By Ralph Sanchez, L.Ac.,CNS,D.Hom
Long before a diagnosis of Dementia or Alzheimer’s disease (AD) is given, brain damage is occurring that leads to, and reflects the gradual downward spiral of mental decline that typifies AD. A cluster of signs that define Mild Cognitive Impairment (MCI), especially memory loss and forgetfulness, may be the early warning indicators that you are at risk for developing AD. If you can visualize a spectrum whereby healthy brain/cognitive function in an individual is on one side of the spectrum, and AD is on the opposite side, MCI would be inching ever so close to the AD side of the spectrum. The individual with MCI is more functional than one who is clinically diagnosed with dementia, albeit with MCI, there is subtle to noticeable problems with memory, judgment, language and other cognitive skills. These symptoms, along with other criteria that define MCI, are now recognized as the transitional stage of brain degeneration that may lead to Dementia and AD. (1)
In essence, MCI often represents cognitive decline that reflects degenerative brain processes that is beyond normal aging, but precedes more severe deterioration and diagnosis of dementia. (2) What has been generally accepted to be normal age-related cognitive decline, may represent to some degree, damage or degenerative processes to brain tissue. A recent study (2006) concluded that the underlying brain deterioration in memory loss related MCI (see classifications of MCI below), represented the early stages of AD brain damage. (3) Autopsies of individuals in this study, revealed the same characteristic brain lesions, neurofibrillary tangles and beta-amyloid plaque, associated with AD.
Whether self reported or observed by a physician, the typical memory loss, or other cognitive impairment, needs to be differentiation from other disorders including depression, drug side effects, and hormonal or nutritional imbalances. Unfortunately, MCI as an early indicator of an advanced risk for developing AD is not assessed routinely in patients that present with memory lapses, or other cognitive problems. Senior moments are often written off as normal age-related memory loss. Due to this fact, a large proportion of patients with MCI may remain undiagnosed until the cognitive decline is more noticeable, or advanced signs of frank dementia or AD are obvious.
In the early stages, MCI may appear or be interpreted as normal aging by either the individual that is affected, those close to him or her, or to the untrained professional. Fortunately, due to the increased awareness of the Alzheimer’s issue in the aging population, many individuals are now expressing concern to their physicians about memory loss. Indeed, the early detection of cognitive problems that represent the early signs of MCI is critical for preventing the progression to, or at the very least, delaying the development of AD.
The problem in diagnosing MCI lies in part with the fact that in the past, cognitive decline in an aging individual was often classified as degeneration associated with a normal aging process. MCI, and its subtypes, is a more recent construct and classification of cognitive impairment, that represents a nuerodegenerative disease process. (4) Prior to the emergence of MCI, and MCI subtypes, as a diagnosable clinical entity, terms such as “benign senescent forgetfulness” and “age-associated memory impairment” (AAMI) were the default labels given to those aging individuals that presented with memory loss. Granted, there is still some resistance, and flat rejection of MCI as a clean window of assessment for a neurodegenerative disease process. (5) Yes, not all diagnosed with MCI progress to dementia or AD. It is not uncommon for a less severe form of MCI (single domain nonamnestic subtype) to revert back to normal. (6) However, the consensus is growing toward the point of this article; the diagnosis of MCI, especially at first signs, may provide the opportunity for prevention of a more serious degenerative disease process. There is now significant and inarguable evidence that demonstrates that MCI can be assessed and identified by objective and measurable testing such as specialized PET scans and MRIs.
Again, the conversion of MCI to AD in any individual will be influenced by a host of factors. Lifestyle, nutrition, stress, education, hormonal factors and genetics will weigh heavily into whether or not one progresses from MCI to dementia or AD. These same factors are the modifiers that determine if a person diagnosed with MCI can delay or prevent the conversion to dementia and AD, or in less complicated cases, revert back to normal. Optimizing brain nutrition can be one of the most powerful interventions for stabilizing and improving brain function.
The early stages of MCI in an individual appear as subtle changes that may not always be noticeable, unless observed by a trained professional, or by a family member or friend that is close to that person. Individuals in the early stages of MCI are functional and will compensate for some impairment by making lists and notes to support daily activities and responsibilities. Independence can actually be maintained for years.
Signs that may signal the onset of MCI are:
• Memory loss – recent recall diminishes, such as what one did yesterday, repeatedly misplacing objects
• Language - difficulty communicating…inability to recall and integrate words into a conversation, or to follow one
• Visuospatial ability – placement of things in time and space becomes more difficult – i.e. having trouble getting the proportions right when drawing a box
• Executive function - difficulty with decision making, planning and organizing
These patterns of cognitive dysfunction have recently been categorized into MCI subtypes.
MCI is differentiated into two basic subtypes:
• amnestic MCI and…
Amnestic MCI is defined as MCI with memory loss, while non-amnestic MCI represents MCI with little or no memory loss, but with other cognitive function impairment (language, visuospatial ability, executive function).
Similarly, in what is considered to be a subtype of amnestic MCI, multiple cognitive domain amnestic-MCI, may include memory loss and the other domains of impairment associated with non-amnestic MCI (visuospatial ability, judgment and language problems – see chart below).
Besides having little or no memory loss associated with it, non-amnestic MCI (single domain), and its subtype, non-amnestic multiple cognitive domain-MCI, includes problems with visuospatial ability, judgment (executive function), or language. (3) If the non-amnestic MCI presents with only a single area of impairment, then it is classified as single cognitive domain non-amnestic MCI.
So we have the two basic subtypes of MCI, amnestic MCI and non-amnestic MCI, and two additional subtypes:
• amnestic MCI and…
Either type of MCI can convert to a dementia diagnosis (. i.e. vascular dementia) or AD, and the classifications may serve to predict the probability of conversion to AD, or the type of dementia that an individual diagnosed with MCI is at risk for. Several studies indicate a higher conversion for amnestic MCI to AD. (7) The greater memory loss, the more severe the impairment may be, and the higher the risk for the impairment progressing to AD.
Cardiovascular disease and diabetes are risk factors for AD. Not surprisingly, these same degenerative disorders, are linked to MCI as well (comormid conditions). In a significant and large population–based Study of Aging conducted at Mayo clinic, patients with history of stroke (cerebrovascular disease) were found to have higher (three times) risk of non-amnestic MCI. Diabetics that had a more advanced form of the disease, doubled their chances for non-amnestic MCI. Similarly patients with other vascular diseases like hypertension and coronary heart diseases were found to be at higher risk of having non-amnestic-MCI. (8) Some research indicates a more likely progression to vascular dementia from non-amnestic-MCI. Similarly, non-amnestic-MCI is associated with the conversion to frontotemporal dementia and dementia with Lewy bodies. (9) Again, individuals with amnestic-MCI are thought to be more likely converters to AD.
The ApoE4 gene variant (please read article: The Alzheimer’s Gene Puzzle – Genetic Links To Late Onset Alzheimer’s Disease-Part 1), a risk factor for AD in and of itself, is linked to MCI and the conversion of MCI to AD as well. Carriers of the ApoE4 gene (genotypes) are more likely to develop amnestic MCI, and ApoE4 genotypes diagnosed with amnestic MCI patients are more likely to progress to AD. (10) Not a surprising link. It is my strong recommendation that if you are diagnosed with MCI, to have an ApoE gene test done. Anyone with MCI, especially amnestic MCI, and who is a carrier of the ApoE4 variant, should have an aggressive dietary, lifestyle and nutritional plan implemented immediately. If it is not part of the current history, assessments for inflammation and oxidative stress should be integrated into a complete health evaluation. Antioxidants have demonstrated in clinical studies to protect and delay progression of AD in at risk individuals. Key nutrients that are important factors in brain health and that are linked to a greater risk for developing AD and/or dementia if deficient, are folate , B12 , Vitamin D , and Vitamin K . Antioxidants and a host of other brain function supportive nutraceuticals such as Acetyl-L-Carnitine , and Phosphatidyl Serine , should also be considered for supplementation. Thyroid function, as well as estrogen and testosterone levels should be checked.
Undoubtedly, the exclusion of, or the definitve diagnosis of MCI, particularly in more at risk individuals with memory and cognitive problems, should be determined as early as possible. Fortunately, there is technology now available that can alert providers and their at risk patients, as to how large that risk may be for conversion of MCI to AD. Please look for my coming articles that overview on how you can screen for the underlying brain damage that is occuring in MCI, and the important nutrients that can help to preserve your vital brain.
This video from a HBO documentary, “The Alzheimer’s Project: Identifying Mild Cognitive Impairment”, is highly recommended.
1. Mild cognitive impairment represents early-stage Alzheimer disease.
Morris JC, Storandt M, Miller JP, McKeel DW, Price JL, Rubin EH, Berg L.
Arch Neurol. 2001 Mar;58(3):397-405.
Authors: José León-Carrión, Margaret Joan Giannini
Markesbery WR, Schmitt FA, Kryscio RJ, et al.
Arch Neurol. Jan 2006;63(1):38-46
Ronald C. Petersen, MD, PhD, and Selamawit Negash, PhD
CNS Spectr. 2008;13(1):45-53
5. Mild Cognitive Impairment Is Not a Clinical Entity and Should Not Be Treated
Gauthier and Touchon
Arch Neurol.2005; 62: 1164-1166.
6. Quantification of Five Neuropsychological Approaches to Defining Mild Cognitive Impairment
Jak, Amy J. Ph.D.; Bondi, Mark W. Ph.D.; Delano-Wood, Lisa Ph.D.; Wierenga, Christina Ph.D.; Corey-Bloom, Jody M.D., Ph.D.; Salmon, David P. Ph.D.; Delis, Dean C. Ph.D.
American Journal of Geriatric Psychiatry. May 2009 – Volume 17 – Issue 5 – pp 368-375
7. Importance of Subtle Amnestic and Nonamnestic Deficits in Mild Cognitive Impairment: Prognosis and Conversion to Dementia
S.D. Rountree, S.C. Waring, W.C. Chan, P.J. Lupob, E.J. Darby, R.S. Doody
Dement Geriatr Cogn Disord 2007;24:476-482
R. Petersen, R. Roberts, D. Knopman, Y. Geda, V. Pankratz, B. Boeve, W. Rocca
Alzheimer’s and Dementia, Volume 4, Issue 4, Pages T130-T130
Boeve B, Ferman TJ, Smith GE, et al.
Neurology. 2004;62(suppl 5):A86.
Gauthier S, Reisberg B, Zaudig M, Petersen RC, Ritchie K, Broich K, Belleville S, Brodaty H, Bennett D, Chertkow H, Cummings JL, de Leon M, Feldman H, Ganguli M, Hampel H, Scheltens P, Tierney MC, Whitehouse P, Winblad B; International Psychogeriatric Association Expert Conference on mild cognitive impairment.
Lancet. 2006 Apr 15;367(9518):1262-70.