SAT/24JAN15 3.00PM - Talk on Challenges In Caring Dementia Sufferers By Dr Yau Weng Keong at Sunway Damansara Residents' Association

To All Caregivers,

We will be having a Talk to Members of the Sunway Damansara Residents’ Association on:

TOPIC:           CHALLENGES IN CARING DEMENTIA SUFFERERS

DATE/DAY:   Saturday, 24 January 2015

TIME:             3.00pm – 5.00pm (3-4pm Talk and 4-5pm Q&As)

VENUE:         28th Residency, Sunway Damansara Residents’ Association, Sunway      Damansara, 47810 Petaling Jaya

The Speaker, DR YAU WENG KEONG, FRCP(Lond), is a registered Geriatrician with the Ministry of Health (MOH) since 2000 and had been working as a Physician and Geriatrician since 1997.

​Dr Yau has been involved in starting the Post-Basic Gerontology Nursing under MOH and instrumental in helping UPM, IMU and RCSI Perdana University to start and run their “Health Care for the Elderly” undergraduate programme. He sits in various ​elderly care committees, including National Specialist Registry for Geriatric Medicine.

Currently, Dr Yau is a Consultant Physician and Geriatrician with the Geriatric Unit, Department of Medicine, Hospital Kuala Lumpur.

Our Caregivers are encouraged to attend the above talk which will be held at the premises of the Association.

Compulsory Registration - Email to jenny@adfm.org.my with full name/s, mobile contacts and indicate whether you are a caregiver or healthcare worker, etc..  More details, call Jenny/Michael at Tel:  03 7931 5850.

Closing Date:  Friday, 23 January before 12.00pm.

Has Stanford University Found A Cure for Alzheimer's Disease?

Scientists at Stanford University believe Alzheimer's disease could be prevented and even cured by boosting the brain's own immune response.

Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.

These cells, called 'microglia' functioned well when people are young, but when they age, a single protein called EP2 stops them operating efficiently.

Now scientists have shown that blocking the protein allows the microglia to function normally again so they can hoover up the dangerous sticky amyloid-beta plaques which damage nerve cells in Alzheimer's disease.

The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animals.

“Microglia are the brain’s beat cops,” said Dr Katrin Andreasson, Professor of Neurology and Neurological Sciences at Stanford University School of Medicine.

“Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

By 2015 there will be 850,000 people with dementia in the UK, with Alzheimer's disease being the most common type. The disease kills at least 60,000 people each year.

Microglial cells make up around 10 to 15 per cent of cells in the brain. They act as a frontline defence, looking for suspicious activities and materials. When they spot trouble, they release substances that recruit other microglia to the scene which then destroy and get rid of any foreign invaders.

They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells including clusters of amyloid-beta which aggregate as gummy deposits and break the connections between neurons, causing loss of memory and spatial awareness. These clusters are believed to play a substantial role in causing Alzheimer’s.

“The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation,” added Dr Andreasson. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”

The scientists discovered that in young mice, the microglia kept the sticky plaques under control. But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.

Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer's disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.

And for those mice who developed Alzheimer's, blocking EP2 reversed memory decline.

Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.

The study was published in the Journal of Clinical Investigation.

 (Source:  The Telegraph, 27 December 2014)