Is alzheimers disease hereditary?
There is at least one gene I know of that has been implicated - specifically, the 4/4 allele of the apoe gene - but my understanding is that it’s still not fully understood.
If I can nitpick myself, technically it’s the 4 allele of the gene, and the homozygous condition thereof that’s known as the 4/4 genotype. Sorry for any confusion that may have caused.
Yeah, you really had me going there for a minute!
I think my mom had it, can’t remember…
j/k
She did have it, and I really hope it’s not hereditary. And if the OP has any predecessor with it, I hope doubly for his/her sake.
There have been genetic studies done. I recommend the book ‘Hannah’s Heirs’ by Daniel Pollen, which goes into some detail on the subject.
The conclusion is that some forms of Alzheimer’s, particularly the early-onset types, do seem to be inherited. However, there may be more recent research. Certainly not all cases are inherited, just some portion.
I heard a report today about a finding that suggests the presence of a precursor molecule that may actually begin some of the actual damage of Alzheimer’s well before any of the physiological evidence is present in the brain - like 20 years before. In fact, it may be that this molecule is more responsible for the cognitive impairment than the protein “junk” that shows up in the interneuronal spaces in Alzheimers patients. If this is so, then it may turn out that the ability to producs this particular molecule is genetically coded and might, in fact, be inherited. This aspect clearly would need further investigation, but as more and more features of the disease are discovered, more and more pieces may be connected to DNA and that would imply that heredity could be more and more involved, I think.
Twin studies are good way to assess the role of heredity in various conditions (especially when there is no obvious single gene or common familial form).
This recent (and large) twin study suggests quite a strong role for heredity in the development of Alzheimer’s Disease - accounting for, perhaps, about two-thirds of the risk (with environmental causes responsible for the other third).
Interestingly, of this high genetic influence, four genes have been identified which account for about 50 percent of the influence (presenilin 1, presenilin 2, amyloid precursor protein, and apolipoprotein E). The genes responsible for the other half remain to be elucidated.
On an individual basis, a person engaged in the care of a parent or other family member with Alzheimer’s very commonly becomes convinced that he or she is getting it also, and can cite a good deal of evidence for it. This appears to support a hereditary basis.
That person should not take it too seriously.
The mechanism for this is the way the brain works. One holds a given thought, plan, or observation in mind (in short-term memory) at the moment, and then writes it to longer-term memory (the plan to make a necessary phone call, say). Alzheimer’s care strongly stresses the family member, and also generates demanding interruptions at random moments.
The interruption puts the first item out of mind before it can be recorded, so the phone call never gets made, and after enough of this, the care-giver begins to think his or her own brain has lost its reliability. This adds one more stress factor.
The false Alzheimer’s clears up when the care-taker stops care-taking, or other factors clear that mechanism.
The genetic evidence is also backed up by the fact that people with Down’s Syndrome (trisomy 21) almost always develop Alzheimer’s in their 40s or 50s.
They have 3 copies of chromosome 21 (the rest of us have 2 copies) and the gene which codes for the Amyoid precursor protein lies on chromosome 21.
Still, many people with late-onset Alzheimers have none of the risky genotypes, and even being homozygous for ApoE 4 isn’t a guarantee that the person will develop Alzheimer’s, it just raises the risk significantly.
Alzheimer’s is just one cause of dementia, and it can only be properly confirmed by looking at the brain post-mortem for Amyloid plaques and tau-protein tangles. When we say that someone has Alzheimer’s Disease, we mean that they have the clinical syndrome associated with that pathology, and we would expect to find the plaques and tangles at autopsy.
Cognitive disfunction is a normal part of ageing. The Mini-Mental State Exam (MMSE) is a quick test used to screening test for cognitive function. A perfect score is 30/30, a score below 25/30 suggests dementia, but the average 90 year old will score 23/30 even if they haven’t got a diagnosis of dementia.
Interesting on the genetic angle. You mention that this is one of the causes. What are others? My step-mother just developed Alzheimer’s at the age of 62 so I’m wondering what else might cause this.
Regards
Testy