Ananova:

Diseases such as Parkinson's and Alzheimer's may be caused when nerve endings in the brain turn "rusty", according to new research.

Scientists found evidence that oxidative damage to the connection points of nerve cells is linked to the development of neurodegenerative diseases.

Oxidation occurs when atoms are stripped of electrons due to a chemical reaction. It causes iron to rust and damages the components of living cells.

US researchers at the University of Pennsylvania, Philadelphia, discovered that in Parkinson's and Alzheimer's patients, a nerve protein called alpha-synuclein suffered oxidative damage.

Alpha-synuclein is found at the synapses of nerve cells, the points where wiring in the brain connects.

Earlier work had shown that mutations in the alpha-synuclein gene caused the inherited form of Parkinson's disease. The protein was also known to be a major component of Lewy bodies, the fibrous lesions characteristic of Parkinson's.

Neurodegenerative diseases such as Parkinson's and Alzheimer's are collectively called synucleinopathies. Their symptoms are normally caused by the deficiency of a neurotransmitter - a chemical that transmits messages across synapses from one nerve cell to another.

When the neurons that produce these chemicals die or become impaired, it can cause tremors or dementia.

The Pennsylvania scientists found that alpha-synucleins damaged by oxidation were widespread in Lewy bodies.

Dr Virginia Lee, co-director of the Centre for Neurodegenerative Disease Research at the University of Pennsylvania, said: "This is a major foothold in beginning to understand how oxidative stress plays a role in causing Parkinson's and other synucleinopathies.

"Our studies provide conclusive evidence of oxidative damage in alpha-synuclein, and that such stress may be a primary event leading to the onset and progression of neurodegenerative synucleinopathies, particularly Parkinson's."

The researchers, who reported their findings in the journal Science, said the work may lead to developing therapies to slow or reverse progression of the diseases by halting or reducing oxidative damage.