State of the science on mild cognitive impairment (MCI)

Abstract

Mild cognitive impairment (MCI) represents a transitional stage between healthy aging and dementia, and affects 10–15% of the population over the age of 65. The failure of drug trials in Alzheimer’s disease (AD) treatment has shifted researchers’ focus toward delaying progression from MCI to dementia, which would reduce the prevalence and costs of dementia profoundly. Diagnostic criteria for MCI increasingly emphasize the need for positive biomarkers to detect preclinical AD. The phenomenology of MCI comprises lower quality-of-life, greater symptoms of depression, and avoidant coping strategies including withdrawal from social engagement. Neurobiological features of MCI are hypoperfusion and hypometabolism in temporoparietal cortices, medial temporal lobe atrophy particularly in rhinal cortices, elevated tau and phosphorylated tau and decreased Aβ42 in cerebrospinal fluid, and brain Aβ42 deposition. Elevated tau can be identified in MCI, particularly in the entorhinal cortex, using positron emission tomography, and analysis of signal complexity using electroencephalography or magnetoencephalography holds promise as a biomarker. Assessment of MCI also relies on cognitive screening and neuropsychological assessment, but there is an urgent need for standardized cognitive tests to capitalize on recent discoveries in cognitive neuroscience that may lead to more sensitive measures of MCI. Cholinesterase inhibitors are frequently prescribed for MCI, despite the lack of evidence for their efficacy. Exercise and diet interventions hold promise for increasing reserve in MCI, and group psychoeducational programs teaching practical memory strategies appear effective. More work is needed to better understand the phenomenology and neurobiology of MCI, and how best to assess it and delay progression to dementia.

Alterations in resting-state network dynamics along the Alzheimer’s disease continuum: a combined MEG-PET/MR approach

“…For its part, MCI is characterized by concerns regarding a change in cognitive capabilities confirmed by an objective deficit (i.e. performance below the norms for the reference population) in one or more cognitive function(s) without an impact on everyday activities 17 (for a recent review, see 18 ).…”

Feasibility of a Functional Medicine Approach to Slowing Clinical Cognitive Decline in Patients over Age 55: A Multiple Case Study Report

“…MCI represents the stage between healthy age-related cognitive decline and dementia but does not always progress to dementia. MCI affects 10% to 15% of people over 65, and the prevalence increases with age [1]. The American Academy of Neurology diagnostic and treatment guidelines for MCI include recommendations to (a) assess with validated screening tools, (b) monitor ongoing cognitive condition, (c) encourage physical exercise and cognitive training interventions, and (d) discuss the current absence of evidence for effective drug treatment [2].…”

“…However, to date there is no definitive remedy, drug, or cure for dementia or cognitive decline [3]. Pharmaceutical interventions such as memantine or cholinesterase inhibitors have been the first-line treatment of many medical practitioners, regardless of the lack of evidence for effectiveness [1][2][3][4]. Yet recent studies abound with recognition of lifestyle changes, such as diet and exercise, for amelioration of cognitive decline [5][6][7].…”

Relationship between subjective memory complaints and social and leisure activities in community‐dwelling older people: Toyoake Integrated Care Study

“…Although there are few studies on social activities as an outcome of subtle cognitive decline, we often observe, in the clinical setting, withdrawal from social/leisure activities by patients in the very early stage of dementia. 13 However, there are few studies that examine the association between SMC and changes in social and leisure activities. [14][15][16][17] The fact that social and leisure activities are not obligatory in life might explain the lack of investigations into the preclinical stage of dementia.…”