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Scientists Pinpoint New Alzheimer's Gene

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WASHINGTON (Jan. 14) - Scientists said on Sunday they have pinpointed a new gene linked to Alzheimer's disease, the incurable brain disorder that is the top cause of dementia in the elderly.

Abnormalities in a gene called SORL1 increased the risk for the disease, and this finding could help scientists develop new treatments, the researchers reported in the journal Nature Genetics.

The researchers looked at DNA samples from 6,000 people from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs. They found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.

The late-onset form, affecting people age 65 and up, represents about 90 percent of Alzheimer's cases. The rarer early-onset form affects people from about age 30 to 65.

Only one other gene, called ApoE4, has been identified as a risk factor for late-onset Alzheimer's. It was identified in 1993.

Several genes are linked with early Alzheimer's, and study of both types might lead to better understanding of how the disease begins and how to tackle it.

Many scientists think Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that clumps together to form plaques. That material stems from a protein called amyloid precursor protein, or APP.

SORL1 controls the distribution of APP inside nerve cells of the brain. When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.

Alzheimer's is a complex disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Scientists have struggled to understand the biology of the disease and its genetic and environmental causes.

'PIECE OF THE PUZZLE'

"It's another clue to the way in which this disease comes about, another piece of the puzzle," Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto and one of the key researchers, said in a telephone interview.

"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.

St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.

"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.

The disease first affects parts of the brain controlling memory and thinking, but as it advances it kills cells elsewhere in the brain. Eventually, if the patient has no other serious illness, the loss of brain function will prove fatal.

Researchers from Boston University and the Mayo Clinic College of Medicine in Jacksonville, Florida, also took part in the five-year study.

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Event Date

Service Center : California Service Center

CIS Office : San Francisco CA

Date Filed : 2008-06-11

NOA Date : 2008-06-18

Bio. Appt. : 2008-07-08

Citizenship Interview

USCIS San Francisco Field Office

Wednesday, September 10,2008

Time 2:35PM

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I worked in special needs facilites. More then not with advanced alzheimers people. It is very sad to see the downward slope of these people. My question is.... why is there more americans with this disease? Is it the chemicals in our every day life? Alzheimers patients have increased over the years...why???

Some have suggested it is the aluminum in our every day products, deodorat.. ect (not sure where I read this however)

It is why I cannot work in this setting any more. To see someone die slowly, transforming, when you get to know them before hand as bright people with just a hint of a problem. The saddest thing is when they have a break though... when they have a lucid moment where they KNOW where they are and why they are there and cant understand why this has happened. They understand the horror of it all... It is sometimes better if they dont have those days...

Wendy

WASHINGTON (Jan. 14) - Scientists said on Sunday they have pinpointed a new gene linked to Alzheimer's disease, the incurable brain disorder that is the top cause of dementia in the elderly.

Abnormalities in a gene called SORL1 increased the risk for the disease, and this finding could help scientists develop new treatments, the researchers reported in the journal Nature Genetics.

The researchers looked at DNA samples from 6,000 people from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs. They found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.

The late-onset form, affecting people age 65 and up, represents about 90 percent of Alzheimer's cases. The rarer early-onset form affects people from about age 30 to 65.

Only one other gene, called ApoE4, has been identified as a risk factor for late-onset Alzheimer's. It was identified in 1993.

Several genes are linked with early Alzheimer's, and study of both types might lead to better understanding of how the disease begins and how to tackle it.

Many scientists think Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that clumps together to form plaques. That material stems from a protein called amyloid precursor protein, or APP.

SORL1 controls the distribution of APP inside nerve cells of the brain. When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.

Alzheimer's is a complex disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Scientists have struggled to understand the biology of the disease and its genetic and environmental causes.

'PIECE OF THE PUZZLE'

"It's another clue to the way in which this disease comes about, another piece of the puzzle," Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto and one of the key researchers, said in a telephone interview.

"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.

St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.

"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.

The disease first affects parts of the brain controlling memory and thinking, but as it advances it kills cells elsewhere in the brain. Eventually, if the patient has no other serious illness, the loss of brain function will prove fatal.

Researchers from Boston University and the Mayo Clinic College of Medicine in Jacksonville, Florida, also took part in the five-year study.

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Filed: AOS (apr) Country: England
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My Stepdad is 64 and 2 years ago was diagnosed with early onset Alzheimer's disease. He was extremely outgoing, confident, athletic, and funny, and is slowly turning into someone who lacks confidence, is losing weight rapidly, and is very dependent on my Mother, losing even his own personality.

As a nurse, I have worked around many illnesses and yet this disease is one of the saddest to watch someone go through. My Stepdad knows ( or at least knew ) what his diagnosis is. He gets so frustrated at doing the simplest things such as getting dressed and feeding himself. The physical decline is very hard to watch , but even more so is watching him struggle to find the words for everyday objects.

I sincerely hope they find a cure for this disease soon.

Karen

Karen ( USA ) and Tony ( UK ) now both residing in USA!!

2/28/05- I-129F sent to TSC

7/29/05- Interview date- Approved!!!!!!!!!!!!!

10/06/05-Tony comes home to Tennessee!!!

10/08/05-WE'RE MARRIED!!! I love this man!

AOS/EAD/AP

11/26/05-filed for emergency AP

11/29/05-filed for AOS/EAD

03/07/06-online EAD approval

03/10/06-received EAD in post and passed driving test (Wow what a day)

07/26/06-AOS Interview---APPROVED!!!!!!

07/31/06-received 'Welcome to America' Letter

08/07/06-received Green card in post wooooooooohoooooooo

03/30/09-received approval to remove conditions!

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