Live. Laugh. Love

Medical Student, medicine is the biggest passion of my life. I love art and philosophy.
neurolove: I had a great question from floating-point that I started to answer earlier this week.  Let’s get back to ApoE e4.  Depending on the number of alleles (you can have up to two, one from each parent), there is an increasing risk of developing Alzheimer’s. People with no ApoE e4 alleles have a 9% risk of getting Alzheimer’s.  Compare that to a 27% risk with one ApoE e4 allele and 55% risk with two ApoE e4 alleles.  Overall, this mutation accounts for about 40% of all Alzheimer’s cases.  The only other genes that are related to Alzheimer’s are causal, which means if you have that mutation, you WILL get Alzheimer’s, but they only account for about .5% of all Alzheimer’s cases.  A few of these genes are AP1 and Presenilin 1 and 2, for example.  The interesting thing is that most of these genes affect APP (Amyloid-Beta Precursor Protein), which is cleaved (cut into a smaller piece) to become amyloid-beta.  It is important to note that amyloid-beta is a normal protein and even with normal aging, there are some amyloid-beta plaques that form.  This makes it extra complicated.  It seems that it might have to do with how amyloid-beta is cleaved (the lengths of the protein once it has been cut normally) and how well it is broken down that might lead to this normal process becoming Alzheimer’s.  There is some evidence that ApoE might help breakdown amyloid-beta and that the e4 allele might not do it as efficiently as the other variants of ApoE, which leads to pathological build up and widespread amyloid-beta plaques.  It isn’t entirely clear at this point, however. I’ve also added a picture to help show the Alzheimer’s brain and degeneration that occurs in the disease progression (above).  It’s pretty marked post-mortem (after death), as you can see. [Image Source]

neurolove:

I had a great question from floating-point that I started to answer earlier this week.  Let’s get back to ApoE e4.  Depending on the number of alleles (you can have up to two, one from each parent), there is an increasing risk of developing Alzheimer’s.

People with no ApoE e4 alleles have a 9% risk of getting Alzheimer’s.  Compare that to a 27% risk with one ApoE e4 allele and 55% risk with two ApoE e4 alleles.  Overall, this mutation accounts for about 40% of all Alzheimer’s cases.  The only other genes that are related to Alzheimer’s are causal, which means if you have that mutation, you WILL get Alzheimer’s, but they only account for about .5% of all Alzheimer’s cases.  A few of these genes are AP1 and Presenilin 1 and 2, for example.  The interesting thing is that most of these genes affect APP (Amyloid-Beta Precursor Protein), which is cleaved (cut into a smaller piece) to become amyloid-beta. 

It is important to note that amyloid-beta is a normal protein and even with normal aging, there are some amyloid-beta plaques that form.  This makes it extra complicated.  It seems that it might have to do with how amyloid-beta is cleaved (the lengths of the protein once it has been cut normally) and how well it is broken down that might lead to this normal process becoming Alzheimer’s.  There is some evidence that ApoE might help breakdown amyloid-beta and that the e4 allele might not do it as efficiently as the other variants of ApoE, which leads to pathological build up and widespread amyloid-beta plaques.  It isn’t entirely clear at this point, however.

I’ve also added a picture to help show the Alzheimer’s brain and degeneration that occurs in the disease progression (above).  It’s pretty marked post-mortem (after death), as you can see.

[Image Source]

  1. pistachito reblogged this from neurolove
  2. the-luminousfisheffect reblogged this from neurolove
  3. oxyj3n reblogged this from neurolove
  4. michelecasandra reblogged this from neurolove
  5. houseboatslove reblogged this from kkimmie
  6. cochicui reblogged this from neurolove
  7. abster2 reblogged this from neurolove
  8. 6catsonedog reblogged this from neurolove
  9. ummaz reblogged this from neurolove
  10. talkingshrimp reblogged this from neurolove
  11. siiiiiigh reblogged this from neurolove
  12. einafets5 reblogged this from neurolove
  13. 1bcg1-onukwughachinenye reblogged this from neurolove and added:
    feel smarticle re-bloging...^^ —I’ll read...later though..i...
  14. ivymatus reblogged this from neurolove
  15. life-forces-maybe reblogged this from neurolove
  16. thaimaishoojew reblogged this from neurolove
  17. thewaytoeden reblogged this from neurolove
  18. daphodillie reblogged this from supriscillious-nonsense
  19. skshawna reblogged this from neurolove
  20. thejoeshow reblogged this from neurolove
  21. theskygazer reblogged this from neurolove
  22. supriscillious-nonsense reblogged this from neurolove
  23. queendan reblogged this from neurolove
  24. gardenfulloflavender reblogged this from neurolove
  25. nckrfkn reblogged this from neurolove
  26. kkimmie reblogged this from neurolove
  27. a-siren-singingyoutoshipwreck reblogged this from neurolove
  28. ashrafaryankhan reblogged this from neurolove
  29. savagebean reblogged this from neurolove and added:
    pretty good explanation...although amyloid is a “normal protein,” in the sense
  30. ladynarwhal reblogged this from nagarothi