Neurocognitive decline and neurodegeneration are one of the most feared issues with aging. It occurs in essentially 100% of individuals to one degree or another. We all want to avoid this from being a health-span determiner. Current approaches are to wait until the person has substantially symptomatic disease and then provide non-disease altering treatment that chases symptom relief (usually only partially) as the underlying disease progresses.
As an Anti-Aging Physician, it is understandable why this is feared.
There is a typical progression for patients who are paying attention to their cognitive status. This is detailed quite nicely done review inNature Mental Health[sadly it does cost a little to read the full article].
#1 At Risk – cognitively unimpaired, but with some risk factors
#2 Pre-clinical – this is commonly where the patient might note some minor changes, and Alzheimer’s Disease (AD) type pathological changes have begun in the brain
#3 Mild Cognitive Impairment (MCI) – this is where there is some memory loss, language issues, executive function issues, but the person continues without “clear impairment of activities of daily living.”
#4 Dementia – Advancement of MCI to where it affects behavior, personality, and executive function.
It is likely that Parkinson’s Disease (PD) prevention approaches are almost identical to that which we might utilize with AD, with some nuances. For the purposes of this series, I am going to lump together all neurodegeneration into one group, albeit, once there is clear disease, the treatment of symptoms certainly utilizes different approaches.
It is critical for patients to understand that the most likely cause of death and disability, remains the traditional conditions of vascular disease, cancer, infection (often related to immune dysfunction that is age related), and trauma (often related to neurocognitive decline and sarcopenia). Managing other traditional and high evidence-based issues must be part of any anti-aging and longevity strategy.
Examples of issues to be managed include lipids, blood pressure and glucose – as each of these independently impact cognitive decline and stroke risk. Additionally, items like Omega 3 index, Vitamin B12 levels, physical activity, sleep, stress management, social connections, learning/mental activity, and a quality diverse diet must be managed and maintained.
Unfortunately, despite having all these items managed, the risk of developing neurodegeneration with aging is substantial, almost certain, if you live long enough.
It would seem that any patient who is thinking about how to manage their risk of neurocognitive decline, should know their ApoE status. This can be ordered by Dr. Fraser by a cheek swab from Boston Heart for $50.This can easily be self-ordered and is a cheek swab for $99.
Figure 1 from this article is available by clicking on the text above. Spend some time on this – unless you are an ApoE2/E2, or if you aren’t trying to live cognitively intact until you are 90 years old, it should result in some contemplation!
Nature Communications Graph as noted above.
One interesting aside, is to understand what ApoE is doing, and that it is significantly relating to lipid metabolism in the body and brain. In elderly Nigerians, there isn’t a huge relationship between ApoE4 and AD. They have one of the highest incidences of ApoE4 in the world, and age matched have unexpectedly low AD. This is felt to be due to their highly plant-based diet, and very low lipids. You can watch a video on this, byDr. Greger here.
So what to do? Do you take the current approach of waiting until disease strikes and progresses to be severe enough to be diagnosed? At that stage you’ll be started on non-disease modifying treatments and have the predictable progression.
Are there medications which might decrease the risk of ever being diagnosed with AD or PD? Do we have drugs or supplements that might prevent or delay a diagnosis of AD or PD? Are these drugs expensive, or have significant risk of side effects? Where is your risk/benefit analysis at, and is it sensible to pre-empt development of disease, even if the evidence isn’t definitive, but instead indicative of benefit?
Looking at the graph above on age vs. AD – if you are planning for a long life without dementia, not to mention neurocognitive decline, it should be a consideration.
Dr. Fraser has an increasing number of patients he is treating in this space and has a focus on what can be done to prevent neurocognitive decline. Interestingly, every one of the therapies considered in this space, also seem to have independent likelihood of improved longevity. However, we are in an area where risk/benefit must be considered, and for most patients, these medications are low risk, and may confer benefit.
As part of this series we will go through the following therapies, one at a time and discuss the pros-cons, contraindications, and evidence for benefit.
We hope you’ll look forward to each addition of this series, and carefully contemplate whether it seems likely that neurocognitive decline can be prevented or delayed. It is theoretically much more difficult to address a condition once it has begun. The philosophical issue is when to act based on lack of certainty. This is a personal decision, but the clock is ticking, and it is unlikely that we’ll have clear evidence of these issues in the next 20 years.
