Age-related changes in brain function can be classified as “mild cognitive assessment.” This isn’t dementia. It’s not as bad as dementia. Impairment may include short-term memory, long-term memory, executive function/attention, language, and visuospatial skills domains. Complex tasks may become more difficult, and the person’s social skills may decline and they may have apathy or depression. Cognitive abilities underlyi the mechanisms of intelligence, so a person with MCI loses some intelligence, although he or she may still be smart. Amnesic MCI is when the person forgets things (people, location of objects, conversations). Non-amnestic MCI doesn't show up as memory loss, but the person may find it harded to hold a conversation and may get mixed up doing routine daily activities.
MCI isn’t a disease. It can be called a neurocognitive disorder. It can be considered a prodrome or precursor to dementia, but it’s not so simple that all MCI leads to dementia. There is no biomarker for MCI - nothing in the person’s body that indicates this condition. Doctors employ “clinical diagnosis” to establish if someone has it. If a patient has symptoms the doctor may search for other diseases that cause them; MCI is what’s left if there is no obvious cause. There is no known cause for MCI just as there is no known cause for Alzheimer's disease. Researchers have identified a gene called APOE-e4 that seems to be present in many patients with Alzheimer’s and MCI, but there no causal link between the gene and the conditions have been shown.
MCI is a true syndrome more than a defined disease. Indeed there is a wide range of cognitive and functional severity among MCI patients.
The person with MCI may notice he or she has reduced capacity and friends and family may also notice. There are tests health care professionals can administer but there is no immediate need to do so. MCI does not typically interfere with the patient’s day to day life. Further, the dividing line between decline due to normal aging and MCI is not firm. The occasional "senior moment" does not indicate MCI if it does not affect the person's life.
MCI a clinical diagnosis. People have tried to find cerebrospinal fluid biomarkers or indicatots in brain images but the way doctors call out MCI is still through a combination of patient self-report, family member self-reports, cognitive tests.
Because it is hard to identify and because diagnostic criteria are unclear and subjective, estimates of incidence and prevalence are all over the place.
Some researchers are classifying patients as having MCI because of underlying AD pathology. In this view, the MCI would be a manifestation of early Alzheimer’s. This is hard to do in a clinical setting because there are no biomarkers for Alzheimer’s in common use; AD is diagnosed by clinical observation the same way MCI is. Retrospectively, we might be able to say a patient had this type of MCI once full blown AD has emerged.
MCI patients can (1) get worse - advance to dementia, (2) remain in MCI, or (3) get better. If a patient has impairment in multiple domains it generally indicates a greaters stage of progression than MCI with impairment in only one area. It is estimated that 20 percent of patients improve in cognitive function although some of them later regress. Indeed, patients who improve to normal function are more likely to later develop dementia than those who never had MCI.
When memory problems are particularly evident the condition can be classified as amnesic MCI (aMCI). There is some thought that this type of impairment is due to neurodegeneration while MCI without amnesia is due to vascular damage https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3081688/ but so much is unknown.
Some geriatricians consider subjective cognitive decline, which is when patients report they cannot think as clearly or remember as much as they once could, but when the decline is not evident on formal tests. It is known that SCD often leads to objective cognitive decline, mild cognitive impairment, and perhaps dementia.
While the term has not been as widely adopted, another classification is Cognitively Impaired, Not Demented (CIND). The boundaries between CIND and MCI are unclear as the definitions for both specify that the patient not show signs of dementia but does show indication of reduced cognitive capacity from the past (either identified by the patient himself or herself or a low score on a mini IQ test administered by a health care professional.) CIND can be applied to younger patients who suffer diminished cognitive capacity due to drug use, injury, etc. MCI is usually applied to older patients.
Vascular illnesses or conditions that affect the vascular system are risk factors. That is, if a person has a risk factor, he or she is more likely to develop MCI. Is MCI merely an early or mild form of vascular dementia? Maybe, but MCI often precedes other forms of dementia also, so it might not be so straightforward. Using advanced medical imaging, scientists can identify plaques inside the brains of patients with Alzheimer's. These plaques are considered a hallmark of Alzheimer's although how of if they actually cause the disease is unknown. Imaging of patients with MCI shows the same plaques, although at lower densities that in Alzheimer's patients.
Other risk factors:
Most studies that have found MCI happens more in men, but some find no difference between sexes and at least one found higher prevalence in women. There is also the presence of the Apoplipoprotein e4 allele in the person's genome which might be a factor. That allele is suspected to be related to Alzheimer's disease.
Can we take measures to reduce the risk of MCI?
More years of education, regular exercise, and a healthy diet appear to help. In particular, the Mediterranean diet rich in monounsaturated and polyunsaturated fats appears protective. Also, keeping engaged with others and with cognitively stimulating tasks helps.
MCI sometimes progresses to dementia - it is estimated that this happens in a quarter to a third of people - but some patients live with it for years. Whether (some) cases of MCI are simply the early stage of Alzheimer's Disease is not clear.
It is possible for people with MCI to get better - experienced increased cognitive capacity. By one estimate 20 percent of MCI patients show better cognitive capacity of a subsequent evaluation, although this does not necessarily mean the patient is back to normal - no evidence of MCI. And even people who do get better still have a greater risk for falling into dementia in the future.
Some of the risk factors for MCI can be alleviated, but there is no direct medical intervention that stops MCI or prevents it from getting worse. If high blood pressure causes MCI (which is not proven; it is more correct to say that hypertension is a risk factor for MCI), we have ways to lower blood pressure.
No treatment for MCI is approved by the FDA. The acetylcholinesterase inhibitors used to treat dementia are not used for MCI. Many herbal supplements are sold that promise to help with memory, but these are unregulated and there is no medical consensus they work. Scientists have tried giving MCI patients the drugs used to treat Alzheimer’s (cholinesterase inhibitors and memantine) in hope that this will forestell the onset of dementia, but there is no evidence these help. Even so, the National Institute on Aging recommendeds people with MCI see a doctor regularly to keep tabs on the condition.
Mentally engaging games such as bridge and chess have been shown to help seniors maintain high scores on IQ tests, but it is not known whether this applies to people with MCI or dementia.
Cognitive fitness is a term for procedures and practices people can do to prevent the onset of mild cognitive impairment, dementia, or any loss of mental functioning. It is supposed to be analogous to physical fitness, which may be defined as the ability of the body to respond to set challenges and to allow the person to thrive.
Framing brain function in terms of cognitive fitness puts the emphasis on what a person can do to stay sharp, rather than the passive approach of accepting decline as an inevitable disease. The recommendations for maintaining cognitive fitness are familiar: eat right, exercise, get enough sleep, have a social life, don't live with high levels of stress, and challenge yourself through puzzles, reading, learning new things.
How we think - how our brain does what it does - may affect how resilient we are to impairment. The brain is still little misunderstood so psychologists and neuoroscientists have come up with the idea of cognitive reserve to describe this ability to cope with disease or injury to the brain. Although not fully characterized, the connection between prevalence of dementia and life experiences are taken seriously by gerontologists. Educational achievement may correlate with cognitive reserve. People who used their brain for much of their lives are better able to cope with illness.
Brain reserve refers to the brain's actual physical capacity and neural networks, which can vary in size and number of neurons between individuals. People with greater brain volume and synapse counts may have more reserve to endure age-related and disease-related changes before clinical symptoms manifest.
In contrast, cognitive reserve reflects the brain's more functional resilience and efficient utilization of networks to aid cognition. Even with brain pathologies, people with higher cognitive reserve can make flexible use of alternate networks and cognitive paradigms to get around limitations better.
In other words:
Brain reserve is quantitative and passive - It dictates how much damage can accumulate before functions are impaired based on fixed structural capacities like volume.
Cognitive reserve is more qualitative and active - It dictates how flexibly networks adapt to damage and make use of backups. It has to do with making efficient use of resources available.
Both concepts play a role. People with innately more neural hardware (brain reserve) likely also develop enhanced cognitive approaches. Therapies aim to boost both by enhancing hardware capacities and efficiency of resources through stimulation and training to delay functional decline.
MCI is a clinical diagnosis; there is no medical sign that shows up in a laboratory test. Healthcare professionals have many cognitive tests they can use to assess a patient’s cognitive abilities. The Montreal Cognitive Assessment https://www.mocatest.org was originally developed to help screen for mild cognitive impairment. The Abbreviated Mental Test Score (AMTS), a 10-item scale, takes only 3–4 min to administer. And the Mini-Mental State Examination is widely used.
The Alzheimer's Association website recommends some assessment tests. These include the Mini-Cog (which can be done in three minutes), the General Practitioner Assessment of Cognition (website), the Short Informant Questionnaire on Cognitive Decline in the Elderly, and the Eight-item Interview to Differentiate Aging and Dementia. Sometimes friends and family get involved.
Do doctors do these tests for MCI? Usually no. There is little action if the person has MCI so many feel there is little reason to diagnose it.
See also: the Super Ager