My MIL passed away at age 64, She developed EOAD at age 59. No other family members have had this and it was quite a shock to all of us. I came across this website because I was wondering it it was heriditary and if her kids (including my husband) and our kids have a highter risk of getting this.

Familial Alzheimer’s disease (FAD) or early-onset Alzheimer’s is an inherited, rare form of the disease, affecting less than 10 percent of Alzheimer’s disease patients. FAD develops before age 65, in people as young as 35. It is caused by one of three gene mutations on chromosomes 1, 14 and 21. If even one of these mutated genes is inherited from a parent, the person will almost always develop FAD. All offspring in the same generation have a 50/50 chance of developing FAD if one parent has it.

Does this mean that for everyone who has EOAD their children have a 50/50 chance of developing this and my kids are at a higher risk too, or maybe not all of those with EOAD there is a gene factor involved. Does anyone who have had a parent with EOAD told they had a 50/50 chance of getting EOAD?

Thanks for any help
Susan

Hello Susan 1215

My name is Mary, I was diagnosed with EOAD at age 49. I have recently turned 50. I carry both APOE3-4 genes.

My grandfather had it on my father's side. I also understand that my great grandmother on my mother's side, had Alz, too.

My primary care physician told me that in my case, Alz skipped a generation and is early onset! Yes, there is a good chance (50/50)that either my children or my grandchildren carry the genes that remains dormant. So far within my family my father, uncle(s), sibling and cousins have not shown signs of Alz disease.

I had a genealogy test to verify the genes. I also had much blood work done to verify that I was not vitamin deficient and that I didn't have thyroid problems. My blood work revealed that everything was at normal range. Therefore, canceling out any other questions in this area.

Finally, I had an MRI w/without imagining which revealed that my brain had significantly shrunk (more so than normal for a person of my age) and that the center cortex of my brain shows white matter---my brain is dead in this area.

You may want to speak with your primary care physician to see what he/she recommends! My understanding is that GP's are only required to have a single course of study regarding dementia! Unless, they are going to continue with this area of study?

M

Mary, that area of your brain that doesn't work anymore? What did it do for you? Problems with it being offline?

Hi, Susan. There are two basic types of AD, i.e., "sporadic" and "early-onset familial (eFAD)." Sporadic AD is by far the most common, and it can strike young people. eFAD, which is the type that is inherited, is quite rare.

For your MIL to have had eFAD, one of her parents would had to have had it, to pass it on to her. eFAD is caused by "dominant" mutations, which means that you only have to have one copy of a mutation for eFAD to develop. Therefore, the odds of a person who has eFAD to pass the disease on to a child are 50:50. However, one of your parents would have to carry a mutation, and pass it on to you, for you to develop eFAD. (And yes, I know this had to have started somewhere, but the odds of eFAD developing spontaneously are vanishingly small.)

The mutations that can cause eFAD are found in the APP, PS1, and PS2.

APOE4 is a risk factor for sporadic AD -- that is, it does not actually cause AD, although people with APOE4 are somewhat more likely to develop AD. You can have APOE4 without developing sporadic AD, and you can develop sporadic AD without carrying the APOE4 allele.

Susan, I understand your concern. My father had EOAD.

If your MIL's own parents did not have Alzheimer's disease early, before 65, then it unlikely that she had one of the few genes that casue FAD. There are two types of early onset,as I understand, Sporadic and FAD. Sporadic early onset is like late onset only with an atypical early onset. Again, this is as I understand it.