Mild cognitive impairment

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Mild cognitive impairment
Classification and external resources
Specialty Lua error in Module:Wikidata at line 446: attempt to index field 'wikibase' (a nil value).
ICD-10 F06.7
ICD-9-CM 331.83
Patient UK Mild cognitive impairment
MeSH D060825
[[[d:Lua error in Module:Wikidata at line 863: attempt to index field 'wikibase' (a nil value).|edit on Wikidata]]]

Mild cognitive impairment (MCI, also known as incipient dementia, or isolated memory impairment) is a brain function syndrome involving the onset and evolution of cognitive impairments beyond those expected based on the age and education of the individual, but which are not significant enough to interfere with their daily activities.[1] It may occur as a transitional stage between normal aging and dementia. Although MCI can present with a variety of symptoms, when memory loss is the predominant symptom it is termed "amnestic MCI" and is frequently seen as a prodromal stage of Alzheimer's disease.[2] Studies suggest that these individuals tend to progress to probable Alzheimer’s disease at a rate of approximately 10% to 15% per year.[2]

Additionally, when individuals have impairments in domains other than memory it is classified as nonamnestic single- or multiple-domain MCI and these individuals are believed to be more likely to convert to other dementias (e.g., dementia with Lewy bodies).[3] However, some instances of MCI may simply remain stable over time or even remit. Causation of the syndrome in and of itself remains unknown, as therefore do prevention and treatment.

Causes

According to some experts, mild cognitive impairment (MCI) may be caused due to alteration in the brain triggered during early stages of Alzheimer’s disease or other forms of dementia. However, exact causes of MCI are still unknown.

But, risk factors of both dementia and MCI are considered to be the same. They are aging, genetic (heredity) cause of suffering from Alzheimer’s or other dementia, and risk of cardiovascular disease. [4]

Diagnosis

The diagnosis of MCI requires considerable clinical judgement,[2] and as such a comprehensive clinical assessment including clinical observation, neuroimaging,[medical citation needed] blood tests and neuropsychological testing are best in order to rule out an alternate diagnosis. MCI is diagnosed when there is:[5]

  1. Evidence of memory impairment
  2. Preservation of general cognitive and functional abilities
  3. Absence of diagnosed dementia

Neuropathology

There is evidence suggesting that although amnestic MCI patients may not meet neuropathologic criteria for Alzheimer's disease, patients may be in a transitional stage of evolving Alzheimer's disease; patients in this hypothesized transitional stage demonstrated diffuse amyloid in the neocortex and frequent neurofibrillary tangles in the medial temporal lobe.[6]

There is emerging evidence that magnetic resonance imaging can observe deterioration, including progressive loss of gray matter in the brain, from mild cognitive impairment to full-blown Alzheimer disease.[7] A technique known as PiB PET imaging is used to clearly show the sites and shapes of beta amyloid deposits in living subjects using a C11 tracer that binds selectively to such deposits.[8] Such tools may help greatly in assisting clinical research for therapies.

Treatment

There is no proven treatment or therapy for mild cognitive impairment. As MCI may represent a prodromal state to clinical Alzheimer’s disease, treatments proposed for Alzheimer’s disease, such as antioxidants and cholinesterase inhibitors, may be useful.[medical citation needed][dubious ] Two drugs used to treat Alzheimer's disease have been assessed for their ability to treat MCI or prevent progression to full Alzheimer's disease. Rivastigmine failed to stop or slow progression to Alzheimer's disease or to improve cognitive function for individuals with mild cognitive impairment,[9] and donepezil showed only minor, short-term benefits and was associated with significant side effects.[10]

A new form of magnesium, namely magnesium l–threonate, has surfaced as a promising avenue in the treatment of cognitive impairment. This form is capable of delivering high amounts of magnesium to the central nervous system and has in preclinical animal studies shown remarkable results, even reversing full-blown dementia in some cases.[11] These findings have now been replicated in the first double-blind placebo controlled human trial which showed similar efficacy in treating cognitive impairment as the animal studies.[12] If corroborated by further human studies this could very well be a landmark in the treatment of age-related cognitive impairment (for which there is presently no effective treatment). The results of this study are also in line with systematic reviews showing that Alzheimer’s patients have lower magnesium status when compared to healthy controls.[13] Despite its apparent simplicity, just replenishing the brains stores of a vital mineral, this study parallels recent findings in other domains of neurobiology, for example the finding that a new copper formulation is able to halt the progression of amyotrophic lateral sclerosis.[14]

In a two-year randomized trial of 168 people with MCI given either high-dose vitamins or placebo, vitamins cut the rate of brain shrinkage by up to half. The vitamins were the three B vitamins folic acid, vitamin B6, and vitamin B12, which inhibit production of the amino acid homocysteine. High blood levels of homocysteine are associated with increased risk of cognitive decline,[15] dementia, and cardiovascular disease.[16][17][18]

Non-pharmacological experimental treatments include transcranial magnetic stimulation and transcranial direct current stimulation.[19]

References

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  4. Mild Cognitive Impairment, Retrieved 3rd February 2016.
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  16. Kelland, K. (2010). B vitamins found to halve aging brain shrinkage. Reuters Health.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  17. Lua error in Module:Citation/CS1/Identifiers at line 47: attempt to index field 'wikibase' (a nil value).
  18. Ravaglia, G. Forti, P., Maioli, F., Matelli, M., Servadei, L., Nicoletta, B., Elisa, Porcellini & Licastor, F. (2005). "Homocysteine and folate as risk factors for dementia and Alzheimer disease". the American Journal of Clinical Nutrition. 82 (3): 636–643. PMID 16155278. <templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  19. Alencastro, A.S., Pereira, D.A., Brasil-Neto, J.P. (2015). "Transcranial direct current stimulation in mild cognitive impairment: methodology for a randomized controlled trial". PeerJ PrePrints. 3:e1610v1. <templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>

External links