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Genetic Variants in the Risk for Late-onset Alzheimer’s Disease—ApoE4 and Beyond
Manage episode 327800129 series 3327910
Kandungan disediakan oleh Ralph Sanchez. Semua kandungan podcast termasuk episod, grafik dan perihalan podcast dimuat naik dan disediakan terus oleh Ralph Sanchez atau rakan kongsi platform podcast mereka. Jika anda percaya seseorang menggunakan karya berhak cipta anda tanpa kebenaran anda, anda boleh mengikuti proses yang digariskan di sini https://ms.player.fm/legal.
How does you unique genome increase the risk for Alzheimer's disease as you age?
In todays episode—#7, I’ll be giving a comprehensive overview on the APOE gene, the ApoE4 genetic variant, and other genes and their genetic variants linked to the risk for late-onset Alzheimer's Disease (LOAD), and how, when, and why Alzheimer's takes root in certain individuals that are carriers of these genes and the variants associated with them.
While the ApoE4 genetic risk variant is widely recognized as a risk factor for LOAD, how ApoE4 contributes to the risk for Alzheimer’s is not as so well recognized by most individuals.
Indeed, the ApoE4 genetic variant is often highlighted as the most significant risk factor for LOAD, but how often have you run across the reasons why ApoE4 raises your risk for LOAD, and how other genetic variants may similarly and synergistically increase the risk for LOAD?
Yes, many other risk variants add to the polygenic (more than one gene) disease profile of LOAD.
The known functional and structural vulnerabilities linked to the ApoE4 variant are multifaceted, and I describe these functional and structural abnormalities that are linked to ApoE4 in my book, "The Diabetic Brain in Alzheimer’s Disease".
However, since the mechanisms that underly the link between ApoE4 in LOAD are a vast topic, I focus on two key points—cholesterol and fat binding and transport, and beta-amyloid deposition and clearance from the brain.
ApoE4, APOJ, ABCA1 and ABCA7, and TREM2 variants greatly determine how these two key mechanisms—cholesterol and beta-amyloid metabolism are factored into the risk for LOAD.
Additionally, I briefly describe another very common variant—MTHFR 677T, that is a critical risk variant in methylation and homocysteine metabolism—yet another pathway that links the importance of the heart-brain axis in the risk for Alzheimer's disease.
Please listen in and get ready for about 35 minutes of a revealing overview on the genes and their variants that are widely available in genetic profiling tests, and are major risk factors in LOAD.
Ralph Sanchez, MTCM, CNS, D.Hom
www.TheAlzheimersSolution.com
https://www.facebook.com/TheAlzheimersSolution
https://www.linkedin.com/in/ralph-sanchez
https://www.instagram.com/alzheimers_solution
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