The gene affects credit - card debt the way other genes have been found to play a role in breast cancer: a particular
version of the gene increases risk, but many other genetic and environmental factors are important, too.
Carrying the APOE4
version of the gene increases risk, while the APOE2 version is protective.
Not exact matches
For more than 20 years, researchers have known that people who carry the E4
version of the APOE
gene are at
increased risk
of developing Alzheimer's.
Carrying a particular
version of the
gene for apolipoprotein E (APOE) is the major known genetic risk factor for the sporadic, late - onset form
of Alzheimer's disease, but exactly how that variant confers
increased risk has been controversial among researchers.
Auriel Willette, an assistant professor
of food science and human nutrition; and Joseph Webb, a graduate research assistant, found on average that Caucasians with one bad
version of the
gene — guanosine triphosphate cyclohydrolase - 1 or GCH1 — developed Parkinson's symptoms five years earlier, and had a 23 percent
increased risk for the disease.
One French study involving nonobese diabetics found that a
version of a
gene for a protein that transports zinc in the pancreas
increased the risk
of this disease.
The paper, entitled «The
gene encoding 5 - lipoxygenase activating protein confers risk
of myocardial infarction and stroke,» presents the results
of a major population study
of heart attack linking a
version of the
gene encoding FLAP with a nearly twofold
increased risk
of heart attack.
The team found that babies with the
version of the
gene linked to an
increased risk
of Alzheimer's were more likely to have smaller medial temporal lobes.
In mouse models in which the endogenous Smn1
gene has been knocked out and human
versions of SMN2 have been swapped in, the Isis therapy — a so - called «antisense oligonucleotide» — delivered to the mouse central nervous system (CNS)
increased the expression
of full - length SMN protein in motor neurons, improved muscle strength in behavioral tests and extended the rodents» median lifespan from 16 days to 26 days3.
The study found that
increased activity in the front
of the brain predicted
increases in the neurotransmitter dopamine in the middle
of the brain in subjects with the suspected schizophrenia - related
version of the
gene.
The NIMH reported today that Clues about how a suspect
version of a
gene may slightly
increase risk for schizophrenia are emerging from a brain imaging study by the National Institute
of Mental Health (NIMH).
Through its population genetics research in Iceland, deCODE identified common
versions of the
gene encoding EP3 (the PTGER3
gene) that confer
increase in risk
of PAOD.
Whilst some
of the lost alleles may be deleterious
versions of genes, the process may at the same time
increase the proportion
of other, mildly deleterious alleles, in the small
gene pool, and thus
increase the incidence
of some diseases.