Medical Treatments

This section will start by describing the medical treatments for dementia, including the Aricept-type drugs (cholinesterase inhibitors) and Namenda. It will also address the non-medical interventions. Will We Ever Cure Alzheimer’s is an good NYT article (11/19) to consult for a current summary of the state of the art in DAT research.

These cholinesterase inhibitors block an enzyme from breaking down acetylcholine which is a neurotransmitter used by neurons to trigger other neurons. Once a neuron releases acetylcholine, it travels across the synapse (gap) seeking to lock into a downstream neuron's receptors. When enough molecules lock in, the neuron's threshold is reached and it fires releasing more acetylcholine, firing tens of thousands more neurons. But, if some of those neurons are dead as the result of dementia, they won't fire before the acetylcholine is broken down by cholinesterase. If this enzyme is blocked or inhibited, that would allow the acetylcholine to exist for a few micro seconds longer which might be enough time to seek a live neuron.

The Aricept-type drugs (including Razadyne and Excelon) are pro-acetylcholine enhancers that work by inhibiting the enzyme (cholinesterase) that breaks them down. Thus, they are called cholinesterase inhibitors. It allows "more gas" to the engine-of-the-brain to run better, but they do little or nothing to slow the underlying disease process killing tens of thousands of neurons due to progressive dementia. Thus, they are not neuroprotective but rather help people have better quality of life in less restrictive environments for longer. In other words, they retain their ability to do Activities of Daily Living (ADL’s) for longer.

Neuroprotective treatments are aimed at slowing down the actual disease process causing dementia. Blood thinners like aspirin, antihypertensive drugs can help protect the brain from microangiopathy (microvascular disease of the tiny blood vessels) of the brain. There is an FDA approved medication called Namenda which was originally used in Germany where it was found useful in treating advanced AD cases with behavioral disturbance, which is what the FDA approved it for in the US; however, our scientists have not seen much benefit from it in agitated dementia patients. Instead, neuroscientists are interested in the anti-glutamate effect the drug has. Namenda blocks a neurotransmitter called glutamate which is used to pre-stimulate nerves so they fire at a lower threshold. Dementia, stroke and MS patients are found to have high amounts of glutamate in their brains on post-mortem leading us to believe that too much glutamate may overstimulate brain cells causing them to die and cause inflammation in the brain contributing to dementia. Thus, Namenda is used "off label" as an anti-inflammatory agent in hope that this may be neuroprotective.

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