place in the brain.

The damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As more neurons die, additional parts of the brain are affected. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly.

Alzheimer’s is currently ranked as the sixth leading cause of death in the United States, but recent estimates indicate that the disorder may rank third, just behind heart disease and cancer, as a cause of death for older people.

What is dementia?

Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living.

Scientists know that Alzheimer’s progresses on a spectrum with three stages—an early, preclinical stage with no symptoms; a middle stage of mild cognitive impairment (MCI); and a final stage of Alzheimer’s dementia. At this time, doctors cannot predict with any certainty which people with MCI will or will not develop Alzheimer’s.

The onset of Alzheimer’s disease is thought by many to be related to the deposition of high concentrations of amyloid beta protein within the brain. If true, and there’s considerable evidence that it probably is, preventing the accumulation of amyloid beta may slow down or reverse the onset of Alzheimer’s.

In a brilliant move, researchers at the École Polytechnique Fédérale de Lausanne in Switzerland created an implantable device that contains live cells that produce anti amyloid beta antibodies.

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Amazingly, this was already tested in laboratory mice with Alzheimer’s. In two models of the disease, the implants significantly reduced the accumulation of amyloid beta in the mice brains compared to controls.Indeed, the constant flow of antibodies produced by the capsule over a course of 39 weeks prevented the formation of Abeta plaques in the brain. The treatment also reduced the phosphorylation of the protein tau, another sign of Alzheimer’s observed in these mice.

A bioactive capsule containing cells that have been genetically engineered to produce antibodies against Abeta proteins. The capsule is implanted in the tissue under the skin, and over time the cells produce and release a steady flow of antibodies into the bloodstream, from where they cross over into the brain to target the Abeta plaques.

The capsule is based on a design which is referred to as a “macroencapsulation device” and it is made of two permeable membranes sealed together with a polypropylene frame. The completed device is 27-mm long, 12-mm wide and 1.2-mm thick, and contains a hydrogel that facilitates cell growth. All the materials used are biocompatible, and the lab specifically used a method that is easily reproducible for large-scale manufacturing.

The cells inside the capsule are important. Not only must they be able to produce antibodies, but they also have to be compatible with the patient, so as to not trigger the immune system against them, like a transplant can. This is where the capsule’s membranes come into play, shielding the cells from being identified and attacked by the immune system. This protection also means that cells from a single donor can be used on multiple patients.

The proof-of-concept work is a landmark. It demonstrates clearly that encapsulated cell implants can be used successfully and safely to deliver antibodies to treat Alzheimer’s disease and other neurodegenerative disorders that feature defective proteins.

Elena-Andrada Szebeni Diana Runcan