Episode # 4
The Alzheimer's Solution Revolution
#4 The Role of Beta-Amyloid Protein in the Progression and Development of Alzheimer’s Disease that Spans Decades
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Episode Summary and Audio
In this fourth episode of The Alzheimer’s Solutions podcast with Ralph Sanchez, I the host, talk with my co-host Susan Brender, who has partnered with me to produce a special “Think Ahead” podcast series.
In this week’s episode, I’ll give an overview of the previous episode #3, and I’ll provide several key insights about a protein that is associated with the pathology of Alzheimer’s disease—beta-amyloid protein, which forms the proverbial amyloid plaque that is often cited as a principal lesion of the disease process.
Additionally, in this Think Ahead podcast, I pick up where we left off on the last episode (#3) with regard to the genesis of Alzheimer’s, disease in the brain, and the role of beta-amyloid protein aggregates in the progression of Alzheimer’s disease in aging. I illustrate how the disease process can progress from the preclinical stage (asymptomatic) to a mild cognitive impairment stage, and eventually a diagnosis of a dementia associated with Alzheimer’s disease.
Please listen in to continue learning how amyloid precursor protein is processed to produce beta-amyloid protein particles and aggregates, which underlies the earliest stage (preclinical) of the Alzheimer’s disease continuum that can span decades before an eventual diagnosis of dementia.
Lastly, we touch on the role of the APOE gene and the ApoE4 variant—the most validated late-onset Alzheimer’s disease genetic risk variant— with regard to beta-amyloid accumulation in the brain, and how research has significantly progressed over the years to illuminate how we can leverage these new findings to reduce the risk for late-onset Alzheimer’s disease.
We end with what to anticipate in an additional podcast coming soon in the Think Ahead series—the role of tau protein and neurofibrillary tangles in Alzheimer’s disease.
Top Takeaways
- Which are the top risk factors—that are often cited by studies—which are associated with an increased risk for Alzheimer’s disease?
- The diagnosis process of Alzheimer’s is difficult, and in the beginning stages there are virtually no symptoms or signs. There are many causes of dementia or cognitive impairment and they are not typically investigated in at-risk individuals.
- The three leading causes dementia are Alzheimer’s, vascular disease, and Lewy body disease. It is very common to have these diseases and the lesions associated with them comingling at the same time.
- Some medications can be a huge risk factor for nutrient deficiencies that can raise the risk for late-onset Alzheimer’s and dementia. For example, regularly taking antacids can block the absorption of B12, which can lead to cognitive impairment in aging.
- Tau and amyloid proteins are constituents of brain function and structure. However, these proteins are abnormally processed and assemble into abnormal aggregations in Alzheimer’s disease.
- Amyloid plague is a result of beta- amyloid protein (peptide) aggregates (oligomers—see illustration at top of page).
- Genetic variants of genes play a role in raising the susceptibility to excess processing and aggregation of amyloid and tau protein. However, just because one is more at genetically at risk for the pathology associated with late-onset Alzheimer’s disease, it does not necessarily mean that you are destined to have it take over your brain as you age.
- Memory and learning mechanisms are a fundamental component of synaptic function and brain plasticity or neuroplasticity. Beta-amyloid protein particles disrupt the vital synaptic signaling mechanisms and cascades that are crucial for memory and learning. Alzheimer’s disease begins—at the synapse!
Timestamp Highlights
In this Episode
[1:58] a brief overview of the first episode, and the clarification made of the terms often used in reference to the two main forms Alzheimer’s disease—early and late-onset Alzheimer’s disease.
[3:43] Why the earliest stages of Alzheimer’s disease—the preclinical stage progresses without any noticeable signs or symptoms associated with the disease process.
[5:55] The difficulty in diagnosing Alzheimer’s disease.
[6:30] Leading causes of dementia.
[7:30] How genetic risk variants and lifestyle choices can play a role in your risk for late-onset Alzheimer’s disease .
[10:39] A description of the hallmark lesions of Alzheimer’s disease that are derived from amyloid and tau protein.
[13:12] A brief overview on how these proteins can aggregate and lead to cognitive impairment, and how they are causative in Alzheimer’s disease.
[14:04] The role of key genetic risk variants (ApoE4) in the risk for late-onset Alzheimer’s disease (LOAD).
[16:55] How research over the last two-plus decades has evolved in the understanding and identification of the causal risk factors linked to LOAD.
[18:39] How memory and learning mechanisms at the synapse are disrupted by the interaction of toxic beta-amyloid aggregates with key synaptic receptors such as the insulin and NMDA receptors. This occurs in the earliest stage of the Alzheimer’s disease process—the preclinical phase. (Described and illustrated in The Diabetic Brain in Alzheimer’s disease)
Please listen in!
Ralph Sanchez, MTCM, CNS, D.Hom
BrainDefend®
www.facebook.com/TheAlzheimersSolution
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