Amnestic MCI vs. Alzheimer's disease: The Crux of It All
This is a tough topic because Amnestic MCI (e.g. impairments in cognition related to memory) is not really distinct from Alzheimer's disease. Its more of a phase that occurs prior to the diagnosis of official "Alzheimer's disease." Yet, the physical manifestations and cognitive symptoms are apparent in this phase and give all indications that an individual is on the path to Alzheimer's disease (AD).
But even that is a hard thing to discuss because AD is difficult to diagnose until there is enough pathology that the deterioration is visible on some measurable medical test, such as a spinal tap or a MRI. At the point, though, when our technology may be able to confirm a diagnosis, the cognitive equivalent of transitioning from MCI to an AD diagnosis has likely occurred.
Should this prevent us from trying? Absolutely not.
We should do everything possible to intervene at the MCI stage of a person's progression, because this stage can last for years to decades. And even at the point where a person cognitively and neurological transitions from the "mild" designation to the "dementia" designation (here being AD), we should still intervene because the dementia stage can 7-15yrs.
Yet, are any of us really certain what a transition from Amnestic MCI to AD looks like?
The answer is: YES.
Clinical science has been spending a considerable amount of time and resources specifically investigating this transition point.
I could go on and on and on and on and on and on about all the literature and research out there and show you a bunch of photos and talk about a lot of things... however, the photo and study shown below really captures the crux of it all.
So this is what I will focus on!
In a study by Whitwell et al. (2007), they looked via neuroimaging and cognitive testing the transition from an Amnestic MCI diagnosis to a diagnosis of AD They were able to see how the neurological changes corresponded to the changes in cognitive functioning and Activities of Daily Living (ADL) functioning.
What they indicated, and has since been replicated a bazillion times in clinical practice, is that there is not so much a HARD LINE that indicates a transition from Amnestic MCI to AD but an overall relationship between the amount of neurological deterioration (in certain areas of the central nervous system) and cognitive/ADL functioning that demonstrates a significant decline beyond what can be considered "mild."
The key, here, is that the neurological deterioration seen in this progression is not random. There are a few possibilities for where Amnestic MCI can progress to, but these options all end up in a variety of dementias that are similar to AD (and a topic for another day!). That means, we can be pretty sure that the Amnestic impairment, meaning the issues with memory, are only going to continue and that other cognitive impairments may arise.
When we look at neuroimaging, we see this very clearly, and the biomarkers from other types of medical testing support the idea that the memory impairment is the issue to focus on in the beginning and throughout treatment.
That is because the medial temporal lobe (seen below in red in each of the 3 photos) is suffering neurological insult. This area is deteriorating because it is being bombarded by plaques (on the outside of the neurons) and tangles (on the inside of those neurons). This pathological deterioration is occurring decades before the first memory issue pops up in a very mild mild mild MCI patient (possibly 35-40yrs before an AD dementia diagnosis is given).
While a lot of people claim that AD is a memory disease, they are in fact, WRONG.
Alois Alzheimer MD identified a type of neurological impairment that has a certain type of biological pathology. That pathology happens to affect neurons in the medial temporal lobe. As an Adverse Effect, anything that part of the cortex does will be impaired. This just happens to be the area associated with memory functioning.
This is also something science has known for years. Memory impairments are the Adverse Effect of an underlying pathology. It is not the target of the destruction. Its just what we can see on the outside.
From there, the progression from the Amnestic MCI stage to the AD dementia stage follows a similar path. It is not that other cognates are under attack. In fact, they are not even a part of the picture. The areas that deteriorate next have neurological, electrical and chemical connections to the medial temporal lobe. So, the plaques and tangles seen in the disease travel to those parts of the cortex and begin to breakdown those areas as well. Whatever cognates those cortical structures serve begin to breakdown as well.
By chance, those cognates are general those that are associated with activity in the prefrontal, inferior parietal and ventral occipital cortices.
The Prefrontal Cortices serve a lot of functions related to our executive control over all other cognates, our personalities and our emotions (because the amygdala is in this area). When this area begins to deteriorate, we see a lot of issues related to task switching, ordering, navigating our environment, fear, depression (specific to AD), carrying on conversations, etc.
The Inferior Parietal Cortices serve a lot of functions related to dreaming, sleep, imagination and integrating information from the entire human experience into something that makes sense. When this area begins to deteriorate, we see issues with sleep disturbances, hallucinations, delusions, violent dreams, altered sensations and interpretations, etc.
The Ventral Occipital Cortices focus more specifically on integrating the tasks of the visual system (e.g. the occipital lobe) with those of the medial temporal lobe like object recognition, identification, language comprehension, etc. When these areas breakdown, we start to see some of the characteristic signs and symptoms of AD: Difficulty recognizing family members and loved ones.
While deterioration of the medial temporal lobe and its corresponding Amnestic impairments are the defining characteristics of Amnestic MCI, it is neurological deterioration in these 3 main areas of the cortex that really comprise the transition from the "mild" stage to the "AD dementia" stage.
At the dementia stage, widespread deterioration in at least one of these other cortical areas plus the initial deterioration of the medial temporal lobe are apparent in medical testing as well as in interactions with the patient. Most often, the additional deterioration is in the prefrontal cortex (e.g. executive dysfunction) and characterizes the Multiple Domain Amnestic MCI patient population (e.g. the largest group of patients who end up with an AD diagnosis). The deterioration they are experience at this transition is significant enough to impede or interrupt their ability to perform ADLs and remain independent.
Again, this does not mean we don't intervene. It just better characterizes that change and helps us to identify individuals who have paths that are progressing. When we cross over into the dementia stages, it just means that things are progressing at a faster rate and we have to become more aggressive in our strategies to slow this process down (or maybe halt the progression altogether!).
Checkout the photo below taken from this study that can be found HERE online. The arrows in this photo point to the region of the medial temporal lobe that deteriorates earliest in AD's progression and is the area that can be neurological tracked to indicate the transition from the Amnestic MCI diagnosis to a diagnosis of dementia of the AD type.
If you are a SLP and would like to learn more through our continuing education opportunities (ASHA approved!), go to dysphagiamanagement.com/ce-courses to get signed up, today! There are 0.9CE available via course topics on Successful Aging, Mild Cognitive Impairment and Alzheimer's disease.
