Changes in enzyme activity on Ach and Bch are involved in different diseases, one of the most important, Alzheimer’s disease

Alzheimer’s is, unfortunately, one of the most common diseases of modern society. It affects about 3% of the population 65-74 years and 50% from 85. A sad news is that it is expected that the number of patients will double in the next 20 years, inevitably affecting much of the population.


Alzheimer’s is considered a kind of “complex disease” since it is not clear the decisive factors for its occurrence. Contrary to popular belief, most cases occur sporadically, further hampering their investigation and cure, except those suffering from genetic disease expressing an early age. Among its more obvious effects include: the progressive loss of memory and recognition of objects and people, the deterioration of cognitive functions (comprehension, speaking, relationship with others) and loss of orientation in space and time.

Acetylcholine is a neurotransmitter with implications for Alzheimer’s

In 1920 it was proposed the theory of Neurotransmission chemistry, and with it the principles needed to distinguish what could be a neurotransmitter and what not. Thus, acetylcholine became the first neurotransmitter to meet all the requirements to become a chemical transmitter. At that time, its discoverers could not imagine not even the enormous importance of Ach and the impressive role that develop in many body processes. And so, when the discovery took place related alterations in the activity of the enzyme and the development of Alzheimer’s.

Acetylcholine is synthesized from acetyl from the metabolism, and choline (considered a member of Vitamin B, largely from the diet). It consists of the most important neurotransmitter in the central and autonomic nervous system and muscle contraction. Once your mission, the enzyme is hydrolyzed in the synaptic cleft by acetylcholinesterase.

Neurofibrillary tangles, senile plaques and the cholinergic hypothesis

The latest research on Alzheimer’s focus on discovering the relationship between the development of the disease and the appearance of neurofibrillary tangles and senile plaques. Neurofibrillary tangles are protein deposits that form inside neurons, similar to senile plaques.

Both are rich in activity acetylcholinesterase and (another enzyme hydrolyzing choline esters). It is unclear whether these formations are the cause of the disease, or conversely, are due to a defense that creates the body against Alzheimer’s. In recent years, the cholinergic hypothesis has had wide acceptance in the scientific world, and has served to explain the causes of loss of function in disease. According to this theory, the cause of dementia is the strong decrease in the content of acetylcholine in the brain regions involved in learning and memory formation.

The increase in acetylcholinesterase activity may explain symptoms of the disease

Thus, it is believed that the brain areas that under normal conditions have a high concentration of acetylcholine, a neurotransmitter functions key to understanding, understanding of new concepts, Alzheimer’s, this concentration is greatly diminished due to increased activity of acetylcholinesterase (hydrolyzed was responsible).

In this way, much of the medication aimed at combating the disease acts as an acetylcholinesterase inhibitor, medications such as the Cognex (Whose active ingredient is tacrine), rivastigmine, etc. However, the problem of these compounds is their high toxicity to certain body organs like the liver. Therefore, much research is focused on finding new inhibitors of this enzyme, with less toxicity and will prevent the disease without reducing both the quality of life of patients.