TBI AND ALZHEIMER'S DISEASE [ back to What's New ]
Some, but not all, cases of Alzheimer's disease (AD) are familial and have a clear genetic component, which gets activated or switched on by an environmental trigger. Recent medical research has shown that traumatic brain injury is a trigger in persons having one specific form of one specific gene known as APOE-e4. In such persons sustaining a TBI will increase their risk of developing AD by 7.7 to 10 times according to various studies. The good news is that this greatly heightened risk has not been found with any of the many other forms of the same gene. It has been suggested that persons with chronic TBI who are refractory to treatment, and manifest little or no spontaneous healing following their brain injury, should be tested for the presence of APOE-e4. Such advice is controversial, at least in part because there is no cure for AD. Being tested is an individual decision.

There are other interesting connections between TBI and AD. Shortage of acetylcholine in the brain is a factor in the poor and progressively worsening memories of patients with AD.  Companies that manufacture and market neuropharmaceuticals, have distributed drugs to increase AcH in the brain by, among other ways, blocking the enzyme acetylcholinesterase which breaks down AcH. Such drugs help some patients to some extent. No magic cure has been found to stop the decline of memory dead in it tracks and reverse it, i.e. restore normal memory function. There has been some "off label" experimentation with these drugs in patients with TBI with some positive indications. Very recently it was discovered that rats have a tremendous number of insulin receptors in their brain, especially in the hippocampus, the part of the brain responsible for encoding short term memory for long term storage elsewhere in the cortex. It was also found that drugs which block insulin signaling in the rat brain impair short term memory function, and that drugs which enhance insulin transmission improve short term memory. Studies are now under way to try insulin enhancing drugs on patients with AD in hopes of boosting their short term memory. One reason for trying this   approach, aside from the rat studies, is that patients with AD have abnormal insulin levels in their spinal fluid, suggesting their brains do not process insulin normally. Everyone who has been forced to keep working until 2 or 3 pm in the afternoon with no lunch can attest to feeling their cognitive speed and efficiency fall off due to hypoglycemia. Studies of college students with slight abnormalities in insulin functioning show these students perform less well on memory tests than their peers. Does TBI cause abnormalities in insulin production or utilization, and can insulin enhancing drugs boost short term memory function in patients with TBI? This is not known, but would seem to be a fruitful area for future biomedical research.