The disease that bears the name of Aloysius Alzheimer was first described in Munich, 1906. Prior to this discovery by Dr. Alzheimer, the loss of memory, forgetfulness and the decline in mental acuity and competence was ascribed to old age. Since that time the clinical symptoms and the changes that occur in the brain are known as a neurological disease and not the inevitable decline of the aging process.
The changes that occur in the brain are well documented, with a variety of different types of dementia now understood to be part of a spectrum of disease. In the last 105 years, the biological mechanisms that kill the neurons of the brain have become defined, but the ultimate cause remains elusive. Recently, the role of the amyloid plaques and neurofibrillary tangles that are a hallmark of Alzheimer’s disease (AD) has been redefined. Previous work assumed that plaques and tangles were the cause of AD, but it appears that these proteins are an attempt by the brain to stop the actual damage.
Currently, there are 5.4 million Americans living with Alzheimer’s disease, with an estimated 13 million Americans providing some sort of assistance or care without compensation. It is estimated that Americans spend $200 billion annually to manage this illness, but even with this much time and money spent on managing this condition, it is the 6th leading cause of death in the U.S. No therapies have been developed that stop AD, merely slow it down.
Clues to Treating Alzheimer’s Disease
In AD, inflammation is a hallmark of the disease. For three decades, non-steroidal anti-inflammatory drugs (NSAIDS; aspirin, acetaminophen, ibuprofen) have been known to reduce the severity of AD. Inflammation does play an important role in the damaged caused by this disease, but the outcomes of inflammation may play an important role in diminishing blood flow to the brain and limits the repair attempts by the body.
Since the early 1990’s the idea of insufficient blood flow in the brain was a major impetus for developing therapies that could stimulate new blood vessel growth in the brain of AD sufferers. This new blood vessel growth, called angiogenesis, appear to be critical components for fighting the ravages of AD and restoration of blood flow helps reduce and reverse cognitive decline associated with AD. Restoring blood flow appears to help clear out accumulating toxic proteins, diminish the signs of inflammation and restore function to areas of the brain.
A tissue known for stimulation new blood vessel growth is the omentum, a lining of the intestine that is routinely used with compromise surgical sections. Reports of omentum transplantation into the brains of AD patients, demonstrated a reversal of symptoms associated with AD and reduction in plaques and tangles where the omentum was transplanted onto the brain. The major limitation with this surgical procedure is the severity (opening the skull) and the lack of long-term effectiveness. But this procedure sheds some important light on potential treatments for AD that BH²F would like to investigate.