Journal of Geriatric Psychiatry and Neurology

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Montreal Cognitive Assessment (MoCA): Validation study for Frontotemporal Dementia

Sandra Freitas, Mário R. Simões, Lara Alves, Diana Duro and Isabel Santana
J Geriatr Psychiatry Neurol 2012 25: 146 originally published online 1 August 2012
DOI: 10.1177/0891988712455235

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 Journal of Geriatric Psychiatry
and Neurology
Montreal Cognitive Assessment (MoCA): 25(3) 146-154
ª The Author(s) 2012
Reprints and permission:
Validation study for Frontotemporal sagepub.com/journalsPermissions.nav
DOI: 10.1177/0891988712455235
Dementia http://jgpn.sagepub.com

Sandra Freitas, PhD1,2, Mário R. Simões, PhD1,2, Lara Alves, PhD1,

Diana Duro1, and Isabel Santana, PhD, MD3,4

Abstract
The Montreal Cognitive Assessment (MoCA) is a brief instrument developed for the screening of milder forms of cognitive
impairment, having surpassed the well-known limitations of the Mini-Mental State Examination (MMSE). The aim of the present
study was to validate the MoCA as a cognitive screening test for behavioral-variant frontotemporal dementia (bv-FTD) by
examining its psychometric properties and diagnostic accuracy. Three matched subgroups of participants were considered:
bv-FTD (n ¼ 50), Alzheimer disease (n ¼ 50), and a control group of healthy adults (n ¼ 50). Compared with the MMSE, the
MoCA demonstrated consistently superior psychometric properties and discriminant capacity, providing comprehensive
information about the patients’ cognitive profiles. The diagnostic accuracy of MoCA for bv-FTD was extremely high (area under
the curve AUC [MoCA] ¼ 0.934, 95% confidence interval [CI] ¼ 0.866-.974; AUC [MMSE] ¼ 0.772, 95% CI ¼ 0.677-0.850). With
a cutoff below 17 points, the MoCA results for sensitivity, specificity, positive predictive value, negative predictive value, and clas-
sification accuracy were significantly superior to those of the MMSE. The MoCA is a sensitive and accurate instrument for screen-
ing the patients with bv-FTD and represents a better option than the MMSE.

Keywords
geriatric assessment, neuropsychological test, validation studies, cognitive impairment, frontotemporal dementia, Alzheimer
disease

Received November 22, 2011. Received revised March 12, 2012. Accepted June 4, 2012.

Introduction
The diagnosis of frontotemporal dementia (FTD) remains a
challenge wrapped in a nosologic controversy. Since the turn
of the century, this clinical condition has been recognized and
referred to as Pick disease, frontal lobe degeneration of non-
Alzheimer type, and dementia of the frontal type, among other
terms.1,2 The task force and consensus for new diagnostic cri-
teria have proposed the designation of ‘‘frontotemporal lobar
degeneration’’3; however, the most frequently used term that
currently gathers larger consensus is FTD.
Frontotemporal dementia refers to a group of degenerative
dementias that are characterized by progressive, bilateral, and
more or less symmetrical pathology in the frontal and anterior
temporal cortex.4-6 With an average onset age of approximately
50 to 60 years,7 FTD is probably the second most prevalent
early-onset cause of degenerative dementia, after Alzheimer dis-
ease (AD) and overcoming Lewy Body dementia which seems to
be more common in late-onset forms.8 The few epidemiological
studies available indicate a wide range of prevalence rates, with
estimates of 15 to 22 per 100 000 people aged 45 to 64 years,
which is almost half of the prevalence of AD in the same age
cohort; the studies also estimate a prevalence rate of 9.4 per
100 000 for the people aged 60 to 69 years and a prevalence of
3.1 per 100 people aged 85 years or more.4,6 Overall, the estimates
suggest that FTD is responsible for up to 20% of presenile demen-
tia cases5,6 figures that overlap with those purposed for vascular
dementia, at least in Western countries.9 The genetic and chromo-
somal locus related to tau and progranulin proteins,10-12 as well as
different neuropathological substrates that are now the basis for a
1
Faculty of Psychology and Educational Sciences, University of Coimbra,
Coimbra, Portugal
2
Centro de Investigação do Núcleo de Estudos e Intervenção Cognitivo
Comportamental (CINEICC), Coimbra, Portugal
3
Faculty of Medicine, University of Coimbra, Coimbra, Portugal
4
Neurology Department of the Coimbra University Hospital, Coimbra,
Portugal
Corresponding Author:
Sandra Freitas, Psychological Assessment Department, Faculty of Psychology and
Educational Sciences, University of Coimbra, Rua do Colégio Novo, Apartado
6153, 3001-802 Coimbra, Portugal
Email: sandrafreitas0209@gmail.com

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Freitas et al
pathological classification of FTD,4,13 were initially described in
this group of young familial cases.
Although FTD is a heterogeneous entity that produces a gra-
dual but variable decline in behavioral, cognitive, and neurolo-
gical domains,3,4,6 it has been widely accepted the division into
3 main subgroups, all of which contain corresponding topogra-
phical cerebral involvement.
Frontal variant or behavioral variant is frequently referred to
as frontotemporal dementia (bv-FTD) and is the most common
subtype. The bv-FTD accounts for approximately half of all
FTD cases.7,14 It is associated with bilateral, and usually sym-
metrical, frontal, and anterior temporal dysfunction.3,4 Despite
the heterogeneity in its clinical presentation, bv-FTD is charac-
terized by an insidious onset and a progressive decline that is
marked by personality and behavioral changes. These changes
lead to an early decline in social interpersonal conduct, early
impairment of regulation of personal conduct, and early emo-
tional blunting and loss of insight.3,15 The cognitive deficits
that are most characteristic of bv-FTD are the impairment of
executive function, attention and working memory deficits,
poor abstraction, and difficulty shifting mental set with perse-
verative tendencies, all of which occur without severe amnesia,
aphasia, or perceptual dysfunction.3,6
Semantic dementia16,17 is also referred to semantic aphasia
and associative agnosia3 or semantic variant of primary progres-
sive aphasia.18 It is usually correlated with left or bilateral atro-
phy of the middle and inferior temporal neocortex.19 The core
feature of this clinical syndrome is a language disturbance that
is characterized by fluent, effortless, and empty spontaneous
speech, with severe deficits in naming and word comprehension
and a loss of word meaning for both verbal and nonverbal con-
cepts; another core feature is a perceptual disorder that includes
prosopagnosia and associative agnosia.3,6 For patients with
semantic dementia, some of the following abilities remain rela-
tively preserved: repetition, articulatory abilities, ability to read
aloud and to write down orthographically regular words that
have been dictated, visuospatial skills, working memory, and
autobiographical memory, at least for the recent past.3,6
Progressive nonfluent aphasia,3 also called nonfluent/
agrammatic variant of primary progressive aphasia,18 is associ-
ated with asymmetric atrophy of the left hemisphere.19 This is a
disorder of expressive language that usually occurs without
impairments in other cognitive domains. These patients present
nonfluent spontaneous speech that is marked by agrammatism,
phonemic paraphasias, and anomia, with difficulties in reading
and writing. Word comprehension remains relatively well pre-
served and behavioral symptoms are less common among these
patients than among sufferers of the other 2 types of FTD.3
Several studies have examined the neuropsychological def-
icits in patients with FTD.20-24 These studies were designed to
identify a global characterization of FTD, which would be a
valuable contribution to distinguishing FTD from other demen-
tia diagnoses. However, the clinical heterogeneity of FTD, its
decline in domains beyond the cognitive, which are not evalu-
ated by neuropsychological tests, the overlap of some cognitive
deficits between FTD and other types of dementia as well as the
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147
methodological differences across study designs have contrib-
uted to inconsistent findings and difficulties in the early dis-
tinction between FTD and others dementias using
neuropsychological tools.1,4,24 This lack of distinction is partic-
ularly relevant for AD, with which there appears to exist
greater misdiagnosis. Moreover, numerical scores on cognitive
tests have a limited value in differentiating between FTD and
AD, while qualitative performances and error types appear to
enhance this distinction.1,21-24
The significant increase in prevalence rates, the high herit-
ability of FTD with estimates of 20% to 40% of familial cases
in referral centers,4,25,26 imposing new challenges in terms of
genetic diagnosis and familial counseling, and issues related
to pharmacological treatment of degenerative dementias, since
drugs used to treat cognitive symptoms of AD or Lewy Body
dementia are not recommended in FTD, all these points high-
light the importance of an accurate screening during early
stages of these disorders. The Mini-Mental State Examination
(MMSE)27 is the most widely used and validated screening
instrument for the assessment of cognitive function. However,
several limitations have been identified in the literature,
namely, the low sensitivity to the early stages of AD and the
inability to differentiate between the various dementia disor-
ders.22,28-31 Regarding FTD, several studies have reported that
the MMSE lacks enough sensitivity to identify cognitive
impairments and frequently results in normal test performance,
which is especially problematic in cases of isolated frontal or
linguistic deficits that are typical of the early stages.6,21,32-34
This lack of sensitivity results from the low complexity of the
tasks for assessment of memory and language dysfunctions and
from the lack of tasks for the evaluation of executive
function.22,35
The Montreal Cognitive Assessment (MoCA)36 is a recent
international brief cognitive screening instrument that was
developed to detect milder forms of cognitive impairment, over-
coming limitations of the MMSE. Previous studies have reported
the usefulness of MoCA in accurately identifying milder forms
of cognitive impairment. Compared with the MMSE, the MoCA
displays a higher sensitivity in detecting patients with MCI and
AD.26,37-42 This improved sensitivity explains the widespread
international use of MoCA and its recognition as one of the best
screening tests.43-45 One of the reasons for the good sensitivity of
the test is that it allows a more comprehensive assessment of the
major cognitive domains, comparatively to other screening tests,
especially executive functions and short-term memory, but also
of language abilities and visuospatial processing. Despite the
recognition that the MoCA has received as a screening tool, its
diagnostic sensitivity cannot be generalized to FTD because
there are no published studies validating the MoCA for these
patients.
The general aim of this study is to validate the MoCA as a
cognitive screening test for bv-FTD by examining its psycho-
metric properties and diagnostic accuracy. Furthermore, we
also investigated the cognitive performances of patients with
bv-FTD on the MoCA and analyzed how their performances
differed from patients with AD.
148
Methods
Participants and Procedures
The total sample includes 150 participants divided into 3 sub-
groups: (i) a bv-FTD group with 50 patients, (ii) an AD group
with 50 patients, and (iii) a healthy group comprising 50 cog-
nitively healthy adults.
Study eligibility was restricted to patients with a compre-
hensive clinical observation, a comprehensive neuropsycholo-
gical evaluation with a validated battery for the Portuguese
population (Bateria de Lisboa para a Avaliação de Demência
[Battery of Lisbon for the Assessment of Dementia]46), as well
as a full investigation using biochemical, structural, and func-
tional imaging (magnetic resonance imaging and single photon
emission computed tomography, and/or positron emission
tomography), which are essential to exclude other causes of
no degenerative dementia and to establish the clinical diagno-
sis. Besides the neuropsychological battery, and as standar-
dized procedures of the Dementia Clinic of the Neurology
Department of Coimbra University Hospital, patients were sub-
mitted to additional tests and scales which are more disease-
specific and are already being purposed in new diagnostic
criteria.47 Considering that this is an extensive global assess-
ment, it was not feasible to carry out this same evaluation in
both clinical groups.
The bv-FTD group included only those patients who dis-
played the behavioral variant of FTD diagnosis, as established
by a multidisciplinary team according to international criteria.3
All the individuals who displayed the aphasic syndromes of
FTD or mixed clinical syndromes were excluded from the
study. In order to better characterize this group, all patients
with bv-FTD were further evaluated using the following instru-
ments: the Neuropsychiatric Inventory.48 the Frontal Behavior
Inventory,49 the Comprehensive Affect Testing System,50 the
Frontal Assessment Battery,51 the MMSE,27 the Trail Making
Test,52 Verbal Fluency,46 the Maze-Tracing Task,53 the Digit
Span Test,54 the Digit Symbol Test,54 the Spatial Span Test,55
the Token Test,56 the Buschke Selective Reminding Test,57 and
the Brief Visuospatial Memory Test.58
The AD group included only those patients who were diag-
nosed by a multidisciplinary team consensus based on interna-
tional criteria for probable AD.59,60 This group was recruited to
match the patients with bv-FTD by gender, age, education
level, and severity of cognitive decline, as assessed by the
MMSE. For patients with AD, the besides the comprehensive
clinical/neuropsychological standard evaluation, patients
underwent the following specific investigation: the MMSE,27
the Alzheimer Disease Assessment Scale,61 the Clinical
Dementia Rating scale (CDR),62 the Irregular Word Reading
Test (TeLPI)63 as an estimate of premorbid intelligence, the
Subjective Memory Complaints scale,64 and the Geriatric
Depression Scale (GDS-30).65
For both clinical groups, the multidisciplinary team was
blind to MoCA scores and to MMSE scores used in this study.
The following patient exclusion criteria were established at the
outset of the study: an unstable clinical condition, with
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Journal of Geriatric Psychiatry and Neurology 25(3)
significant comorbidities; high severity dementia (only those
patients with CDR 2 and MMSE 12 points were included
in the study); recent pharmacotherapy changes; recent psychia-
tric comorbidity (clinically diagnosed within the 6 months prior
to the current neuropsychological evaluation); and significant
motor, visual or auditory deficits, all of which may influence
neuropsychological assessment.
The healthy group comprised cognitively healthy commu-
nity members who resided in the Portuguese continental terri-
tory. This group was selected from the database of normative
study of MoCA for the Portuguese population in order to match
each patient on variables that were found to be predictive of the
MoCA performance (educational level and age),66 and addi-
tionally on gender. Several demographic and clinical inclusion
criteria were considered in the initial participant selection for
the normative study of MoCA for the Portuguese population:
age 25 years and older; Portuguese as their native language and
schooling in Portugal; absence of significant motor, visual or
auditory deficits, all of which may influence performance on
tests; and to ensure that participants were cognitively healthy
adults: autonomy in daily living activities; no history of alco-
holism or substance abuse; absence of neurological or psychia-
tric diseases, as well as of chronic unstable systemic disorders
with impact in cognition; absence of significant depressive
complaints and medication with possible impact in cognition
(eg, psychotropic or psychoactive drugs). In order to imple-
ment and confirm these general criteria, the recruited partici-
pants were interviewed by a psychologist with a standard
questionnaire including a complete sociodemographic ques-
tionnaire, an inventory of current clinical health status, and past
habits and medical history. In case of older participants, this
information was always also checked with general practioner,
community center directors, and/or an informant, usually an
individual in cohabitation or a close relative. For further inclu-
sion in the study, all the participants were required to display
normal performance on others tools of the assessment battery
especially composed for the normative study of MoCA for the
Portuguese population.66 From the initial community-based
sample of the 936 volunteers, 194 (20.73%) were excluded
after the interview (most frequent reasons were history of neu-
rological or psychiatric disorder and history of alcohol abuse),
and 92 (9.83%) were excluded because of their performance on
the assessment battery, suggesting the presence of cognitive
impairment or depressive symptoms according to Portuguese
cutoff points. The final sample of the normative study of
MoCA for the Portuguese population was composed by 650
cognitively healthy adults that met all the inclusion criteria
defined.66
Informed consent was obtained from all the participants
after a member of the research team provided them with a full
explanation of the research aims and procedures as well as con-
fidentiality requirements. For the patients who were not capa-
ble of providing the informed consent, a legal representative
fulfilled that requirement on their behalf. The present research
complies with the ethical guidelines on human experimentation
stated in the Declaration of Helsinki and was approved by the
Freitas et al
Portuguese Foundation for Science and Technology and by the
Faculty of Psychology and Educational Sciences Scientific
Committee.
Materials and Neuropsychological Testing
In the clinical interview, data were collected through a compre-
hensive sociodemographic questionnaire and an inventory of
the patients’ current clinical health status, past habits, and med-
ical history. The diagnosis of bv-FTD requires significant input
from a close informant; thus, an extensive interview was con-
ducted with each patient’s caregiver. The informants also con-
tributed to the completion of some of the assessment tests listed
above. For the purposes of this study, the neuropsychologist
administered the MMSE27,67 and the MoCA36,68 in a single ses-
sion; according to protocol, all participants first received the
MMSE and screening instruments were not counterbalanced
because with the administration of the MMSE in the first place,
we increase the time between verbal tasks, thus resulting in a
reduced possible influence of the MMSE verbal items on the
MoCA verbal tasks. Besides, and given the lower complexity
of the MMSE tasks, the predicable effects on MoCA would
be less significant. For the interrater reliability analysis, 2
neuropsychologists blindly scored the performance of the
patient in a single assessment.
The MMSE is the most widely recognized and used brief
screening instrument for detecting cognitive deficits. Both the
MMSE and the MoCA are brief cognitive screening tools that
are administered in paper-and-pencil format. For both tests, a
score is derived by summing the points from each successfully
completed task, for a total range from 0 to 30 points; higher
scores indicate better cognitive performance. The MoCA was
developed to screen milder forms of cognitive impairment
through the assessment of a wide range of cognitive functions,
such as short-term memory, executive functions, visuospatial
abilities, language, attention, concentration, working memory,
and temporal and spatial orientation.36,69 It comprises a 1-page
test, which requires a short administration time (10-15 minutes).
The MoCA is accompanied by a manual that explicitly describes
the instructions for administering the tasks and objectively
defines the scoring system. In the current study, the total score
of MoCA refers to the raw score without the one correction point
for education effects that was recommended in the original
study36 because this correction is not used in the Portuguese
population.66
Statistical Analyses
Statistical analyses of the data were computed using the Statis-
tical Package for the Social Sciences (SPSS, version 19.0; IBM
SPSS, Chicago, Illinois). Descriptive statistics were used for
the sample’s characterization. The w2 test, the 2-sample t test,
the one-way between-groups analysis of variance, and the
Tukey HSD and Bonferroni post hoc test were conducted to
examine group differences. Cronbach alpha was used as an
index of internal consistency. The Pearson correlation
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149
coefficients were used to analyze interrater reliability and con-
vergent validity and to explore the correlations between items,
cognitive domains, and the total test score.
The diagnostic accuracy of the MoCA and the MMSE for
predicting clinically diagnosed bv-FTD was assessed through
the receiver operating characteristics (ROC) curve analysis
implemented in MedCalc (version 11.6; MedCalc Software,
Mariakerke). The area under the curve (AUC) was calculated,
which can vary between 0.5 and 1, with a larger AUC signify-
ing better diagnostic accuracy. The ROC curves were com-
pared according to Hanley and McNeil AUC comparison
method.70 For each instrument, the optimal cutoff points that
yielded the highest Youden index were selected, with a higher
Youden index indicating the maximization of the instrument’s
sensitivity and specificity. To analyze the predictive value of
the tests, for each cutoff point, we calculated the sensitivity (the
probability that participants with cognitive impairment will test
positive), specificity (the probability that participants without
cognitive impairment will test negative), positive predictive
value (PPV; the probability of disease in participants who test
positive), negative predictive value (NPV; the probability of a
lack of disease in participants who test negative), and classifi-
cation accuracy (the probability of correctly classifying partici-
pants who either do or do not have cognitive impairment).
Results
Sample Characterization
Table 1 presents the characteristics of the sample, including
details of all the subgroups. The following variables were
included in the sample characterization: sample size, gender,
age, educational level, time progression of the disease, family
history, MMSE score, and MoCA score.
As presented in Table 1, there are no gender differences
between the 3 groups. Similarly, no statistically significant dif-
ferences were found between groups for age (F2,147 ¼ 1.808,
P ¼ .168) or educational level (F2,147 ¼ 0.013, P ¼ .987). In
addition, the clinical groups did not differ from each other in
terms of MMSE score (t98 ¼ 1.622, P ¼ .108), which suggests
an equivalence across groups in the severity of cognitive
decline. Regarding the time of progression disease, no statisti-
cally significant differences were found between the clinical
groups (t98 ¼ 1.295, P ¼ .198). Finally, half of the AD group
patients had a family history of dementia in first-degree rela-
tives, whereas the bv-FTD group and the healthy group did not
differ from each other; approximately 14% of each group pre-
sented positive cases in their family history.
Psychometric Properties
Internal consistency reliability of the MoCA was estimated
using Cronbach a. In the total sample, we found a Cronbach
a of .906 that confirms the overall reliability of the scale when
used to examine Portuguese participants (the respective value
for MMSE was 0.832). A more detailed analysis reveals that
excluding any single item from the scale does not improve the
150
Table 1. Demographic and Clinical Characteristics of the Subgroupsa
bv-FTD AD
n 50 50 50
Gender 25 (50.0) 25 (50.0) 25 (50.0)
Age 67.96 + 7.69 70.64 + 7.51 70.12 + 7.22
Educational level 6.18 + 3.71 6.14 + 3.88 6.26 + 3.83
Time progression of 3.24 + 2.80 3.94 + 2.60 —
disease
Family history 7 (14.0) 25 (50.0) 7 (14.0)
MMSE score 23.86 + 4.76 22.46 + 3.81 27.88 + 1.71
MoCA score 13.34 + 5.03 11.04 + 4.46 22.50 + 3.44
Abbreviations: bv-FTD, behavioral variant of frontotemporal dementia; AD,
Alzheimer disease; Healthy, healthy adults; MoCA, Montreal Cognitive
Assessment (maximum score ¼ 30); MMSE, Mini-Mental State Examination
(maximum score ¼ 30).
a
Gender is characterized by the number of females and respective percentage
(%). Time progression of disease is expressed in years. Family history is
characterized by number of positive cases and respective percentage (%). Data
of others variables are presented as mean + standard deviation.
reliability coefficient value. This reliability coefficient was
also computed for each clinical group: a (bv-FTD) ¼ .847 and
a (AD) ¼ .835. The interrater reliability was calculated for a
subsample of 30 patients with bv-FTD and resulted in a high
Pearson correlation of .976. The correlations between the
MoCA scores and the MMSE scores were also explored. A
high positive correlation was observed between the scores from
both tools in the total sample (r ¼ .802, P < .001) and in the
bv-FTD group (r ¼ .838, P < .001), which is indicative of con-
vergent validity. Both the correlations between each item and
the cognitive domains, and between each cognitive domain and
the overall MoCA score were also analyzed in the bv-FTD
group. All the items showed a significantly higher correlation
with their respective domains than with any other domain. In
this group, the Phonemic Fluency task showed a higher corre-
lation with the Executive Function domain than with Language
domain. The same result was found for the AD and healthy
groups. Furthermore, we found a significant (P < .001)
positive correlation between each cognitive domain and the
total score of the scale, ranging from .349 to .787. These corre-
lations are suggestive of construct-related validity.
Furthermore, each domain showed significantly higher
correlations with the MoCA total score than with any other
domain, illustrating the discriminative power of the domains.
Group Differences
There were statistically significant differences between the
groups in the MoCA total scores (F2,147 ¼ 96.700, P < .001).
According to post hoc tests, these differences occurred between
all group comparisons. Thus, although the clinical groups were
previously matched for the severity level of their cognitive
decline, as assessed by the MMSE (t98 ¼ 1.622, P ¼ .108), the
patients with AD obtained significant lower MoCA scores
(11.04 + 4.46) than the patients with bv-FTD
(13.34 + 5.03), and both clinical groups obtained lower scores
than the healthy group (22.50 + 3.44).
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Journal of Geriatric Psychiatry and Neurology 25(3)
As expected, a more detailed analysis regarding the sub-
scores from the MoCA cognitive domains revealed that the
Healthy
healthy participants performed higher in all cognitive domains
than both clinical groups. Comparing the 2 clinical groups, sta-
tistically significant differences in both the short-term Memory
domain and the Attention, Concentration and Working Mem-
ory domain were observed, with the patients with AD perform-
ing worse than the patients with bv-FTD, according to post
hoc tests (AD group: Memory domain [range 0-5] ¼ 0.16
+ 0.510; Attention, Concentration, and Working Memory
domain [range 0-6] ¼ 2.42 + 1.655; bv-FTD group: Memory
domain ¼ 0.72 + 1.230; Attention, Concentration and Work-
ing Memory domain ¼ 3.30 + 1.799). These cognitive
domains correspond to the test subscores as described by the
authors36 and corroborated by confirmatory factor analysis in
a previous study from our group.69
Cutoff Points
The ROC curve analyses were computed to evaluate the diag-
nostic accuracy of the MoCA and the MMSE to discriminate the
patients with bv-FTD from the cognitively healthy adults. Gra-
phic representations of the ROC curves are provided in Figure 1.
The MoCA discriminant potential for bv-FTD was excel-
lent, with an AUC of 0.934 (95% confidence interval
[CI] ¼ 0.866-0.974). In contrast, the MMSE showed an accep-
table discriminant potential, with a corresponding AUC of
0.772 (95% CI ¼ 0.677-0.850). These AUC were significantly
different from each other (z ¼ 4.472, P < .001), according to the
AUC comparison method of Hanley and McNeil,70 indicating
that the instruments were different in the accuracy of their
classifications.
Figure 1 illustrates that the ROC curve for the MoCA fully
included the curve for the MMSE, which is a clear indication
that there is always a cutoff for the MoCA, with higher sensi-
tivity and specificity, for any cutoff chosen for the MMSE. The
optimal cutoff point for maximum accuracy (Youden index)
and the respective values of sensitivity, specificity, PPV, NPV,
and classification accuracy are described for both instruments
in Table 2.
Discussion
This study was primarily motivated by the lack of studies vali-
dating the MoCA as a brief cognitive screening instrument for
patients with bv-FTD and by the need for a sensitive, reliable,
and accurate instrument to briefly assess the cognitive impair-
ments in these patients. In this context, 3 matched subgroups of
participants (bv-FTD, AD, and healthy groups) were
investigated to validate the MoCA in patients with bv-FTD,
to establish the MoCA corresponding cutoff point, and to
evaluate its diagnostic classification accuracy. Our findings
demonstrate the MoCA adequacy and usefulness for this task
and indicate that the MoCA is superior to the widely used
MMSE as a brief cognitive assessment of patients with bv-
FTD.
Freitas et al
Figure 1. The ROC curve analysis of the MoCA (dark gray) and
MMSE (medium gray) to detect bv-FTD, with reference line (light gray
diagonal). Abbreviations: MoCA, Montreal Cognitive Assessment;
MMSE, Mini-Mental State Examination; bv-FTD, frontotemporal
dementia, behavioral variant; ROC, receiver operating characteristics.
The MoCA consistently displayed superior psychometric
properties than the MMSE, which confirm the overall reliabil-
ity of the scale when used to examine Portuguese participants.
We consider that the presence of a manual with administration
and scoring rules for the tasks contributed to the excellent
interrater reliability of MoCA. The correlation coefficient
between the total scores of MoCA and MMSE was high,
suggesting convergent validity. Finally, significant positive
correlations were found between each item and its respective
cognitive domain, and all the items were more highly corre-
lated with their own respective domain than with any other
domain. Each cognitive domain was more highly correlated
with the MoCA total score than with any other domain. These
correlations support both the MoCA construct-related validity
and the discriminative power of the cognitive domains.
As expected, the healthy participants obtained higher MoCA
scores than either of the clinical groups. Despite the previous
matching according to the severity level, as assessed by the
MMSE, we found statistically significant differences between
the 2 clinical groups in the MoCA scores, with a lower
performance displayed by the patients with AD. This finding
demonstrates that the MoCA has better discriminant capacity
than the MMSE. At the level of the MoCA’s cognitive
domains, the healthy participants also had significantly higher
performances than both patient groups in all cognitive
domains. Between clinical groups, statistically significant dif-
ferences were observed in the MoCA’s Short-term Memory
and Attention, Concentration and Working Memory domains,
with the patients with AD performing worse than the patients
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151
Table 2. Diagnostic Classification Accuracya
Classification
Cutoff Sensitivity Specificity PPV NPV Accuracy
MoCA <17 78 98 98 82 88
MMSE <26 58 88 83 68 73
Abbreviations: MoCA, Montreal Cognitive Assessment (maximum score ¼
30); MMSE, Mini-Mental State Examination (maximum score ¼ 30); AUC, area
under the operating characteristic curve; PPV, positive predictive value; NPV,
negative predictive value.
a
Sensitivity, specificity, PPV, NPV, and classification accuracy values were
expressed in percentage. Cutoff values indicate the minimum score required
for absence of signal.
with bv-FTD. However, these results should be interpreted
cautiously because they contribute to a literature that already
presents several inconsistencies. Various factors have contrib-
uted to the difficulties in distinguishing between FTD and
other dementias at early stages of the disease using neuropsy-
chological tools,1,4,24 including (a) the clinical heterogeneity
of FTD; (b) its decline in other domains beyond the cognitive,
which are not evaluated by neuropsychological tests; (c) the
overlap in some cognitive deficits between FTD and other
types of dementia; (d) the insufficient breadth of representa-
tion of the cognitive abilities relevant to cognitive impairment
associated with the disease in the cognitive assessment tools,
an essential condition for the accurate and comprehensive
cognitive assessment; and (e) and the methodological differ-
ences across the study designs (eg, variation in the mean age
of participants and others characteristics, diagnostic criteria,
and assessment instruments used; the use of the mixed clinical
groups that include different FTD subtypes; and different
stages of the disease’s evolution). Furthermore, the MoCA
is a brief cognitive instrument, which by its nature has a
restricted range of tasks to assess each cognitive domain,
which constitutes an additional limitation to the analysis of
differences in cognitive profile between clinical groups
explored in this study.
The MoCA displayed excellent diagnostic accuracy in dis-
criminating patients with bv-FTD from cognitively healthy old
adults, and it exhibited an AUC that was significantly higher
than the AUC of MMSE. The optimal cutoff point for detecting
bv-FTD that allowed the maximization of the sensitivity and
specificity was below 17 points. This cutoff point is equivalent
to the optimal cutoff point established in our prior validation
studies of MoCA for patients with AD 71 and for patients with
vascular dementia (Freitas, Simões, Alves, Vicente, and San-
tana, 2012).72 With this cutoff point, the MoCA showed high
levels of sensitivity (78%), specificity (98%), PPV (98%), NPV
(82%), and classification accuracy (88%); all the values were
consistent and significantly higher than the respective MMSE
values. In this sample, the optimal cutoff point of MMSE to
detect bv-FTD was below 26 points.
We propose that the strengths of the current study include
the homogeneity of the sample regarding groups’ size, gender,
age, educational level, and severity level of cognitive decline
(as assessed by the MMSE in the clinical groups) as well as the
152
homogeneity in the FTD group (for which only the behavioral
variant was considered). These strengths allowed a clearer
analysis and minimized the influence of these individual and
methodological variables. Additionally, contributions to the
current study’s methodological rigor included the previous
well-validated clinical diagnosis of groups by a multidisciplin-
ary team using standard criteria and based on a full investiga-
tion, the presence of a control group composed of cognitively
healthy adults from the community, and the reduced interrater
variability due to evaluation of the participants by 1 of 2 expert
neuropsychologists.
However, some limitations of current study must be
addressed, mainly, that our analyses included only those
patients with FTD who displayed the behavioral variant. Cau-
tion should be used when generalizing these results to other
FTD syndromes. Besides, the sample of the present study
showed a low educational level, which is representative of the
demographic profile of our country, where the older strata of
the population are characterized by a very low educational
level. This feature should be taken into account in generalizing
the results of this study to other samples. It is also important to
consider that the aim of our study was the evaluation of mild-
to-moderate levels of severity of dementia. Future studies with
homogeneous samples of other FTD syndromes will be essen-
tial to corroborate the ability of MoCA to identify early cogni-
tive decline associated with bv-FTD. Finally, the current study
is the first to validate the MoCA for screening bv-FTD and to
examine its diagnostic accuracy with the establishment of cut-
off points; thus, we cannot compare it with other studies.
In conclusion, MoCA was confirmed as a valid, reliable,
sensitive, and accurate instrument for the brief assessment of
cognitive impairments in patients with bv-FTD. The MoCA
results were systematically superior to the MMSE results for
both discriminant validity and diagnostic accuracy. Therefore,
MoCA is a better cognitive screening instrument for bv-FTD
than the MMSE.
Authors’ Note
This study was done at the Dementia Clinic of the Neurology Depart-
ment of Coimbra University Hospital (Coimbra, Portugal) and at the
Faculty of Psychology and Educational Sciences, University of Coim-
bra (Coimbra, Portugal). Our results were partially presented on poster
session at the 21st Meeting of the European Neurological Society, Lis-
bon, Portugal (Freitas S, Simões MR, Santana I. Validity study of the
montreal cognitive assessment in patients with frontotemporal demen-
tia. Poster presented at the 21st Meeting of the European Neurological
Society; March, 2011; Lisbon, Portugal.).
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Funding
The author(s) disclosed receipt of the following financial support for
the research, authorship and/or publication of this article: the Funda-
ção para a Ciência e Tecnologia (Portuguese Foundation for Science
Downloaded from jgp.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 13, 2014
Journal of Geriatric Psychiatry and Neurology 25(3)
and Technology) through of a PhD fellowship (SFRH/BD/38019/
2007) and PIC/IC/83206/2007.
References
1. Hutchinson AD, Mathias JL. Neuropsychological deficits in fron-
totemporal dementia and Alzheimer’s disease: a meta-analytic
review. J Neurol Neurosurg Psychiatry. 2007;78(9):917-928.
2. Kertesz A, Blair M, McMonagle P, Munoz DG. The diagnosis and
course of frontotemporal dementia. Alzheimer Dis Assoc Disord.
2007;21(2):155-163.
3. Neary D, Snowden JS, Gustafson L, et al. Frontotemporal lobar
degeneration: a consensus on clinical diagnostic criteria. Neurol-
ogy. 1998;51(6):1546-1554.
4. Seelaar H, Rohrer JD, Pijnenburg YA, Fox NC, van Swieten JC.
Clinical, genetic and pathological heterogeneity of frontotem-
poral dementia: a review. J Neurol Neurosurg Psychiatry. 2011;
82(5):476-486.
5. Snowden JS, Neary D, Mann DM. Frontotemporal dementia. Br J
Psychiatry. 2002;180:140-143.
6. Weder ND, Aziz R, Wilkins K, Tampi RR. Frontotemporal
dementias: a review. Ann Gen Psychiatry. 2007;6:15.
7. Seelaar H, Kamphorst W, Rosso SM, et al. Distinct genetic forms
of frontotemporal dementia. Neurology. 2008;71(16):1220-1226.
8. Harvey RJ, Skelton-Robinson M, Rossor MN. The prevalence and
causes of dementia in people under the age of 65 years. J Neurol
Neurosurg Psychiatry. 2003;74(9):1206-1209.
9. Rossor MN, Fox NC, Mummery CJ, Schott JM, Warren JD. The
diagnosis of young-onset dementia. Lancet Neurol. 2010;9(8):
793-806.
10. Cruts M, Gijselinck I, van der Zee J, et al. Null mutations in pro-
granulin cause ubiquitin-positive frontotemporal dementia linked
to chromosome 17q21. Nature. 2006;442(7105):920-924.
11. Hutton M, Lendon CL, Rizzu P, et al. Association of missense and
5’-splice-site mutations in tau with the inherited dementia
FTDP-17. Nature. 1998;393(6686):702-705.
12. Baker M, Mackenzie IR, Pickering-Brown SM, et al. Mutations in
progranulin cause tau-negative frontotemporal dementia linked to
chromosome 17. Nature. 2006;442(7105):916-919.
13. Mackenzie IR, Neumann M, Bigio EH, et al. Nomenclature and
nosology for neuropathologic subtypes of frontotemporal lobar
degeneration: an update. Acta Neuropathol. 2010;119(1):1-4.
14. Johnson JK, Diehl J, Mendez MF, et al. Frontotemporal lobar
degeneration: demographic characteristics of 353 patients. Arch
Neurol. 2005;62(6):925-930.
15. McKhann GM, Albert MS, Grossman M, et al. Clinical and patho-
logical diagnosis of frontotemporal dementia: report of the Work
Group on Frontotemporal Dementia and Pick’s Disease. Arch
Neurol. 2001;58(11):1803-1809.
16. Snowden JS, Goulding PJ, Neary D. Semantic dementia: a form of
circumscribed cerebral atrophy. Behav Neurol. 1989;2:167-182.
17. Hodges JR, Patterson K, Oxbury S, Funnell E. Semantic demen-
tia. Progressive fluent aphasia with temporal lobe atrophy. Brain.
1992;115 (pt 6):1783-1806.
18. Gorno-Tempini ML, Hillis AE, Weintraub S, et al. Classification
of primary progressive aphasia and its variants. Neurology. 2011;
76(11):1006-1014.
Freitas et al
19. Neary D, Snowden J, Mann D. Frontotemporal dementia. Lancet
Neurol. 2005;4(11):771-780.
20. Diehl J, Monsch A U, Aebi C, et al. Frontotemporal dementia,
semantic dementia, and Alzheimer’s disease: the contribution
of standard neuropsychological tests to differential diagnosis.
J Geriatr Psychiatry Neurol. 2005;18(1):39-44.
21. Gregory CA, Orrell M, Sahakian B, Hodges JR. Can frontotem-
poral dementia and Alzheimer’s disease be differentiated using
a brief battery of tests?. Int J Geriatr Psychiatry. 1997;12(3):
375-383.
22. Mathuranath PS, Nestor PJ, Berrios GE, Rakowicz W, Hodges JR.
A brief cognitive test battery to differentiate Alzheimer’s disease
and frontotemporal dementia. Neurology. 2000;55(11):1613-1620.
23. Perry RJ, Hodges JR. Differentiating frontal and temporal variant
frontotemporal dementia from Alzheimer’s disease. Neurology.
2000;54(12):2277-2284.
24. Thompson JC, Stopford CL, Snowden JS, Neary D. Qualitative
neuropsychological performance characteristics in frontotem-
poral dementia and Alzheimer’s disease. J Neurol Neurosurg
Psychiatry. 2005;76(7):920-927.
25. De Jesus-Hernandez M, Mackenzie IR, Boeve BF, et al.
Expanded GGGGCC hexanucleotide repeat in noncoding region
of C9ORF72 causes chromosome 9p-linked FTD and ALS. Neu-
ron. 2011;72(2):245-256.
26. Renton AE, Majounie E, Waite A, et al. A hexanucleotide repeat
expansion in C9ORF72 is the cause of chromosome 9p21-linked
ALS-FTD. Neuron. 2011;72(2):257-268.
27. Folstein M, Folstein S, McHugh P. Mini-mental State. A practical
method for grading the cognitive state of patients for the clinician.
J Psychiatr Res. 1975;12(3):189-198.
28. Freitas S, Santana I, Simões MR. The sensitivity of the MoCA and
MMSE to cognitive decline: a longitudinal study. Alzheimers
Dement. 2010;6(4):S353-S354 [Abstract].
29. Ihl R, Frölich L, Dierks T, Martin EM, Maurer K. Differential
validity of psychometric tests in dementia of Alzheimer type.
Psychiatry Res. 1992;44(2):93-106.
30. Tombaugh TN, McIntyre NJ. The Mini-Mental State Examina-
tion: a comprehensive review. J Am Geriatr Soc. 1992;40(9):
922-935.
31. Wind AW, Schellevis FG, Van Staveren G, Scholten RP, Jonker
C, Van Eijk JT. Limitations of the Mini-Mental State
Examination in diagnosing dementia in general practice. Int
J Geriatr Psychiatry. 1997;12(1):101-108.
32. Gregory CA, Hodges JR. Dementia of frontal type: use of
consensus criteria and prevalence of psychiatric features.
Neuropsychiatr Neuropsychol Behav Neurol 1996;9:145-153.
33. Miller BL, Cummings JL, Villanueva-Meyer J, et al. Frontal lobe
degeneration: clinical, neuropsychological, and SPECT charac-
teristics. Neurology. 1991;41(9):1374-1382.
34. Hodges JR, Patterson K, Ward R, et al. The differentiation of
semantic dementia and frontal lobe dementia (temporal and frontal
variants of frontotemporal dementia) from Alzheimer’s disease: a
comparative neuropsychological study. Neuropsychology. 1999;
13(1):31-40.
35. Naugle RI, Kawczak K. Limitations of the Mini-Mental State
Examination. Cleve Clin J Med. 1989;56(3):277-281.
Downloaded from jgp.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 13, 2014
153
36. Nasreddine Z, Phillips NA, Bédirian V, et al. The Montreal Cog-
nitive Assessment, MoCA: a brief screening tool for mild cogni-
tive impairment. J Am Geriatr Soc. 2005;53(4):695-699.
37. Fujiwara Y, Suzuki H, Yasunaga M, et al. Brief screening toll for
mild cognitive impairment in older Japanese: validation of the
Japanese version of the Montreal Cognitive Assessment. Geriatr
Gerontol Int. 2010;10(3):225-232.
38. Lee J, Lee Dong Woo, Cho SJ, et al. Brief screening for mild cog-
nitive impairment in elderly outpatient clinic: validation of the
Korean version of the Montreal Cognitive Assessment. J Geriatr
Psychiatry Neurol. 2008;21(2):104-110.
39. Luis CA, Keegan AP, Mullan M. Cross validation of the Montreal
Cognitive Assessment in community dwelling older adults resid-
ing in the Southastern US. Int J Geriatr Psychiatry. 2009;24(2):
197-201.
40. Rahman TT, Gaafary MM. Montreal Cognitive Assessment Ara-
bic version: reliability and validity prevalence of mild cognitive
impairment among elderly attending geriatric clubs in Cairo. Ger-
iatr Gerontol Int. 2009;9(1):54-61.
41. Smith T, Gildeh N, Holmes C. The Montreal Cognitive Assess-
ment: validity and utility in a memory clinic setting. Can J Psy-
chiatry. 2007;52(5):329-332.
42. Zhao S, Guo C, Wang M, et al. A clinical memory battery for
screening for amnestic mild cognitive impairment in an elderly
Chinese population. J Clin Neurosci. 2011;18(6):774-779.
43. Ismail Z, Rajji TK, Shulman KI. Brief cognitive screening instru-
ments: an update. Int J Geriatr Psychiatry. 2010;25(2):111-120.
44. Lonie JA, Tierney KM, Ebmeier KP. Screening for mild cognitive
impairment: a systematic review. Int J Geriatr Psychiatry. 2009;
24(9):902-915.
45. Jacova C, Kertesz A, Blair M, Fisk JD, Feldman HH. Neuropsy-
chological testing and assessment for dementia. Alzheimers
Dement. 2007;3(4):299-317.
46. Garcia C. A Doença de Alzheimer: Problemas de diagnóstico
clı´nico [Alzheimer’s disease: Difficulties in clinical diagnosis]
[dissertation]. Lisbon: University of Lisbon; 1984.
47. Rascovsky Hodges JR, Knopman D, et al. Sensitivity of revised
diagnostic criteria for the behavioural variant of frontotemporal
dementia. Brain. 2011;134(pt 9):2456-2477.
48. Cummings JL, Mega M, Gray K, Rosenberg-Thompson S, Carusi
DA, Gornbein J. The Neuropsychiatric Inventory comprehensive
assessment of psychopathology in dementia. Neurology. 1994;
44(12):2308-2314.
49. Kertesz A, Nadkami N, Davidson W, Thomas AW. The Frontal
Behavioral Inventory in the differential diagnosis of frontotem-
poral dementia. J Int Neuropsychol Soc. 2000;6(4):460-468.
50. Schaffer SG, Wisniewski A, Dahdah M, Froming KB. Emotion
Processing: The Comprehensive Affect Testing System. User’s
manual. Sanford, FL: Psychology Software Inc; 2006.
51. Dubois B, Slachevsky A, Litvan I, Pillon B., The FAB: A Frontal
Assessment Battery at bedside. Neurology. 2000;55(11):
1621-1626.
52. .Partington JE, Leiter RG Pathway Test. Psychol Serv Center
Bull. 1949;1:9-20.
53. Lezak MD, Howieson DB, Loring DW. Neuropsychological
Assessment. New York, NY: Oxford University Press; 2004.
154
54. Wechsler D. Wechsler Adult Intelligence Scale. 3rd ed. Portu-
guese version. Lisbon, Portugal: Cegoc-Tea; 2008.
55. Wechsler D. Wechsler Memory Scale. 3rd ed. Portuguese version.
Lisbon, Portugal: Cegoc-Tea; 2008.
56. De Renzi E, Vignolo LA. The Token Test: a sensitive test to
detect receptive disturbances in aphasics. Brain. 1962;85:
665-678.
57. Buschke H. Selective reminding for analysis of memory and
learning. J Verb Learn Verb Behav. 1973;12:543-550.
58. Benedict RH. Brief Visuospatial Memory Test. Revised. Odessa,
FL: Psychological Assessments Resources Inc; 1997.
59. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorder., 4th ed, text revised. Washington,
DC: American Psychiatric Association; 2000.
60. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Sta-
dlan EM. Clinical diagnosis of Alzheimer’s disease: report of the
NINCDS-ADRDA Work Group under the auspices of Depart-
ment of Health and Human Services Task Force on Alzheimer’s
disease. Neurology. 1984;34(7):939-944.
61. Rosen WG, Mohs RC, Davis KL. A new rating scale for Alzhei-
mer’s disease. Am J Psychiatry. 1984;141(11):1356-1364.
62. Hughes CP, Berg L, Danziger WL, Coben LA, Martin RL. A new
clinical scale for the staging of dementia. Brit J Psychiatry. 1982;
140:566-572.
63. Alves L, Simões MR, Martins C. Teste de Leitura de Palavras
Irregulares (TeLPI) [Reading Word Irregular Test]. Coimbra, Ser-
viço de Avaliação Psicológica da Faculdade de Psicologia e de
Ciências da Educação da Universidade de Coimbra; 2009.
64. Schmand B, Jonker C, Hooijer C, Lindeboom J. Subjective mem-
ory complaints may announce dementia. Neurology. 1996;46(1):
121-125.
Downloaded from jgp.sagepub.com at TOBB Ekonomi ve Teknoloji Üniversitesi on May 13, 2014
Journal of Geriatric Psychiatry and Neurology 25(3)
65. Yesavage JA, Brink TL, Rose TL, et al. Development and valida-
tion of a geriatric depression screening scale: a preliminary report.
J Psychiatr Res. 1983;17(1):37-49.
66. Freitas S, Simões MR, Alves L, Santana I. Montreal Cognitive
Assessment (MoCA): normative study for the Portuguese popula-
tion. J Clin Exp Neuropsychol. 2011;33(9):989-996.
67. Guerreiro M. Contributo da Neuropsicologia Para o Estudo
Das Demeˆncias [Contribution of Neuropsychology to the study
of dementia] [dissertation]. Lisbon: University of Lisbon;
1998.
68. Simões MR, Freitas S, Santana I, Firmino H, Martins C, Nasred-
dine Z, Vilar M. Montreal Cognitive Assessment (MoCA): Versão
final portuguesa [Montreal Cognitive Assessment (MoCA): Por-
tuguese Final Version]. Coimbra, Serviço de Avaliação Psicoló-
gica, Faculdade de Psicologia e de Ciências da Educação da
Universidade de Coimbra; 2008.
69. Freitas S, Simões MR, Marôco J, Alves L, Santana I.
Construct validity of the Montreal Cognitive Assessment
(MoCA). J Int Neuropsychol Soc. 2012;18(2):1-9. doi:10.
1017/S1355617711001573.
70. Hanley JA, McNeil BJ. A method of comparing the areas under
receiver operating characteristic curves. Radiology. 1983;
148(3):839-843.
71. Freitas S, Simões MR, Alves L, Santana I. Montreal Cognitive
Assessment (MoCA): validation study for Mild Cognitive Impair-
ment and Alzheimer’s disease. Alzheimer Dis Assoc Disord. 2012.
doi: 10.1097/WAD.0b013e3182420bfe.
72. Freitas S, Simões M R, Alves L, Vicente M, Santana I.
Montreal Cognitive Assessment (MoCA): Validation study for
Vascular Dementia. J Int Neuropsychol Soc. 2012; doi:10.
1017/S135561771200077X..