INTRODUCTION — The concept of mild cognitive impairment (MCI) as an intermediate state between normal cognition and dementia has been long recognized. While a gradual decline in cognition is a characteristic of normal aging, there is increasing evidence that some forms of cognitive impairment are recognizable as an early manifestation of dementia [1].
This topic review will discuss MCI. Topics related to dementia, including diagnosis, treatment, risk factors, and prevention of dementia, are discussed separately. (See "Dementia syndromes" and see "Treatment of dementia" and see "Risk factors for dementia" and see "Prevention of dementia").
DEFINITIONS — Mild cognitive impairment (MCI) refers to cognitive impairment that does not meet the criteria for dementia. Various researchers have proposed several criteria for and subtypes of MCI [1-3]. These criteria and subtypes differ somewhat, although there is considerable overlap. The Mayo criteria are the ones most commonly applied in the literature [4]:
Memory complaint, preferably corroborated by an informant
Objective memory impairment (for age and education)
Preserved general cognitive function
Intact activities of daily living
Not demented
It is important to emphasize that these criteria are imprecise. Considerable judgment is involved in making the distinction between impairments that are normal for the elderly population and, on the other extreme, that do not represent dementia. Also, some investigators challenge the inclusion of intact activities of daily living as a criterion [5,6]. These and other judgments likely differ between assessors and account for some of the conflicting results in studies of this disorder.
MCI is heterogeneous in terms of clinical presentation, etiology, and prognosis [3,7,8]. There are now accepted definitions for subclasses of MCI: amnestic MCI, multiple-domain MCI, and the single non-memory domain MCI [4,9]. The amnestic type of MCI is generally thought to represent prodromal Alzheimer's disease (AD) [10]. Other subclasses may have different underlying mechanisms of cognitive impairment, and may be associated with other non-AD disease processes (eg, vascular dementia, dementia with Lewy bodies), but there is little supporting evidence for this paradigm [11]. Studies of parkinsonian signs among patients with MCI have conflicted as to their greater association with amnestic versus nonamnestic MCI [12,13].
The term MCI, without qualification, was traditionally and is still often used to refer to the amnestic type; however, using MCI without qualification is somewhat ambiguous.
Amnestic MCI — Amnestic MCI refers to those individuals with significantly impaired memory who do not meet criteria for dementia. The criteria outlined above were initially developed to define MCI in general but subsequently have been understood to identify only this type [1,4].
Memory impairments that qualify for MCI are generally represented by defects that are 1.5 standard deviations (SD) or more below age-corrected norms. While this seems straightforward, different tests of memory likely have different sensitivity and specificity, and norms are not available for all populations [7]. (See "Screening cognitive examinations" below).
Many individuals with amnestic MCI complain only of memory loss; however, they may have additional subtle impairments in other cognitive domains that are revealed with careful neuropsychological testing [9,14-16]. Some would interpret the latter finding as excluding patients from this subtype of MCI according to the criteria listed above [7]. This highlights operational difficulties with the application of the criteria.
Amnestic MCI is often thought of as a precursor to AD [10]. Although memory performances are often similar in patients with amnestic MCI and AD, impairments in multiple cognitive domains are also prominent in patients with AD [1].
Multiple-domain MCI — Individuals with multiple-domain MCI have cognitive performances and complaints that reflect slight deficiencies in multiple domains of cognitive and behavioral functioning. Their cognitive complaints and objective performances do not reflect a circumscribed impairment. Such persons may manifest subtle problems with activities of daily living, but they do not meet criteria for a formal diagnosis of dementia [8]. The multiple domains are, by definition, only slightly impaired (ie, less than 0.5 SD below age and education-matched normal subjects).
Often these individuals progress to meet criteria for AD or vascular dementia; in a minority of cases, the cognitive profile may simply reflect normal aging [8]. The multiple-domain form of MCI may be a particularly unstable condition, with some individuals even returning to a baseline level of functioning over time [9].
Single non-memory domain MCI — The concept of single non-memory domain MCI is similar to amnestic MCI, except that this form of MCI is characterized by a relatively isolated impairment in a single non-memory domain, such as executive functioning, language, or visual spatial skills [8]. Depending upon the domain, individuals with this subtype of MCI may progress to other syndromes, such as frontotemporal dementia, primary progressive aphasia, or dementia with Lewy bodies.
Related terminology — There are a multitude of loosely related terms that have been used to describe constructs that are similar to or perhaps even the same as MCI, eg, incipient dementia, isolated memory impairment, dementia prodrome, minimal AD, predementia AD, prodromal AD, and early AD [1,2,4,8,17,18]. In a glossary of these and other terms that describe cognitive impairment in elderly people without dementia, most of these definitions do not fully overlap with the definition of MCI [19].
The concept of MCI perhaps reflects most closely the idea of "cognitive impairment, no dementia" (CIND) [20]. However, in contrast to the definition for the amnestic form of MCI, CIND less heavily relies on the presence of prominent memory deficits and includes in its definition the presence of a functional disability. It is a more inclusive definition than MCI, as is reflected by its higher prevalence. (See "Epidemiology" below).
"Age-associated memory impairment" and "age-associated cognitive decline" are also widely used and fairly well known terms. However, these terms differ from MCI in that they refer to the memory impairments in older adults as referenced to young normal adult individuals [1,21,22]. In MCI, memory impairments are referenced to age-adjusted norms.
Studies of "preclinical AD" should be distinguished from studies of MCI [23]. In MCI studies, patients meet cognitive criteria for diagnosis, and are then followed prospectively to assess for conversion to AD. In contrast, "preclinical AD" studies examine information retrospectively, following the diagnosis of AD.
EPIDEMIOLOGY — Findings from epidemiological studies vary significantly, partially due to the differing diagnostic criteria, measuring instruments, and definitions.
In cohorts and treatment trials that more strictly apply the criteria for amnestic mild cognitive impairment (MCI), prevalence rates in elderly populations are estimated between 2 and 4 percent [5,7,24].
Studies using different measures, such as "age-associated cognitive decline," "cognitive impairment, no dementia," and "minimal dementia," estimate higher prevalences of 16 to 19 percent [2,5,20,25].
Gender, race, increased age, and lower education are inconsistently associated with MCI in various studies [5,7,25-27,91,92]. Elevated blood pressure and diabetes (even in the absence of symptomatic cerebrovascular disease) and apolipoprotein E epsilon 4 genotype have also been associated with the risk of MCI, particularly amnestic MCI [26-30,91,92].
CONVERSION TO DEMENTIA — It is generally accepted that individuals with mild cognitive impairment (MCI) are at increased risk of developing Alzheimer's disease (AD). In a prospective study of 798 older Catholic clergy without dementia, participants were categorized at baseline as having MCI (n = 211) or no cognitive impairment (n = 587) and were followed for an average of 4.5 years with cognitive tests [31]. The group with MCI developed AD at a rate 3.1 (CI 2.1-4.5) times higher than the group with no cognitive impairment.
However, not all studies have agreed that MCI is an important predictor of conversion to AD. In one retrospective study, a diagnosis of age-associated cognitive decline was a better predictor of conversion to AD than MCI [5]. One criticism of this study is that the MCI criteria were applied retrospectively to neuropsychological test scores [32]. These findings also highlight the general difficulty in defining MCI.
In various studies, a substantial percentage (11 to 40 percent) of patients with MCI improve, even to normal, over a one to three-year follow-up time [5,7,24,33,34]. This finding emphasizes the clinical heterogeneity of MCI. In one study, patients who improved did not appear to be at a higher risk of dementia compared with controls [33].
Rates — Rates of conversion from MCI to dementia have been estimated from treatment trials and population cohorts. In elderly populations, annual rates range from 8 to 16 percent [1,7,11,24,29,33,35-40]. This contrasts with incidence rates for AD in the general population of 1 to 3 percent per year [1,24,36]. The cumulative incidence of dementia in patients with MCI may be as high as 80 percent at six years [1]. The interval between MCI diagnosis and conversion may be as long as eight years in some cases [17].
Predictors — Given the heterogeneity of outcomes among individuals with MCI, many studies have investigated factors that might further identify those with MCI who will develop dementia. Risk factors for dementia in the general population are discussed separately. (See "Risk factors for dementia").
Some studies suggest that socioeconomic variables are equivocal predictors. Gender and education level are not predictors [41].
Age — Aging is a primary predictor of progression of MCI to AD [7,27,38,42,43,92]. With every year of age increase, MCI is slightly more likely to convert to AD. MCI is relatively unlikely to represent a predementia condition in patients less than 50 years [38].
Neuropsychological testing — A variety of observational studies suggest that neuropsychological testing may be helpful in defining individuals at risk for dementia.
Prospective cohort studies of patients with MCI or "cognitive impairment, no dementia" have shown that within this group, more severely affected patients are at greater risk for dementia than those who are less affected [33,44,45]. This was seen as early as nine years prior to diagnosis. A number of specific test measures, such as short delayed verbal recall, visual recognition memory, and other cued memory tasks, as well as measures of instrumental activities of daily living, have been found to have high predictive value for dementia in some studies [42,45-51]. However, these have not been independently and prospectively validated in a manner that allows application to individual cases.
Follow-up neuropsychological testing provides more helpful information, in that intraindividual change in cognitive function is more sensitive than comparison with group norms [52]. In one cohort study, acceleration of cognitive decline occurred approximately three years prior to the diagnosis of AD [44]. Educational level was an important modulator of test performance and rate of decline. These findings have been corroborated in other cohort studies [10,53-55]. One of these studies emphasized that a decline in cognitive measures is a necessary but not sufficient predictor of dementia, having good negative predictive value (as high as 90 percent), but poor positive predictive value (30 percent) in their cohort [54].
ApoE epsilon 4 — Apolipoprotein E (APOE) epsilon 4 (e4) genotype has been associated with the risk of AD in the general population but has had mixed association with conversion to AD among individuals with MCI. In one study, MCI patients carrying the APOE e4 allele had a greater degree of cognitive impairments and hippocampal atrophy on MRI compared with noncarriers [56]. Some studies have found that APOE e4 is a strong risk factor for conversion from MCI to AD [29,43,45,57], but others have found only a marginal or even no association [27,41,42,58-60].
CSF biomarkers — Because the pathological process of AD and other degenerative dementias is likely well underway before clinical symptoms manifest, biomarkers would seem to have potential utility in the early diagnosis of dementia. A number of small studies have examined the use of cerebrospinal fluid (CSF) markers for predicting conversion from MCI to dementia [48,61]. Associations have been suggested for:
Increased levels of tau or phosphorylated tau protein [37,43,62,63]
Lower activity of neprilysin, an amyloid beta peptide degrading enzyme [64]
Lower levels of amyloid beta 42 (Aß42) peptide, a low ratio of Aß42 to Aß40 levels, and a low ratio of Aß42 to tau levels [37,65-67,94]
The applicability of these findings to large populations is unclear, and these tests do not have an established role in the evaluation of patients with MCI. Moreover, the absence of a clinical treatment imperative for MCI makes this relatively invasive test less appealing.
Neuroimaging — Pathologic studies find that the earliest and most severe manifestations of AD are found in the medial temporal lobe. Neuroimaging studies have focused attention to these areas to define abnormalities that may predict conversion from MCI to AD as this appears to be more closely associated with MCI than other findings, such as white matter abnormalities [93].
MRI studies — Volume loss or brain atrophy can be identified on magnetic resonance imaging (MRI) in patients at risk for AD [68]. Temporal lobe atrophy may be an early specific marker for preclinical AD; similar patterns of temporal lobe atrophy are seen in patients with amnestic MCI and AD, which are not seen in individuals with multiple cognitive domain MCI, whose scans are similar to healthy controls [69]. While most studies use a specialized technique for volumetric measurements, visual assessment using a standardized rating scale seems to perform nearly as well [70-72].
Both the degree and progression of medial temporal lobe atrophy on MRI are associated with conversion to dementia in patients with MCI as well as in people with normal baseline cognition [41,42,60,70-79]. These changes can be observed one to two years prior to cognitive decline. Similarly, higher baseline apparent diffusion coefficient (ADC) values in the hippocampus on diffusion-weighted MRI (DWI) may predict conversion to dementia in patients with amnestic MCI [80,81]. However, there is overlap in the degree of atrophy for patients who do and do not progress to dementia, and the same is true for ADC values. Thus, these findings are not a practical way to predict progression to dementia for individual patients. While some investigations suggest that these MRI changes may be useful in combination with other risk factors in predicting risk of AD, such multivariate models require independent validation [79].
PET and SPECT studies — Preliminary data suggest that identification of regional patterns of cortical hypometabolism using fluorodeoxyglucose (FDG) positron emission tomography (PET) may be useful for predicting conversion from MCI to AD, especially in the presence of the APOE e4 allele [82-86]. However, it is unclear as to whether this method will have sufficient predictive value in non-APOE e4 carriers, and the limited availability of PET in most medical centers is an additional obstacle.
One study suggested that a subset of patients with amnestic MCI who perform poorly on a test of visual recognition memory also exhibit patterns of temporomesial and temporoparietal hypoperfusion on single photon emission CT (SPECT), a pattern seen in early AD [87]. However, there were no follow-up data on these patients assessing their risk of developing AD. Another study followed 105 patients with MCI; the 24 who developed AD within four years had reduced perfusion on baseline SPECT in specific brain areas compared with those who remained stable [88]. However, in the brain area most sensitive for early changes, the posterior cingulate, the average perfusion reduction was just 8 percent, which had limited ability to discriminate converters from nonconverters with a sensitivity and specificity of 79 and 67 percent.
Others — One study has found that impaired motor performance, in particular a parkinsonian gait and bradykinesia, was associated with conversion from MCI to AD [89]. In addition, individuals with MCI had levels of motor performance significantly inferior to those with normal cognition and superior to those with AD.
In another small cohort study of 139 individuals with MCI, less than one drink of alcohol per day was associated with decreased progression to dementia compared with those who abstained (HR = 0.15) [90]. Higher amounts of alcohol intake were not associated with increased or decreased risk of dementia.
PATHOLOGY — Support for the idea that mild cognitive impairment (MCI) represents an early clinical expression of age-related neurologic disease comes from neuropathological studies:
Among 180 Catholic clergy who had died at a mean age of 76 years, 37 subjects had MCI, 83 had dementia, and 60 did not have cognitive impairment at a time proximate to their death. [95]. Although there was marked overlap of Alzheimer's disease (AD) pathology among the groups, the MCI group had an intermediate level of AD pathology, compared with individuals with dementia (more AD pathology) and those without cognitive impairment (less AD pathology). Additional age-related neurologic diseases were also identified; about a third of the MCI group had one or more cerebral infarctions, and 8 percent had Lewy body disease. The neuropathologist was blinded to the clinical data.
Similarly, the neuropathologic features in 15 patients classified as amnestic MCI at the time of death were found to be intermediate between the neurofibrillary changes of aging, seen in 28 individuals free of dementia, and early AD, as identified in 23 age-matched patients with a premortem diagnosis of probable AD [96]. These findings were corroborated in a similar study [97].
In a series of 25 patients with MCI, 21 had pathology consistent with AD, three had diffuse Lewy body disease, and 14 had cerebrovascular disease; only one patient had no clear neuropathologic diagnosis [10].
Among 34 patients identified in a community-based study as having MCI and who then developed dementia, pathology at postmortem was consistent with AD in most (71 percent); other diagnoses included vascular dementia, dementia with Lewy bodies, frontotemporal dementia, and progressive supranuclear palsy [98]. Amnestic versus multi-domain MCI did not distinguish those patients who developed AD versus another dementia diagnosis.
SYMPTOMS — Patients with MCI, particularly the amnestic subtype, complain primarily of impaired memory. In contrast to the impaired awareness of deficits commonly present in patients with Alzheimer's disease (AD), patients with MCI are often particularly troubled by their symptoms [99]. However, over time, patients with MCI who convert to AD shift to a relatively greater preponderance of informant- over self-reported symptoms [100]. This phenomenon may be helpful in following an individual patient's progression to dementia.
As with dementia, behavioral symptoms are common in patients with MCI. In a clinical trial of 1010 patients with MCI, 59 percent had behavioral problems [101]. Depression was most prevalent (in almost half) followed by irritability, anxiety, aggression, and apathy. Patients with behavioral symptoms were significantly more impaired on cognitive measures than those without behavioral symptoms.
Population-based studies comparing MCI and AD patients find a similar range of neuropsychiatric symptoms, with AD patients having them in somewhat higher frequency and severity [102,103]. (See "Treatment of behavioral symptoms related to dementia").
The relationship between depression and cognitive impairment is complicated. Cognitive impairment may be a presenting symptom of depression, so-called pseudodementia. Depression may also be an early manifestation of cognitive impairment. A number of population-based studies have studies have found an association between various measure of depression and the presence of MCI [104-106]. However, follow-up data has yielded somewhat mixed results:
Among 500 85-year-old persons, impaired cognition at baseline was associated with increasing depressive symptoms over four years of follow-up, but baseline depression was not associated with accelerated cognitive decline [104].
In contrast, other large cohort studies have found that depressed mood and/or anxiety is associated with increased risk of MCI in patients with normal cognition, and with progression to dementia in patients with MCI [105,106].
Finally, an analysis of MCI diagnostic criteria used in six clinical trials found that excluding patients with depression significantly reduced the sensitivity rates of MCI diagnosis for future AD diagnosis [107].
In the aggregate, these results suggest that depression is more likely to be an early manifestation of cognitive decline rather than an independent risk factor for MCI or progression to dementia.
DIFFERENTIAL DIAGNOSIS — Psychiatric disease, particularly depression, may present with cognitive rather than mood complaints. Adverse effects of medications (eg, antihistamine use) and sleep disturbances are also common causes of cognitive complaints, particularly in elderly populations [114]. Metabolic disturbances, particularly vitamin B12 deficiency and hypothyroidism, should be considered in the differential diagnosis of mild cognitive impairment (MCI). Structural brain disease is an uncommon cause of MCI in the absence of focal neurologic findings.
In one community sample, patients with "cognitive impairment, no dementia" were diagnosed with depression and other psychiatric disease (10.2 percent), alcohol and drug related causes (6.9 percent), and delirium (1 percent) [20]. Approximately one-quarter of cases had neurologic disease (brain tumor, Parkinson's disease, multiple sclerosis, cerebrovascular disease, and epilepsy). Among the remaining 57.5 percent, most (31.7 percent) had circumscribed memory impairment.
EVALUATION — The evaluation in patients who present with cognitive complaints is focused on ruling out treatable conditions as well as establishing the severity of the impairments and providing a baseline for follow-up. These goals overlap in the specific tests that might be ordered. In general, the evaluation of patients with mild cognitive impairment (MCI) should be similar to that performed in patients presenting with dementia and include a neuroimaging study (brain CT or MRI) and screening for B12 deficiency and hypothyroidism. (See "Evaluation of cognitive impairment and dementia").
Despite the high rate of progression from MCI to dementia, the absence of an established treatment limits the value of early detection and routine monitoring for progression to dementia. Nonetheless, this can be valuable for proactive decision making on the part of individual patients and family members.
Screening cognitive examinations — The Quality Standards Subcommittee of the American Academy of Neurology has provided practice parameters, including evaluation guidelines for MCI [4]. Neuropsychological testing and screening cognitive evaluations (eg, mini mental status examination) are recommended to evaluate patients with suspected cognitive impairment.
Neuropsychological testing includes an objective measure of memory impairment [8]. It may also have additional value in the detection of contributing or causative depression. Once a patient meets criteria for MCI, it is recommended that the patient return for neuropsychological reassessment in approximately one year to monitor cognitive and functional decline [4,102]. Improved performance on the examination argues against neurodegenerative disease, while declining performance supports that diagnosis.
Neuropsychological testing should not be used in isolation; clinical judgment is critical to diagnosing both Alzheimer's disease (AD) and MCI [99]. There are no uniformly accepted criteria for the diagnosis of MCI using neuropsychological testing. Some suggest a 1.5 standard deviation (SD) threshold value for tests of memory impairment; others have used 1 SD [1,7,35,108]. In amnestic MCI, other cognitive domains may be impaired, but test abnormalities are generally milder and are usually within 0.5 SD of appropriate comparison groups. In multiple-domain MCI, several cognitive domains may be impaired in the 0.5 to 1.0 SD range. These ranges are not used as cutoff scores, but they provide a sense of the impairments seen in MCI.
Other rating scales have been used to define MCI but not with uniform acceptance. These include the Clinical Dementia Rating Scale (CDRS) (show table 1) and the Mini-Mental Sate Examination (MMSE). (See "Evaluation of cognitive impairment and dementia", section on Mini-Mental State Examination). A CDRS of 0.5 and a score of 24/30 on the MMSE have been used by some investigators to define MCI or CIND. An informant-based questionnaire of cognitive decline may also provide relevant information regarding the diagnosis and prognosis of MCI, but this needs further validation [109].
TREATMENT — This section covers studies that have evaluated treatments for mild cognitive impairment (MCI) specifically. Treatment of dementia is discussed separately. (See "Treatment of dementia").
Acetylcholinesterase inhibitors — Vitamin E and donepezil were evaluated for treatment of patients with the amnestic subtype of MCI in a double-blind study in 769 participants [35]. Vitamin E had no benefit in patients with MCI. Donepezil therapy was associated with a lower rate of progression to Alzheimer's disease (AD) during the first year. However, the cumulative rate of progression of AD after three years was not lower among patients treated with donepezil than among those given placebo. Another randomized controlled trial in 270 patients examined the effects on cognitive function after 24 weeks of treatment and found no significant treatment effect of donepezil for MCI in the primary efficacy measures [110]. Some secondary measures suggested benefit. Withdrawals due to adverse events (mostly gastrointestinal) were higher in the treatment group (32 versus 17 percent) [111].
In April 2005, the US Food and Drug Administration (FDA) and the manufacturer of galantamine reported data from two randomized controlled trials; each was of two years duration and involved a total of 2048 subjects with MCI. Death in patients receiving galantamine was significantly higher than in those receiving placebo (13 patients versus 1 patient). About half of the deaths in the galantamine group appeared to result from vascular causes, such as myocardial infarction, stroke, and sudden death [112].
Based on these results, cholinesterase inhibitors are not routinely recommended for patients with MCI [111]. However, if memory difficulties are particularly troublesome to an individual patient, a trial of donepezil for symptomatic benefit may be warranted. (See "Cholinesterase inhibitors in dementia").
Vascular risk factor modification — Some feel that the association of MCI and vascular dementia has been underappreciated relative to AD:
Patients with MCI and AD have a higher than expected prevalence of atherosclerosis risk factors. (See "Epidemiology" above).
Patients with MCI are likely to have cerebrovascular as well as AD pathology on postmortem examination. (See "Pathology" above).
Cerebrovascular disease may play a prominent pathogenic role in dementia in many patients with AD. (See "Etiology, clinical manifestations, and diagnosis of vascular dementia", section on "Mixed dementia").
These observations suggest that atherosclerosis risk factors should be aggressively treated in patients with MCI. There have been no randomized controlled clinical trials to support this; however, treatment of hypertension has been shown to reduce the incidence of dementia in the general population. There is less compelling evidence for the efficacy of antiplatelet therapy, statin therapy, and diabetes management in the treatment or prevention of dementia. (See "Treatment and prevention of vascular dementia").
Elevated homocysteine levels have been associated with risk of vascular disease, dementia, and decreased cognitive performance. (See "Risk factors for dementia", section on Homocysteine and see "Overview of homocysteine"). However, a systematic review of clinical trials concluded that supplementation with either vitamin B6, B12, and/or folate has not been shown to improve cognition in individuals with MCI or normal cognition [113].
SUMMARY AND RECOMMENDATIONS — Mild cognitive impairment (MCI) represents a state between normal aging and dementia.
MCI includes patients with cognitive deficits that are insufficiently severe to meet criteria for dementia. There are not well defined clinical criteria for diagnosis. Subtypes of MCI based on the affected cognitive domains (amnestic MCI, multiple domain MCI, and single nonmemory domain MCI) are individually recognized. (See "Definitions" above).
Patients with MCI, particularly amnestic MCI, appear to be at risk for dementia. (See "Conversion to dementia" above).
Neuropsychological test measures, cerebrospinal fluid (CSF) biomarkers, and neuroimaging studies are being evaluated as predictive tools for assessing patients' risk for conversion to dementia. These lack standardization, and there is no clinical imperative for general use. (See "Predictors" above).
Patients with cognitive complaints should be evaluated for treatable causes of dementia. (See "Evaluation of cognitive impairment and dementia"). Follow-up evaluations of cognitive complaints are recommended to monitor a patient's progression to dementia. (See "Evaluation" above).
Based on the available clinical trial data and lack of convincing benefit, we recommend NOT routinely treating MCI with cholinesterase inhibitors (Grade 1B). For an individual patient with troublesome memory difficulties, a trial of donepezil for symptomatic benefit may be warranted. Patients and families should be informed of the potential risk. (See "Treatment" above).
Patients with MCI and clinical or radiologic evidence of cerebrovascular pathology should be screened and treated for vascular risk factors, especially hypertension, although this has been shown to be helpful in preventing dementia in the general rather than the MCI population. (See "Treatment and prevention of vascular dementia").
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