REVIEW

Overlay of Late-Life Depression and Cognitive

Impairment
Rehan Aziz, M.D., and David Steffens, M.D., M.H.S.

This article appraises several facets of the linkage between depression and cognitive impairment, including dementia, mild
cognitive impairment, and vascular dementia. Potential mechanisms for this association are examined. This review was
crafted to be extensive but not exhaustive. The authors searched PubMed, using the terms depression, late-life depression,
cognitive impairment, and dementia. Articles included are seminal articles from the field as well as representative, heuristic
studies. A link between depression and cognitive impairment was found. Depression likely serves as both a risk factor and a
prodromal symptom of dementia. Mechanisms whereby depression could induce cognitive impairment include hippocampal
atrophy, alterations in glucocorticoid secretion, cerebrovascular compromise, deposition of b-amyloid plaques, chronic
inflammation, apolipoprotein E status, and deficits of nerve growth factors. This article will benefit the practicing clinician by
increasing awareness of the links between depression and dementia and encouraging greater emphasis on screening for
cognitive impairment among individuals with depression or a history of depression.
Focus 2017; 15:35–41; doi: 10.1176/appi.focus.20160036

OVERVIEW mechanisms whereby depression may result in lasting cog-

Cognitive deficits are a core feature of depression among both
adults and elders, which makes depression a “cognitive dis-
order” for many people (1). Cognitive deficits are consistently
found in the domains of memory, verbal learning, motor
speed, executive functioning, and processing speed (2). In the
past, such deficits were thought to be temporary and isolated
to periods of dysphoria. They were labeled “pseudodementia”
or “reversible dementia.” Increasingly, there is evidence to
suggest that cognitive deficits persist despite remission of
depression. Continuing cognitive deficits may be related to
underlying brain changes, including hippocampal atrophy,
alterations in glucocorticoid secretion, and cerebrovascular
compromise (3–5). Other biological mechanisms linking
depression to cognitive impairment include increased de-
position of b-amyloid plaques, chronic inflammation, and
deficits of nerve growth factors, such as brain-derived neu-
rotrophic factor (6).
Fifteen years ago, Jorm (7) proposed three hypotheses to
explain the relationship between dementia and depression.
Depression can, first, be an early prodromal sign of dementia;
second, bring forward the clinical manifestations of dement-
ing disease; and third, lead to hippocampal damage through a
glucocorticoid cascade. He concluded that depression is likely
a risk factor for dementia in general and Alzheimer’s disease
specifically (7).
This article appraises several facets of the linkage between
depression and cognitive impairment, including whether de-
pression is a risk factor or a prodromal feature of dementia.
Other areas of exploration include the impact of midlife, late-
life, and vascular depression on cognition and possible
nitive impairment. This review was crafted to be extensive,
although not exhaustive, because this is a rapidly expanding
area of inquiry.
DESCRIPTION
Depression among older adults can have a variety of presen-
tations. It may arise as recurrent disease stemming from earlier
life. This has been termed early-onset or midlife depression.
Late-onset or late-life depression is described as depression
that initially occurs past the age of 60 to 65 years. Depression
can also occur as a mood disorder secondary to another
medical condition or as mood symptoms secondary to sub-
stance use or medication.
Symptomatic differences have been noted in early-onset
depression and late-life depression. Early-onset depression
has been characterized by greater personality abnormalities,
a family history of psychiatric illness, and dysfunctional past
maternal relationships. The mood is often depressed, hope-
less, and accompanied by suicidal thoughts (8). Late-life de-
pression has been described by fearfulness, poor appetite,
weariness, hopelessness, worthlessness, guilt, and anger. Peo-
ple with late-life depression have fewer crying spells and less
sadness (8, 9). Anxiety, somatic complaints, and thoughts
of death, rather than outright suicide ideation, may occur
more frequently (9).
As noted, cognitive deficits are a core feature of depression
for both adults and elders. Among younger adults, decreased
concentration and indecisiveness are seen, whereas cognitive
complaints of older adults may include selective attention,
problems in working memory, impaired memory retrieval,

Focus Vol. 15, No. 1, Winter 2017 focus.psychiatryonline.org 35

OVERLAY OF LATE-LIFE DEPRESSION AND COGNITIVE IMPAIRMENT
TABLE 1. Adult Versus Geriatric Depression (13, 14)
Symptom Domain Adult Presentation
Mood Depressed mood, anhedonia, Depressed, hopeless, feels worthless,
suicidal thoughts psychic anxiety, thoughts of death
Somatic Sleep changes, appetite changes, Activity changes, general somatic symptoms
activity changes
Cognitive Decreased concentration, Decreased processing speed, executive
indecisiveness function, selective attention, working
memory, verbal fluency, spatial planning
difficulties in learning, slowed processing speed, and exec-
utive dysfunction (10–12). Table 1 summarizes these pre-
sentations. Cognitive deficits persist even during euthymic
periods, and, compared with healthy others, euthymic pa-
tients postdepression have had significantly poorer cognitive
function (11). Cognitive deficits seem to be more common
among patients with late-onset depression, compared with
those with early-onset disease. This supports theories sug-
gesting that vascular and neurodegenerative factors, which
are more common in late life, affect a substantial number of
these patients (11) and that etiologically, late-life depression
may be different from early-onset depression.
DEPRESSION AND DEMENTIA
The crux of the association between depression and dementia
has focused on whether depression is a risk factor for de-
mentia, a prodrome of dementia, or some combination of
both. The majority of published studies have highlighted an
increased risk of dementia among people with previous di-
agnoses of depression. However, approximately one quarter
of studies have not shown any statistically significant increase
in this risk (15), which has led to continued uncertainty
regarding this association. Other areas of inquiry have been
whether there is differential risk for dementia among patients
with early-onset, late-life, vascular, or recurrent depression.
Cognitive deficits can persist despite remission of de-
pressive symptoms, which indicates that depression may have
a longer term pernicious effect on cognition. In one study,
conducted over three years, irreversible dementia developed
significantly more frequently among depressed elders with
reversible dementia or pseudodementia (43%) than among
the group with depression alone (12%). The group with re-
versible dementia had a 4.69 times higher chance of de-
veloping dementia than patients with depression alone (16).
Cognitive areas affected included visuoperception, processing
speed, and memory function (13). Researchers have continued
to find deficits up to 18 months and four years later postde-
pression, so that cognitive impairment among elderly patients
with depression may be a trait characteristic, such that even
when depression has remitted, cognitive impairment persists (3).
With respect to depression as a risk factor for dementia,
data have been mixed (7, 17). A large systematic review and
meta-analysis concluded that depression was a risk factor
for dementia. The researchers appraised 20 studies involv-
ing 102,172 patients. They separated case-control studies,
36 focus.psychiatryonline.org
which are retrospective and
Geriatric Presentation subject to recall bias, from
cohort studies, which are pro-
spective. The authors found
calculated pooled odds ratios
(ORs) of 2.03 for case-control
studies and 1.90 for cohort
studies. The interval between
diagnoses of depression and
Alzheimer’s dementia (AD)
was positively related to increased risk of developing AD,
which suggests that rather than a prodrome, depression may
be a risk factor for AD (18). Another meta-analysis involving
older adults and elders over age 50 found that depression was
also associated with a significant risk of all-cause dementia
(OR51.85), AD (OR51.65), and vascular dementia (VaD;
OR52.52) (14).
The hypothesis that depression is a prodrome to dementia
is most compatible with studies in which depression occurs
near the onset of dementia. The MIRAGE study was a case-
control study involving more than 4,000 individuals. A sig-
nificant association was found between depression and AD,
with an OR of 2.13. Where depression first occurred within
one year before onset of AD, the OR was 4.47. Where de-
pression first occurred more than one year before onset of AD,
the OR was 1.38. Where depression first occurred more than
25 years before onset of AD, the OR was 1.71 (19). The data
suggested that depression is a significant prognostic indicator
for dementia, as well as a risk factor. Barnes et al. (20) con-
ducted a retrospective cohort review of 13,535 Kaiser Per-
manente patients with an average age of 81.1 years. Depressive
symptoms were present among 14.1% of patients in midlife
only, 9.2% in late-life only, and 4.2% in both. During six years
of follow-up, 22.5% of the patients received a diagnosis of
dementia. The adjusted hazard ratio of dementia was in-
creased by approximately 20% for midlife depressive symp-
toms only (OR51.19), 70% for late-life symptoms only
(OR51.72), and 80% for both (OR51.77). When AD and VaD
were examined separately, patients with late-life depressive
symptoms had a twofold increase in AD risk (OR52.06),
whereas patients with midlife and late-life symptoms had
more than a threefold increase in VaD risk (OR53.51). In this
analysis, late-life depressive symptoms were more predictive
of dementia than early-life depressive symptoms (20). Other
studies have also found that a history of current depression
and increasing depressive symptoms in late life increase the
risk of cognitive impairment, whereas a history of past de-
pressive symptoms or low depression is not associated with
cognitive impairment. These data suggest that depression in
later life may also represent a prodromal phase of cognitive
impairment (21, 22).
Recurrent depression seems to present a greater risk for
dementia than single-episode depression, such that patients
with many prior hospitalizations for depression have an in-
creased risk of developing subsequent dementia. On aver-
age, each depressive episode has been associated with
Focus Vol. 15, No. 1, Winter 2017

a 13% increased rate of dementia (23). This result has been
confirmed in a prospective study of 1,239 older adults from
the Baltimore Longitudinal Study of Aging. In that study,
each depressive episode was associated with a 14% increase
in risk for all-cause dementia (24).
In sum, the proposals of depression as either a risk factor
or a prodrome for dementia are not mutually exclusive. Data
currently seem to reflect that depression is both a risk factor
and a prodrome for dementia (15, 18–20, 25, 26), although
there is evidence to the contrary (21, 27–29), likely because of
heterogeneity in methodology, populations, and other factors.
More data support early-onset depression’s serving as a risk
factor for dementia (17, 30) than support late-life depression’s
acting as a prodromal symptom of dementia (20, 21). How-
ever, in studies looking across age ranges, the magnitude of
risk ratios decreases with the time between depression onset
and dementia diagnosis (1, 19, 20), which makes it more likely
that later onset of depression may be a more significant pro-
dromal symptom or risk factor for later dementia (1). There
also seems to be a dose-response relationship between de-
pression and dementia, such that each depressive episode is
associated with an increased rate of dementia (23, 24).
DEPRESSION AND MILD COGNITIVE IMPAIRMENT
The term mild cognitive impairment (MCI) is used to charac-
terize nonnormal cognitive function that is not severe enough
to meet diagnostic criteria for dementia (1). It has been con-
ceptualized as a predementia state or a warning sign that the
risk of dementia is high. Depression occurs commonly among
people with MCI and has been found in 30%245% of patients
with MCI (31, 32). More than 20% of patients with MCI
convert to dementia within a three-year period (33). However,
the majority of MCI patients do not convert. Researchers
have attempted to determine which factors lead to dementia
conversion and have looked at depression, apolipoprotein E
(APOE) genotypes, and amnestic MCI (aMCI).
Studies have shown that the presence of depressive
symptoms increases the rate of conversion of MCI to de-
mentia (34). In one study of MCI patients, after a mean period
of three years, 85% of the patients with depression developed
dementia, in comparison with 32% of the patients without
depression. The relative risk (RR) was 2.6. Patients with MCI
and depression had more than twice the risk of developing AD
as those without depression (32). This finding was confirmed
in a large meta-analysis. Eighteen studies were included, with
a sample size of 10,861 patients with MCI. The pooled RR of
progressing to dementia was 1.28 for the group of MCI
patients with depressive symptoms, compared with non-
depressed patients with MCI (35).
Other factors that might affect the role of depression in
conversion of MCI to dementia include APOE status and the
presence of aMCI. The risk of developing AD has been sig-
nificantly higher among depressed aMCI groups than among
depressed nonamnestic groups (36). The role of APOE status
in conversion to dementia and the development of MCI has
Focus Vol. 15, No. 1, Winter 2017
AZIZ AND STEFFENS
been more mixed. In one study, 21% of depressed elders met
criteria for aMCI. Among depressed elders, aMCI and age
were most associated with incident dementia and AD. Any
APOE ε4 allele was not significant (37). Another study found
significance only for depression and ε3/ε4 or ε4/ε4 geno-
types in the development of MCI (hazard ratio55.1) (38).
Researchers have used imaging studies to further explore
the relationship between depression and MCI. A synergistic
effect of depressive symptoms and smaller left hippocampal
volume among MCI patients has been found to accelerate
conversion to dementia (39). In the Alzheimer’s Disease Neu-
roimaging Initiative study, those with persistent depressive
symptoms had higher conversion to AD, compared with those
who remained without neuropsychiatric symptoms. Patients
with MCI who had comorbid depressive symptoms showed
more frontal, parietal, and temporal white matter atrophy than
asymptomatic patients (40).
VASCULAR DEPRESSION AND DEMENTIA
The vascular depression hypothesis postulates that cerebro-
vascular disease predisposes, precipitates, or perpetuates a
depressive syndrome among some older adult patients (4). The
hypothesis is supported by the known comorbidity of de-
pression, vascular disease, vascular risk factors, and ischemic
lesions with distinctive behavioral symptoms. Researchers
have postulated that the central mechanisms are disruption
of prefrontal systems and their limbic and hippocampal con-
nections or their modulating pathways by single lesions or by
an accumulation of lesions exceeding a threshold (39).
Patients with vascular depression have characteristic features.
With respect to clinical symptoms, patients have significant psy-
chomotor retardation, little psychomotor agitation, less guilt,
poorer insight, and limited depressive symptoms, compared with
healthy others (41). Individuals have tended to be older, have
higher levels of hypertension and other cerebrovascular risk
factors, and have less family history of depression (42, 43). They
also have greater overall cognitive impairment and disability
than those with nonvascular depression. Cognitively, fluency and
naming are impaired (4, 41). However, the core cognitive deficits
in late-life depression seem to be slowed processing speed, fol-
lowed by executive dysfunction. Changes in processing speed
most fully mediate the effect of age, depression severity, educa-
tion, race, and vascular risk factors on other cognitive domains,
including episodic memory and visuospatial performance. These
declines persist even after remission of depression (44, 45).
Supporting the vascular depression hypothesis, a large
proportion of elders with depression have had either a stroke
or other evidence of cerebrovascular compromise (41, 46, 47).
Pooled data from studies have found poststroke prevalence
rates for major depression of 19.3% among hospitalized pa-
tients and 23.3% among outpatients (47). These numbers are
higher than the prevalence of major depressive disorder in the
general population (8.3%) (48).
High rates of cerebrovascular disease, along with white
matter hyperintensities (WMHs) on MRIs, have also been
focus.psychiatryonline.org 37
OVERLAY OF LATE-LIFE DEPRESSION AND COGNITIVE IMPAIRMENT
found among depressed elders (49). WMHs are thought to be
caused by small, silent cerebral infarctions. They are char-
acterized by arteriosclerosis, perivascular demyelination, di-
lated periventricular spaces, and ischemia (50, 51). They can
predispose individuals to depression (49, 52) by disrupting the
fiber tracts connecting cortical and subcortical structures (52)
in areas such as the dorsolateral prefrontal cortex and the
anterior cingulate cortex (50). In one study involving patients
with late-life depression, silent cerebral infarctions were ob-
served among 65.9% of those with early-onset depression and
among 93.7% of those with late-life depression (53). A sys-
tematic review (54) confirmed this finding. The authors found
that late-life depression was characterized by more frequent
and intense white matter abnormalities than early-onset de-
pression. The odds of having white matter changes were over
4 for late-onset illness, compared with early-onset illness.
These differences suggest different etiological mechanisms
for late-life depression, in keeping with the vascular de-
pression hypothesis (54). Last, considering structural brain
changes, Kramer-Ginsberg et al. (55) found that among
elders with depression, hyperintensity location/severity
and the presence or absence of depression had a significant
interaction with cognitive performance. Depressed pa-
tients with moderate-to-severe deep WMH had worse per-
formance on general and delayed recall memory, executive
function, and language testing than depressed patients
without WMH and normal elders with or without deep
white matter changes. (54).
Regarding vascular depression and vascular dementia, the
similarity of risk factors and findings for the two conditions
implies a connection. Both conditions encompass cerebrovas-
cular compromise through vascular risk factors, ischemic le-
sions, and the detection of WMHs, among other potential
findings. However, the path from vascular disease to vascular
depression to vascular dementia has not been elucidated.
Furthermore, the road may be reciprocal and not direct or
sequential, given that depression can also increase the risk of
vascular disease and vice versa (4). Unfortunately, research
linking vascular depression to dementia, including vascular
dementia, is limited (27, 56). However, it is likely that a con-
nection exists between these conditions and that structural
brain changes may be a distinctive feature of late-life de-
pression linking it to cognitive impairment.
DEPRESSION IN DEMENTIA
Symptoms of depression are often present in dementia and
may constitute one of the many behavioral and psychological
symptoms of dementia. A considerable minority of AD pa-
tients, during the course of their illness, exhibit depressed
mood (40%250%), whereas depressive disorders are en-
countered in 10%220% of patients (57). Depression may
occur more commonly as a symptom in VaD than in AD (58).
It is also common among patients with other forms of de-
mentia, such as dementia with Lewy bodies, Parkinson’s
disease, and Huntington’s disease (1). The high prevalence of
38 focus.psychiatryonline.org
depressive symptoms in dementia seems to indicate an on-
going association between these conditions.
DEPRESSION AND CEREBRAL DISRUPTION
Depression is associated with disruption in a number of
brain regions. Some described areas include the hippocam-
pus, prefrontal systems and their limbic-hippocampal con-
nections, the orbitofrontal cortex (OFC), the dorsolateral
prefrontal cortex (DLPFC), the anterior cingulate gyrus, and
the amygdala (1, 59).
The hippocampus plays a critical role in learning, recall,
and affect regulation (1). Depression serves as a neurobiolog-
ical stressor. Overall, it leads to excess circulating glucocorti-
coids, which result in hippocampal neurotoxicity and volume
loss (60). Decreased hippocampal volume may result from
many factors. First, it has been demonstrated in animal studies
that stress induces decreased cell proliferation in the hippo-
campal region, which leads to reduced neurogenesis (61).
Second, the glucocorticoid hypothesis (62) postulates that a
prolonged physical reaction to stress elicits sustained gluco-
corticoid secretion. There are glucocorticoid receptors in the
hippocampus. Over time, glucocorticoid hypersecretion leads
to excessive activation of these receptors. This overstimulation
is eventually toxic and leads to neuronal cell death and atro-
phy. Such damage has been recorded in imaging studies (63),
has been associated with cognitive decline and dementia
(64, 65), and has been demonstrated in clinical studies (5, 66).
Sheline et al. (66) found that females, ages 23–86, with a
history of depression (postdepression) had smaller hippo-
campal volumes bilaterally than did case-matched others
without depression but with similar age and education. They
scored lower on verbal memory, a neuropsychological mea-
sure of hippocampal function, which suggested that the
volume loss was related to cognitive functioning. There was
also a significant correlation with hippocampal volume loss
and total lifetime duration of depression. This suggested a
dose-response relationship between depression and cogni-
tive impairment, which indicated that repeated stress from
recurrent depressive episodes may result in cumulative
hippocampal injury, reflected in volume loss (66).
A later prospective study of elders found that over two
years, the depressed group showed a greater reduction in left
hippocampal volume than the nondepressed group. The study
found that hippocampal change from baseline to two years
was associated with subsequent change in Mini–Mental State
Examination scores from two years to two and a half years in
the depressed group. Thus, depressed elders with hippocam-
pal volume loss were at greater risk of cognitive decline (5).
Age of depression onset seems to correlate negatively with
hippocampal volume, so that patients with late-life depression
have smaller hippocampal volumes compared with controls
and those with early-onset depression (59, 63). However, others
have found different results and have connected reductions in
hippocampal volume with earlier onset depression (66) and
longer duration of untreated depression (67).
Focus Vol. 15, No. 1, Winter 2017

Last, with respect to other brain areas in- FIGURE 1. Some Pathways Linking Depression With Dementia
volving depression and cognition, the OFC
seems to have a role in selectively processing
affective stimuli. This makes depressed indi-
viduals predisposed to cognitive errors if they
have received negative feedback on preceding
tasks (68). Increased lesion density has been
found in the OFC among patients with late-life
depression (69). The anterior cingulate gyrus
seems to be involved in initiation and sup-
pression of behavior through conflict moni-
toring and appraisal of motivational content
(1). It is also involved in spatial planning and
working memory. Individuals with depression
have demonstrated lower activation of this
region on the Tower of London task, which is a test of plan-
ning (70). The DLPFC is involved in working memory,
retrieval of episodic memory, planning, and response moni-
toring (1). Late-life depression has also been associated
with microstructural changes in the white matter of the
DLPFC (71).
CONCLUSION
Summary of the Literature on Cognitive Deficits With
Late-Life Depression
Cognitive deficits are a core feature of depression among
both adults and elders, which makes depression a cognitive
disorder (1). Deficits are consistently found in the domains
of memory, verbal learning, motor speed, executive function,
and processing speed (2). Depression may be associated with
cognitive impairment through a variety of mechanisms, in-
cluding hippocampal volume loss from excess secretion
of glucocorticoids, resulting in neurotoxicity; inhibition
of hippocampal neurogenesis (61, 62); cerebrovascular com-
promise, including disruption of prefrontal systems and
their limbic-hippocampal connections (4); increased de-
position of b-amyloid plaques; chronic inflammation; and
deficits of nerve growth factors, such as brain-derived
neurotrophic factor (6). Studies of late-life depression
have demonstrated a reduction in hippocampal volume
(63, 72), and this has been linked to impaired cognition (5,
66). Late-life depression and total lifetime duration of
depression may have the greatest overall effects on volume
loss (59, 66). Depression could also be an important marker
for increased risk of conversion from depression to de-
mentia among patients with MCI and especially aMCI. A
partial model depicting some of these relationships is
presented in Figure 1.
It also seems that depression is a both a risk factor and a roimaging, such as a brain MRI or head CT. Future tools
prodrome for dementia (15, 18–20, 25, 26). The quantity of
data is greater for early-onset depression’s serving as a risk
factor for dementia (17, 30) than for late-life depression’s
serving as a prodromal symptom of dementia (20, 21). How-
ever, the strength of the linkage decreases with increasing time comprise soluble Abeta, tau, synuclein, and others for
between depression onset and dementia diagnosis (1, 19, 20).
Focus Vol. 15, No. 1, Winter 2017
AZIZ AND STEFFENS
This suggests that older age at depression onset may be more
important as a prodromal symptom or a risk factor for
dementia than earlier onset illness (1). There also seems to be
a dose-response relationship between depression and de-
mentia, such that each depressive episode is associated with
an increased rate of dementia (23, 24). Future studies will
probably continue to suggest one relationship, both rela-
tionships, or neither. This is likely a reflection of the hetero-
geneous presentations and diverse pathologies of depression
and dementia. Perhaps the more vital issues are identifying
factors that cause depression to become a risk factor for de-
mentia and determining which factors cause depression to
develop into prodromal dementia (1).
Clinical Relevance
The evidence that late-life depression may represent a pro-
drome for dementia and that midlife depression may be a
risk factor for dementia should be concerning for clinicians.
Increased vigilance in screening for signs and symptoms of
depression and cognitive impairment is imperative, espe-
cially among elders (60). Researchers have estimated that
10% of dementia cases could be attributed to depression. A
10% reduction in depression prevalence, through aggressive
screening and management, could result in more than
325,000 fewer AD cases worldwide and 67,000 fewer cases
in the United States (73).
Although strategies for identifying depression and cog-
nitive impairment are beyond the scope of this review,
common methods include obtaining a patient history and
a functional assessment; collecting collateral information;
excluding reversible causes of dementia; using standardized
assessment measures, such as the Montreal Cognitive
Assessment (74) and the Geriatric Depression Scale (75);
considering neuropsychological testing; and ordering neu-
that are not currently the standard of care may include
fluorodeoxyglucose–PET imaging (76), PiB-PET imaging
for amyloid deposition (77), and APOEε4 allele screening
(78), among many others. Biomarkers being investigated
brain inflammation (77). Clinicians caring for older adults
focus.psychiatryonline.org 39
OVERLAY OF LATE-LIFE DEPRESSION AND COGNITIVE IMPAIRMENT
with depression should also emphasize vascular risk factor
reduction: “A healthy brain starts with a healthy heart.” As
a consequence, they could collaborate with primary care
providers and support patient adherence with medications,
dietary and lifestyle modifications, follow-up visits, and other
recommendations.
AUTHOR AND ARTICLE INFORMATION
Dr. Aziz is associate professor of psychiatry with the Departments of
Psychiatry and Neurology, Robert Wood Johnson Medical School,
Rutgers University, New Brunswick, New Jersey (email: (raziz@rwjms.
rutgers.edu). Dr. Steffens is professor and chairman of psychiatry,
Department of Psychiatry, University of Connecticut Health Center,
Farmington.
Dr. Steffens has received royalties from the American Psychiatric As-
sociation for textbooks related to geriatric psychiatry. Dr. Aziz reports
no financial relationships with commercial interests.
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