TPG Online Daily

Drug Treatment for Alzheimer’s

Ron Conte, Pharm.D.

Alzheimer’s Times Publishing Group Inc tpgonlinedaily.comThere are many types of dementia. Alzheimer’s is the most common type comprising sixty to eight percent of patients diagnosed with dementia. Currently there are 5 million people in the U.S. diagnosed with Alzheimer’s. Fifty percent of all people over the age of 85 will develop Alzheimer’s.

Dementia is defined as a group of symptoms associated with a decline in memory or other thinking skills that reduces a person’s ability to perform everyday activities. Symptoms of Alzheimer’s include a decrease in memory of recent events and difficulty to reason that may lead to unsafe situations, lack of proper decision-making, as well completing complex tasks. Furthermore, Alzheimer’s may include difficulty in recognizing people you know, mood swings, impaired speaking, reading, and/or writing.

Symptoms develop as a result of Alzheimer’s disease due partly to the formation of specific protein formation within the brain known as amyloid plaques. However, there seems to be other factors involved in the development of Alzheimer’s. There is one neurotransmitter that is depleted in patient’s with Alzheimer’s, namely acetylcholine. Without boring you with much detail, acetylcholine is metabolized (broken down) by an enzyme named acetylcholinesterase. Acetylcholine is necessary for acting as a signal for muscle movement, detecting the sensation of pain, learning and memory formation, the regulation of the endocrine system, and rapid eye movement (REM) sleep cycles.

The drug treatment of Alzheimer’s is geared currently to prevent the depletion of acetylcholine. This is accomplished by inhibiting acetylcholinesterase with use of the drugs known as acetylcholinesterase inhibitors. The main drugs in the group include donepezil (Aricept), galantamine (Razadyne), rivastigmine (Exelon), and tacrine (Cognex). Some common side effects of these agents include nausea, diarrhea, insomnia, headaches, vomiting, and fatigue.

Another drug is memantine (Namenda). It works a little differently by reducing glutamate levels in the brain. Toxic levels of glutamate are harmful to brain tissue. At times Namenda is added to an acetylcholinesterase inhibitor to treat more serious forms of Alzheimer’s disease. Common side effects of Namenda may include dizziness, confusion, headache, constipation, cough, and an increase in blood pressure.

As you know, there is no cure for Alzheimer’s disease. Additional drug therapy may be needed to decrease symptoms of the disease. These drugs include antidepressants, anti-anxiety meds, anti-parkinsonism agents, anti-seizure meds, and beta-blockers (to decrease blood pressure and heart rate, as well as produce a calming effect).

I am no expert in non-drug therapy for any disease, including Alzheimer’s. But I should mention there are two therapies with questionable effects: transcranial magnetic stimulation (TMS) and light flashes. However, these two types of therapies may be the starting point leading to the discovery of additional or more refined therapies.

Although amyloid plaques paint part of the picture for Alzheimer’s, there must be other factors involved.


There have been studies analyzing the brains of some elderly patients, showing amyloid plaques on autopsy but who never developed Alzheimer’s when they were alive. Why? What else must be contributing to the development of Alzheimer’s?

I am a believer of chemical balance within the human body. Take for example the pancreas which secretes two hormones: insulin and glucagon.

They work in balance with one another, based on the blood sugar level. An imbalance of these two hormones leads to pancreatic dysfunction, possibly diabetes.

I believe the same is true of Alzheimer’s disease. However, there are more than 30 neurotransmitters within the brain, ten that are more prominent than the others. What type of balance needs to be maintained? Do some neurotransmitters have a more profound effect on others?

We do know that an imbalance of some neurotransmitters leads to depression and forms of psychosis. Why not the same for dementia particularly Alzheimer’s disease?

At this point there are many more questions than there are answers.

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For more info: rrxconte@gmail.com

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