Acetylcholine receptor
The neurotransmitter acetylcholine unfolds its effect via various receptors, which are built into the membrane of corresponding cells. Since some of them are also stimulated by nicotine, they are called nicotinic acetylcholine receptors. Another class of acetylcholine receptors is stimulated by the poison of the fly agaric (muscarin).
Muscarinic acetylcholine receptors (mAChR) belong to the group of G-protein coupled receptors and can be divided into different subtypes (isoforms) which are numbered M1 to M5. The M1 isoform can be found in the brain, for example in the corpus striatum. It is called the neural type.
The M2 isoform is found at the heart. The M3 mAChR is located on the smooth muscles of blood vessels and glands, such as the salivary glands and pancreas. It is also responsible for the acid production of the cells in the stomach.
Both M4 and M5 have not yet been conclusively researched, but both occur in the brain. The nicotinic acetylcholine receptors (nAChR) are mainly found at the motor endplate. Here they serve to transmit nerve impulses to the muscles. nAChR are particularly well known in connection with the disease myasthenia gravis, in which the nicotinic receptors are destroyed by autoantibodies, which ultimately leads to a disturbance of muscle excitation.
Alzheimer’s disease
Morbus Alzheimer, known after its first describer Alois Alzheimer, is a so-called neurodegenerative disease. It occurs particularly in people over the age of 65 and results in gradually increasing dementia. Alzheimer’s disease is based on the death of nerve cells due to plaque deposits of beta-amyloid peptides within the cells.
This cell death is known as brain atrophy. Acetylcholine producing neurons are particularly affected, resulting in an ACh deficiency in the brain. Since numerous cognitive abilities and processes are bound to this messenger substance, the patients increasingly experience behavioural problems and an inability to participate in activities of everyday life in the course of the disease.
Since a causal therapy is not yet available, the disease is treated symptomatically in the best possible way. This is mainly achieved by the drug administration of acetylcholinesterase inhibitors such as galantamine or rivastigmine, which inhibit the acetylcholine-degrading enzyme. This results in a higher concentration of the neurotransmitter in the brain.
The same effect can also be achieved by administering precursor proteins of ACh. Precursor proteins are inactive protein precursors which are converted into their active form by enzymatic cleavage. Precursor proteins of acetylcholine include deanol and meclophenoxate.
Parkinson’s disease
Parkinson’s disease (also known as idiopathic Parkinson’s syndrome, or IPS for short) is a neurodegenerative disease. The disease is characterised by its main symptoms, which include muscle stiffness (rigor), lack of movement (bradykinesis), muscle tremor (tremor) and postural instability (postural instability) (see: Parkinson’s disease symptoms). The main cause of this serious disease is the gradual death of nerve cells of the so-called substantia nigra, which is located in the midbrain.
Since these nerve cells are mainly responsible for the production of dopamine, there is an increasing lack of dopamine in the brain structure of the basal ganglia, which is essential for movement, during the course of the disease. In other words, an excess of the other neurotransmitters can also be spoken of. In particular, these are mainly norepinephrine and acetylcholine.
The excess of acetylcholine in particular is regarded as the cause of the leading symptomatology of Parkinson’s disease. The therapy of Parkinson’s disease mainly involves the administration of dopaminergic drugs, i.e. a medication that increases the supply of dopamine in the brain. Another therapeutic approach, which is hardly ever used anymore due to strong side effects, is the administration of so-called anticholinergics, also called parasympatholytics.
These are substances which suppress the ACh effect by inhibiting the muscarinic acetylcholine receptors. In this way, a balance of the imbalance of neurotransmitters can be achieved. Frequently occurring side effects of anticholinergics mainly concern limitations of the patients’ cognitive performance, as well as states of confusion, hallucinations, sleep disorders, and minor side effects such as dry mouth.
