Professor Julie Williams, from Cardiff University's School of Medicine, led a genome study that involved 16,000 people
A scientist who has discovered two new genes associated with Alzheimer's disease said they could help in the race to find a cure for the condition.
Julie Williams, professor of Neuropsychological Genetics at Cardiff University, said new treatments for dementia could also be found.
Previously only one gene had been known as a risk factor for Alzheimer's.
Professor Williams said the new genes identified protect the brain but that changes may turn them into "attackers".
There are currently around 700,000 people with dementia in the UK - 37,000 of them from Wales.
Two Alzheimer's genes identified
The new genes were discovered after Prof Williams completed a genome study involving 16,000 people.
Scientists had known that one gene - APOE4 - had been shown to be a risk factor for Alzheimer's disease.
But the study revealed for the first time that there are a further two genes - CLU and PICALM - which work in the brain and are related to the onset Alzheimer's disease.
Professor Williams said: "We do not really understand what causes common Alzheimer's disease - we thought we had a good idea but what our data is showing is that there are new things going on there and we really need to focus on those and work on those.
"And I think a few years and we may get a very good idea about the full picture of what causes the disease.
"It appears that the genes we have identified have a role in protecting the brain so changes in these genes associated with Alzheimer's disease may either remove this protection or possibly change these protectors into attackers of the brain."
She said that CLU is a clusterin - a type of protein - which normally protects the brain in a variety of ways.
PICALM is important at synapses - connections between brain cells - and is involved in the transport of molecules into and inside of nerve cells, helping form memories and other brain functions.
"We know that the health of synapses is closely related to memory performance in Alzheimer's disease, thus changes in genes which affect synapses are likely to have a direct effect on disease development," she said.
It is also important to recognise the contribution many Welsh people who have acted as subjects for this research over the years
Professor Julie Williams
She said the research helped "change our understanding of what causes the common form of Alzheimer's disease and provides valuable new leads in the race to find treatments and possibly cures".
"It also shows that other genes can be identified using this method, and we are already planning a larger study involving 60,000 people, which can be achieved within the next year," she added.
"It is also important to recognise the contribution many Welsh people who have acted as subjects for this research over the years."
The study was funded by the Wellcome Trust, Medical Research Council, Alzheimer's Research Trust and the Welsh Assembly Government.
First Minister Rhodri Morgan said the findings were a "feather in the cap" for Wales' reputation as a centre for "world-class research".
"This major breakthrough in the battle to understand and develop treatments for Alzheimer's is good news for the 37,000 people in Wales and their carers who are affected by Alzheimer's or other forms of dementia," he said.
"World-class research like this will help lead to improved treatment for this distressing disease, and may one day even mean we can cure dementia."
The university-led research also involved scientists from universities in London, Cambridge, Nottingham, Southampton, Manchester, Oxford, Bristol and Belfast, who collaborated with Irish, German, Belgian, Greek and American institutions.
This page is best viewed in an up-to-date web browser with style sheets (CSS) enabled. While you will be able to view the content of this page in your current browser, you will not be able to get the full visual experience. Please consider upgrading your browser software or enabling style sheets (CSS) if you are able to do so.