Faulty gene may cause Alzheimer's in women
Your support helps us to tell the story
From reproductive rights to climate change to Big Tech, The Independent is on the ground when the story is developing. Whether it's investigating the financials of Elon Musk's pro-Trump PAC or producing our latest documentary, 'The A Word', which shines a light on the American women fighting for reproductive rights, we know how important it is to parse out the facts from the messaging.
At such a critical moment in US history, we need reporters on the ground. Your donation allows us to keep sending journalists to speak to both sides of the story.
The Independent is trusted by Americans across the entire political spectrum. And unlike many other quality news outlets, we choose not to lock Americans out of our reporting and analysis with paywalls. We believe quality journalism should be available to everyone, paid for by those who can afford it.
Your support makes all the difference.Medicine A faulty gene on the female X chromosome may contribute to the development of Alzheimer's disease in women, scientists said yesterday.
The discovery is the first evidence of a sex-specific risk factor for the disease. Scientists identified a variant in the gene PCDH11X that significantly correlated with susceptibility to late-onset Alzheimer's disease (Load).
When the data was analysed to account for sex, the association was found to be almost entirely confined to women. PCDH11X lies on the female X chromosome, one of the "packages" of DNA inside the cell nucleus.
It provides the coded building instructions for a protein called protocadherin.
There is evidence that protocadherins may be affected by an enzyme linked to early-onset forms of Alzheimer's. Dr Steven Younkin of the Mayo Clinic College of Medicine in Jacksonville, Florida, led the research, reported in the Nature Genetics. The researchers wrote: "Further study should open new therapeutic possibilities for this devastating disease."
Join our commenting forum
Join thought-provoking conversations, follow other Independent readers and see their replies
Comments