Mild cognitive impairment

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Mild cognitive impairment
Classification and external resources
Specialtypsychiatry, neurology, neuropsychology
ICD-10F06.7
ICD-9-CM331.83
Patient UKMild cognitive impairment
MeSHD060825

Mild cognitive impairment (MCI), also known as incipient dementia and isolated memory impairment, is a neurological disorder that occurs in older adults which involves cognitive impairments with minimal impairment in instrumental activities of daily living.[1] MCI involves the onset and evolution of cognitive impairments beyond those expected based on an individual's age and education, but which are not significant enough to interfere with her or his daily activities.[2] It may occur as a transitional stage between normal aging and dementia. The specific etiology of the disorder remains unclear, as well as its prevention and treatment.

Types[edit]

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.[3] Studies suggest that these individuals tend to progress to probable Alzheimer's disease at a rate of approximately 10% to 15% per year.[3]

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).[4]

Causes[edit]

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.

Risk factors of both dementia and MCI are considered to be the same. They are ageing, genetic (heredity) cause of Alzheimer’s or other dementia, and risk of cardiovascular disease.[5]

Oxidative damage[edit]

Individuals with MCI have increased oxidative damage in their nuclear and mitochondrial brain DNA.[6] A widely studied biomarker of DNA damage, 8-hydroxyguanine was found to be elevated in nuclear DNA of the frontal and temporal lobe of individuals with MCI and in mitochondrial DNA of the temporal lobe compared with age matched control subjects.[6] Other oxidized DNA bases were also increased in the brains of individuals with MCI. These findings suggested that oxidative damage to DNA occurs in the earliest detectable phase of Alzheimer’s disease and thus may play a significant role in the pathogenesis of this disease[6](see Aging brain).

Diagnosis[edit]

The diagnosis of MCI requires considerable clinical judgement,[3] 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:[7]

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

Neuropathology[edit]

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.[8] Alternatively, many individuals develop neurofibrillary tangles without amyloid, a pattern termed primary age-related tauopathy.

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.[9] 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.[10] Such tools may help greatly in assisting clinical research for therapies.

Treatment[edit]

As of January 2018, there are no USFDA-approved medications for the treatment of mild cognitive impairment.[1] Moreover, as of January 2018, there is no high-quality evidence that supports the efficacy of any pharmaceutical drugs or dietary supplements for improving cognitive symptoms in individuals with mild cognitive impairment.[1] A moderate amount of high-quality evidence supports the efficacy of regular physical exercise for improving cognitive symptoms in individuals with MCI.[1] The clinical trials that established the efficacy of exercise therapy for MCI involved twice weekly exercise over a period of six months.[1] A small amount of high-quality evidence supports the efficacy of cognitive training for improving some measures of cognitive function in individuals with mild cognitive impairment.[1] Due to the heterogeneity among studies which assessed the effect of cognitive training in individuals with MCI, there are no particular cognitive training interventions that have been found to provide greater symptomatic benefits for MCI relative to other forms of cognitive training.[1]

The American Academy of Neurology's (AAN) clinical practice guideline on mild cognitive impairment from January 2018 stated that clinicians should identify modifiable risk factors in individuals with MCI, assess functional impairments, provide treatment for any behavioral or neuropsychiatric symptoms, and monitor the individual's cognitive status over time.[1] It also stated that medications which cause cognitive impairment should be discontinued or avoided if possible.[1] Due to the lack of evidence supporting the efficacy of cholinesterase inhibitors in individuals with MCI, the AAN guideline stated that clinicians who choose to prescribe them for the treatment of MCI must inform patients about the lack of evidence supporting this therapy.[1] The guideline also indicated that clinicians should recommend that individuals with MCI engage in regular physical exercise for cognitive symptomatic benefits;[1] clinicians may also recommend cognitive training, which appears to provide some symptomatic benefit in certain cognitive measures.[1]

As MCI may represent a prodromal state to clinical Alzheimer's disease, treatments proposed for Alzheimer's disease, such as antioxidants and cholinesterase inhibitors, could potentially be useful;[medical citation needed][dubious ] however, As of January 2018, there is no evidence to support the efficacy of cholinesterase inhibitors for the treatment of mild cognitive impairment.[1] 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;[11] donepezil showed only minor, short-term benefits and was associated with significant side effects.[12]

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,[13] dementia, and cardiovascular disease.[14][15][16] A single study from 2012 showed a possible connection between macronutrient intake and development of MCI. It is also suggested that a dietary pattern with relatively high caloric intake from carbohydrates and low caloric intake from fat and proteins may increase the risk of MCI or dementia in elderly persons [17]

Experimental non-pharmacological treatments for MCI include transcranial magnetic stimulation and transcranial direct current stimulation;[18][19] the efficacy of these interventions for the treatment of MCI has not yet been established.

Prevalence[edit]

The prevalence of MCI varies by age.[1] The prevalence of MCI among different age groups is as follows: 6.7% for ages 60–64; 8.4% for ages 65–69, 10.1% for ages 70–74, 14.8% for ages 75–79, and 25.2% for ages 80–84.[1] After a two-year follow-up, the cumulative incidence of dementia among individuals who are over 65 years old and were diagnosed with MCI was found to be 14.9%.[1]

Globally, approximately 16% of the population over the age of 70 experiences some type of mild cognitive impairment.[14][15]

Outlook[edit]

MCI does not usually interfere with daily life, but around 50 percent of people diagnosed with it go on to develop the far more severe Alzheimer's disease within five years.[14] However, some instances of MCI may simply remain stable over time or even remit[citation needed].

References[edit]

  1. ^ a b c d e f g h i j k l m n o p Petersen RC, Lopez O, Armstrong MJ, Getchius T, Ganguli M, Gloss D, Gronseth GS, Marson D, Pringsheim T, Day GS, Sager M, Stevens J, Rae-Grant A (January 2018). "Practice guideline update summary: Mild cognitive impairment – Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology". Neurology. Special article. 90 (3): 1–10. doi:10.1212/WNL.0000000000004826. PMC 5772157. PMID 29282327. Lay summaryExercise may improve thinking ability and memory (27 December 2017). In patients with MCI, exercise training (6 months) is likely to improve cognitive measures and cognitive training may improve cognitive measures. ... Clinicians should recommend regular exercise (Level B). ... Recommendation
    For patients diagnosed with MCI, clinicians should recommend regular exercise (twice/week) as part of an overall approach to management (Level B).
  2. ^ Petersen RC, Smith GE, Waring SC, Ivnik RJ, Tangalos EG, Kokmen E (1999). "Mild cognitive impairment: clinical characterization and outcome". Arch. Neurol. 56 (3): 303–8. doi:10.1001/archneur.56.3.303. PMID 10190820.
  3. ^ a b c Grundman M, Petersen RC, Ferris SH, et al. (2004). "Mild cognitive impairment can be distinguished from Alzheimer disease and normal aging for clinical trials". Arch. Neurol. 61 (1): 59–66. doi:10.1001/archneur.61.1.59. PMID 14732621.
  4. ^ Tabert MH, Manly JJ, Liu X, et al. (2006). "Neuropsychological prediction of conversion to Alzheimer disease in patients with mild cognitive impairment". Arch. Gen. Psychiatry. 63 (8): 916–24. doi:10.1001/archpsyc.63.8.916. PMID 16894068.
  5. ^ "Mild Cognitive Impairment". Alzheimer's Association. Retrieved July 9, 2017.
  6. ^ a b c Wang J, Markesbery WR, Lovell MA (February 2006). "Increased oxidative damage in nuclear and mitochondrial DNA in mild cognitive impairment". J. Neurochem. 96 (3): 825–32. doi:10.1111/j.1471-4159.2005.03615.x. PMID 16405502.
  7. ^ Morris, J C.; Storandt, M.; Miller, J. P.; McKeel, D. W.; Price, J. L.; Rubin, E.H. & Berg, L. (2001). "Mild cognitive impairment represents early-stage Alzheimer disease". Archives of Neurology. 58 (3): 387–405. doi:10.1001/archneur.58.3.397.
  8. ^ Petersen RC, Parisi JE, Dickson DW, et al. (2006). "Neuropathologic features of amnestic mild cognitive impairment". Arch. Neurol. 63 (5): 665–72. doi:10.1001/archneur.63.5.665. PMID 16682536.
  9. ^ Whitwell JL, Shiung MM, Przybelski SA, et al. (2008). "MRI patterns of atrophy associated with progression to AD in amnestic mild cognitive impairment". Neurology. 70 (7): 512–20. doi:10.1212/01.wnl.0000280575.77437.a2. PMC 2734138. PMID 17898323.
  10. ^ Jack CR, Lowe VJ, Senjem ML, et al. (2008). "11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment" (PDF). Brain. 131 (Pt 3): 665–80. doi:10.1093/brain/awm336. PMC 2730157. PMID 18263627.
  11. ^ Feldman HH, Ferris S, Winblad B, et al. (2007). "Effect of rivastigmine on delay to diagnosis of Alzheimer's disease from mild cognitive impairment: the InDDEx study". Lancet Neurol. 6 (6): 501–12. doi:10.1016/S1474-4422(07)70109-6. PMID 17509485.
  12. ^ Birks J, Flicker L (2006). Birks J, ed. "Donepezil for mild cognitive impairment". Cochrane Database Syst Rev. 3 (3): CD006104. doi:10.1002/14651858.CD006104. PMID 16856114.
  13. ^ McCaddon, A.; et al. (2001). "Homocysteine and cognitive decline in healthy elderly". Dement Geriatr Cogn Disord. 12 (5): 309–313. doi:10.1159/000051275. PMID 11455131.
  14. ^ a b c Kelland, Kate (September 8, 2010). "B vitamins found to halve brain shrinkage in old". Reuters. Retrieved July 8, 2017.
  15. ^ a b Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, Oulhaj A, Bradley KM, Jacoby R, Refsum H (2010). "Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: A Randomized Controlled Trial". PLoS ONE. 5 (9): e12244. Bibcode:2010PLoSO...512244S. doi:10.1371/journal.pone.0012244. PMC 2935890. PMID 20838622.
  16. ^ Ravaglia, G.; Forti, P.; Maioli, F.; Matelli, M.; Servadei, L.; Nicoletta, B.; Porcellini E. & 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.
  17. ^ Rosebud O. Roberts, Lewis A. Roberts, Yonas E. Geda, Ruth H. Cha, V. Shane Pankratz, Helen M. O’Connor, David S. Knopman, and Ronald C. Petersen (2012). "Relative Intake of Macronutrients Impacts Risk of Mild Cognitive Impairment or Dementia" (PDF). Journal of Alzheimer's Disease. 32 (2): 329–339. doi:10.3233/JAD-2012-120862. PMC 3494735. PMID 22810099.
  18. ^ 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. doi:10.7287/peerj.preprints.1610v1.
  19. ^ Yun, Kyongsik; Song, In-Uk; Chung, Yong-An (2016-01-01). "Changes in cerebral glucose metabolism after 3 weeks of noninvasive electrical stimulation of mild cognitive impairment patients". Alzheimer's Research & Therapy. 8 (1): 49. doi:10.1186/s13195-016-0218-6. ISSN 1758-9193. PMC 5131431. PMID 27903289.

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