It is slowly dawning on politicians and health care providers that Alzheimer’s dementia is about to overwhelm the health sector, not only with the sheer number of affected patients, but also through the cost, and societal impact associated with the predicted further increase in prevalence of the disease. It’s estimated that currently about 25% of those over 85 years have Alzheimer’s dementia, and 5% of those over 65.
When we say dementia, we mean a global impairment of cognition with normal levels of consciousness. An early sign is often impairment in memory function, but we also see mood swings, disruption of sleeping patterns, intellectual decline, and in some dementias, personality change. The disease progresses mercilessly, and leads to death within 8-10 years through pneumonia or inanition. The histological changes in the Alzheimer brain are illustrated here :
We don’t know much at all about the why, but we do know some of the how of Alzheimer’s, some of the biochemical pathways and immune mechanisms that lead to deposition of plaques of Amyloid between nerve cells in the brain, which disrupt synaptic function and cause secondary inflammatory reactions, that lead to neuron loss and neurotransmitter disturbances.
We know for example that the deposition of b-Amyloid is caused by mutations in substances called presinilins 1 and 2, and in the amyloid precursor protein gene.
Which brings me to this study from researchers at the University of Buffalo. 2 things are interesting to me about this admittedly very small study. They found, apparently for the first time, that the immune cells that circulate in our blood, can produce these precursor proteins (the presenilins and APP). And they also found that a low dose of Insulin, a naturally occurring hormone in humans, that is central to glucose metabolism and for some inflammatory reactions, was able to suppress the release of 4 of these Alzheimer precursors in patients with Type-2 Diabetes.
Now, that is pretty cool research, and good to know as a base for further and bigger studies (for one, you would have to show that this effect is also there in non-diabetics, who have naturally circulating Insulin in their blood, and target cells that can make use of it). But it doesn’t mean that we will prevent Alzheimer’s dementia from tomorrow on, by shooting up Insulin. What has to happen is, that much more money is made available for Alzheimer research in the coming years, and that politicians start making plans for the millions of Alzheimer sufferers (and their carers) that will hit us in the next 2 or 3 decades.
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