Brussels, 25 Sep 2006
Researchers from Germany, Belgium and the US have found that an enzyme necessary for the normal development of the central nervous system is an important player in the development of Alzheimer's disease.
The enzyme, beta-secretase or BACE1, is essential in normal nervous development because it organises the coating of nerve fibres with myelin, the insulator essential for quick transmission of nerve impulses, and for ensuring the impulses reach their destination.
The researchers found that when the gene responsible for regulating BACE1 was switched off, then the development of Alzheimer's stopped. At least this was the case in genetically modified mouse studies. However, these mice also lacked proper myelin insulation, which means that they would be susceptible to other neurodegenerative diseases.
'These findings allow us for the first time to also look very closely at the side effects of Alzheimer's inhibitors,' said Professor Christian Haass from LMU Munich.
Alzheimer's is characterised by a build up of a protein fragment, known as beta-amyloid. These fragments are the result of enzymes eating away at a protein known as amyloid precursor protein. BACE1 is one of enzymes responsible for this process. If the enzyme is deactivated, the process stops. So does the progression of Alzheimer's disease.
However, this will also stop the enzyme performing its proper function, which is to generate myelin insulation for nerve fibres. 'BACE1 has therefore also positive functions, not only bad ones,' explained Dr. Alistair Garratt from MDC, Berlin-Buch.
The researchers believe that the negative effect of switching off the BACE1 gene would only occur during development, and that in an adult, there would be little or no effect on the myelin insulation of nerve fibres. 'We have thus been able to bring together the field of developmental biology with that focusing on neurodegenerative diseases,' said Dr Garratt.
This new research opens a new line of enquiry for the treatment of Alzheimer's disease, and could lead to the development of drugs to inhibit the action of BACE1, and so limit the effects of the disease.