REVIEW ARTICLE

Working memory in early Alzheimers disease:

a neuropsychological review
J. D. Huntley and R. J. Howard
Section of Old Age Psychiatry, Institute of Psychiatry, London, UK
Correspondence to: Dr J. D. Huntley, E-mail: jonathan.huntley@iop.kcl.ac.uk

Background: Reports of the extent of working memory (WM) impairment in early Alzheimers disease
(AD) have been inconsistent. Using the model of WM proposed by Baddeley, neuropsychological
evidence for the impairment of WM in early AD is evaluated.
Method: Literature searches were performed using Medline, PsycINFO and Embase databases. Individual
papers were then examined for additional references not revealed by computerised searches.
Results: Phonological loop function is intact at the preclinical and early stages of AD, becoming more
impaired as the disease progresses. In mild AD, there is impairment on tasks assessing visuospatial
sketchpad (VSS) function; however, these tasks also require executive processing by the central executive
system (CES). There is evidence that the CES is impaired in mild AD and may be affected in the earlier
preclinical stage of the disease. Episodic buffer function may be impaired but further research is required.
Conclusions: Future research into central executive functioning at the earliest stages of the disease,
combined with further longitudinal studies, needs to be carried out. Tasks to assess the proposed
functions of the episodic buffer and specific tests of the VSS suitable for AD subjects need to be developed
and validated. Learning more about these processes and how they are affected in AD is important in
understanding and managing the cognitive deficits seen in the early stages of AD. Copyright # 2009 John
Wiley & Sons, Ltd.
Key words: working memory; Alzheimers Disease; central executive
History: Received 20 October 2008; Accepted 8 April 2009; Published online 11 August 2009 in Wiley InterScience
(www.interscience.wiley.com).
DOI: 10.1002/gps.2314

Introduction impairments of everyday tasks, such as keeping track

The predominant cognitive deficit in Alzheimers
disease (AD) is episodic memory impairment. This
inability to acquire, encode and retrieve memories is
present at the earliest stages of the disease (Aggarwal
et al., 2005) and progresses with disease severity.
There has been growing interest in how other
cognitive processes, such as working memory (WM)
are affected in the early stages of the disease. WM
encompasses aspects of attentional and executive
control and is involved in many cognitive processes.
Deficits of WM in AD are therefore thought to
contribute to a range of significant problems. For
example, difficulties in dividing attention and manip-
ulating remembered information are reflected in
of conversations (Alberoni et al., 1992), walking whilst
talking (Camicioli et al., 1997) or packing a bag
(Ramsden et al., 2008). Clarifying how WM is affected
in early AD is therefore important in understanding
the cognitive and functional difficulties faced by
individuals with the disease and may aid early
diagnosis (Belleville et al., 2007).
Different theoretical models of WM have been
proposed including the hypothesis that active repres-
entations of long term memory constitute WM
(Cowan, 1995; Ruchkin et al., 2003).
However, in this review we use the influential model
of WM proposed by Baddeley, which provides a useful
framework to evaluate neuropsychological evidence for
the impairment of WM in AD.

Copyright # 2009 John Wiley & Sons, Ltd. Int J Geriatr Psychiatry 2010; 25: 121132.
122
Method
Literature searches were performed using Medline,
PsycINFO and Embase databases combining search
terms Alzheimer disease, mild cognitive impairment or
MCI, with WM, short term memory (STM), phono-
logical loop, phonological store, visuospatial sketchpad
(VSS), central executive, episodic buffer, digit span, dual
task, primary memory and short term forgetting.
Individual papers were then examined for relevance
and for additional references not revealed by compu-
terised searches.
Models of working memory
The concept of STM was based on the model of
Atkinson and Shiffrin (1968). STM was conceptualised
as a temporary store, through which information passed
prior to being encoded in long term memory or retrieved
from long-term memory stores (Atkinson and Shiffrin,
1968). Neuropsychological data cast doubts as to the role
of STM as a gatekeeper controlling input and output
from long term memory through a simple serial process.
Patients were described with specific STM deficits but
who appeared to have preserved long term memory
(Shallice and Warrington, 1970) and vice versa
(Baddeley and Warrington, 1970).
These findings led Baddeley and Hitch to suggest a
new model of STM, consisting of subcomponents,
which they termed the working memory model
(Baddeley and Hitch, 1974). According to this model,
information is held in subsidiary slave systems, the
phonological loop, which holds verbal information
and the visuospatial sketchpad (VSS), which holds
visual images. A third component of the model, the
central executive system (CES), acts as an attentional
controller, allowing manipulation and executive
control of information within WM (Baddeley, 1996).
The functions of the central executive overlap conside-
rably with other models of attention, including Norman
and Shallices (1980) model of a supervisory attentional
system (SAS) (Norman and Shallice, 1980) and involve
executive processes, such as the ability to shift and divide
attention, inhibit irrelevant information and manipu-
late information within verbal and visual stores. In 2000,
the model was extended by Baddeley to include an
episodic buffer (Baddeley, 2000), placing WM at the
interface of episodic memory and executive function.
Investigating working memory
Prior to the WM model, the function of STM was
investigated using memory span tasks (Miller, 1956).
Copyright # 2009 John Wiley & Sons, Ltd.
J. D. Huntley and R. J. Howard
As the length of the span sequence increases, the ability
to correctly recall the sequences decreases, with the
length of the longest list a subject can correctly recall
referred to as their memory span. These tasks have
demonstrated that WM is limited in capacity with a
span length of approximately 7 digits (Miller, 1956;
Baddeley, 2000). Subjects can be asked to recall the
span sequence in reverse, referred to as the backward
span. This is thought to require increased processing and
therefore to involve the CES as well as the subsidiary
system (Carlesimo et al., 1994; Cherry et al., 1996).
Impairment of memory span tasks in AD
Several studies using digit and word spans have found
them reduced in AD subjects compared to elderly
controls (Miller, 1973; Morris, 1984; Kopelman, 1985;
Morris, 1987a; Becker, 1988; Spinnler et al., 1988;
Hulme et al., 1993; Cherry et al., 1996), with no
significant difference between elderly and young
control groups (Belleville et al., 1996).
However, as can be seen from Table 1, some studies
have found normal digit and word spans in individuals
at the early or mild stages of AD (Martin et al., 1985;
Carlesimo et al., 1994; Perry et al., 2000). It appears
that rather than reflecting heterogeneity of WM deficits
in AD, some of these conflicting results may be
explained by differences in disease severity amongst
subjects. Some investigators have examined subjects at
the very early stages of AD, referred to as minimal AD
and at the preclinical or mild cognitive impairment
(MCI) stage. There is evidence that digit spans are
preserved in MCI and minimal AD but become signi-
ficantly impaired across mild and moderate groups
(Corkin, 1982; Orsini et al., 1988; Lines et al., 1991;
Greene et al., 1995; Hodges and Patterson, 1995;
Traykov et al., 2007). This may reflect initially normal
functioning within the phonological loop and CES
which becomes impaired as the disease progresses.
Longitudinal studies have found that digit span
performance is normal at the preclinical stage of the
disease (Backman et al., 2001; Twamley et al., 2006)
and does not predict advancement to AD (Bondi et al.,
1994).
The Corsi block tapping test is used as a measure of
spatial memory span. This involves encoding of visual
stimuli, short term storage of spatial location and
sequence order and maintenance of information over
time (Fischer, 2001). As reviewed in Table 2, impair-
ment on this task has been found in both mild and
moderate AD groups compared to both young and
elderly controls but not in MCI (Corkin, 1982; Orsini
Int J Geriatr Psychiatry 2010; 25: 121132.
Working memory in early Alzheimers disease 123

Table 1 Studies of digit and word span in AD

Study Subjects Severity of AD (scale used if not MMSE) Results AD (vs. EC)

(Miller, 1973) 15 AD Presenile dementia Impaired

15 EC No comment on severity
(Corkin, 1982) 18 AD MILD (n 1) Intact
15 EC MOD (n 8) Impaired
5 Global amnesia SEV (n 9) Impaired
(WAIS and clinical/functional evidence)
(Morris, 1984) 17 AD MOD Impaired
17 EC (Moderate severe anterograde amnesia
and moderately disorientated)
(Martin et al., 1985) 14 AD MILD Intact
11 EC (WAIS, WMS)
(Kopelman, 1985) 16 AD MILDMOD Impaired
16 Korsakoff (NART, IQ, Wechsler logical memory)
16 EC
(Morris, 1987a) 21 AD MILD Impaired
21 EC (WAIS and clinical evidence)
(Becker, 1988) 71 AD MILD (MMSE 22.5 (5.2)) Impaired
89 EC
(Spinnler et al., 1988) 29 AD MILDMOD Impaired
42 YC (Psychometric assessment)
58 EC
(Orsini et al., 1988) 51 AD MILD (n 24) Intact
30 EC MOD (n 27) Impaired
(History, orientation, visual retention test,
clinical judgement)
(Lines et al., 1991) 16 AD MILD (n 8, MMSE 22 (2026)) Intact
8 EC MOD (n 8, MMSE 1119) Impaired
(Hulme et al., 1993) 14 AD MILD Impaired
14 EC (relatively early stage of dementia,
Clifton assessment procedure)
(Carlesimo et al., 1994) 18 AD MILD Intact
18 MID (Global performance index)
26 EC
(Hodges and Patterson, 1995) 52 AD MIN (n 17, MMSE 25.6 (1.8)) Intact
24 EC MILD (n 17, MMSE 20.9 (1.7)) Impaired
MOD (n 18, MMSE 10 (4.6)) Impaired
(Greene et al., 1995) 33 AD MIN (n 17, MMSE 26.2 (2.2) Intact
30 EC MILD (n 16, MMSE 20.3 (3.3) Impaired
(Belleville et al., 1996) 20 AD MILD (n 9), Impaired
12 EC MOD (n 8),
12 YC MODSEV: (n 3)
(Reisberg global deterioration scale)
(Cherry et al., 1996) 49 AD MILD (n 26), Impaired
49 EC MOD (n 20),
SEV (n 3)
(Clinical dementia rating scale)
(Perry et al., 2000) 27 AD MIN (n 13 MMSE 26.08 (1.6)) Intact
77 EC MILD (n 14 MMSE 20.4 (2)) Intact
(Traykov et al., 2007) 20 MCI MMSE 28.95 (1.1) Intact
20 EC

AD: Alzheimers disease; EC: elderly controls; YC: young controls; MMSE: mini mental state examination (score (SD)); MIN: minimal; MOD: moderate;
WAIS: Wechsler adult intelligence scale; WMS: Wechsler memory scale; MCI: mild cognitive impairment; MID: multi infarct dementia.

Copyright # 2009 John Wiley & Sons, Ltd. Int J Geriatr Psychiatry 2010; 25: 121132.
124 J. D. Huntley and R. J. Howard

Table 2 Studies of spatial span in AD

Study Subjects Severity of AD (scale used if not MMSE) Results AD (vs. EC)

(Corkin, 1982) 18 AD MILD (n 1) Impaired

15 EC MOD (n 8) Impaired
5 Global amnesia SEV (n 9) Impaired
(WAIS and clinical/functional evidence)
(Spinnler et al., 1988) 29 AD MILDMOD Impaired
42 YC (Psychometric assessment)
58 EC
(Orsini et al., 1988) 51 AD MILD (n 24) Impaired
30 EC MOD (n 27)
(History, orientation, visual retention test,
clinical judgement)
(Lines et al., 1991) 16 AD MILD (n 8, MMSE 22 (2026)) Intact
8 EC MOD (n 8, MMSE 1119) Impaired
(Sahgal et al., 1992) 15 AD MILD (n 8, MMSE 2024) Impaired
8 EC MOD (n 7, MMSE 1519) Impaired
(Grossi et al., 1993) 39 AD MILD (MMSE21.4 (4.9)) Impaired
62 EC
(Carlesimo et al., 1994) 18 AD MILD Impaired
18 MID (Global performance index)
26 EC
(Trojano et al., 1994) 30 EC MILD (MMSE 22.6) Impaired
38 AD
(Cherry et al., 1996) 49 AD MILD (n 26) Impaired
MOD (n 20)
49 EC SEV (n 3)
(Clinical dementia rating scale)
(Traykov et al., 2007) 20 MCI MMSE 28.95 (1.1) Intact
20 EC

AD: Alzheimers disease; EC: elderly controls; YC: young controls; MMSE: mini mental state examination (score (SD)); MIN: minimal; MOD: moderate;
SEV: severe; WAIS: Wechsler adult intelligence scale; MID: multi infarct dementia; MCI: mild cognitive impairment.

et al., 1988; Spinnler et al., 1988; Sahgal et al., 1992;
Grossi et al., 1993; Carlesimo et al., 1994; Trojano et al.,
1994; Cherry et al., 1996). As the Corsi block tapping
task requires both visuospatial storage and executive
processing (temporal sequencing), the impairment
seen in early AD, on both forward and backward spatial
spans, has been interpreted as reflecting deficits in both
the VSS and central executive (Carlesimo et al., 1994).
Specific subcomponents of WM
Phonological loop. It is thought that two functional
components make up the phonological loop. The first
is a phonological short term store (PSS); a temporary
storage system, from which verbal information traces
spontaneously fade after a few seconds. Evidence for
this component comes from observations that similar
sounding items are more difficult to remember than
dissimilar items in STM (Conrad and Hull, 1964;
Morris, 1994). Memory span capacity is therefore
greater when tested with sequences of phonologically
dissimilar items, than when tested with phonologically
similar items, referred to as the phonological similarity
effect (PSE).
The second component is the articulatory rehearsal
mechanism (ARM). The function of the ARM has been
investigated using the word length effect (WLE)
(Baddeley et al., 1975). This refers to the observation
that normal subjects are more able to recall lists of
shorter, compared to longer words, which require
more time to be rehearsed and can therefore be
refreshed less frequently than short words. Another
method for investigating ARM function is to measure
the degree to which memory span decreases when the
ARM is suppressed by concurrent articulation (e.g.
mouthing an irrelevant word), which interferes with
subvocal articulation by the ARM (Morris, 1994).

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Working memory in early Alzheimers disease 125

Phonological loop function in AD
The PSE, WLE and suppression of the ARM by
concurrent articulation, have been used to investigate
subcomponents and functioning of the phonological
loop in individuals with AD with inconsistent results,
reviewed in Table 3.
Morris (1984) has attributed Millers (1972) findings
of a reduced PSE to a floor effect in individuals with
severe AD and concluded that the phonological loop
was intact in AD, with observed deficits in memory
span tasks attributed to impairments in the central
executive (Morris, 1994).
By contrast, other experimenters have found evidence
of phonological loop dysfunction in AD. Belleville et al.
(1996) found evidence of a decreased PSE in AD but a
normal WLE. However, individual case analysis of AD
subjects revealed that, of those classed as having mild
AD, all had normal WLE and 5 out of 6 of them had
normal PSE. All subjects with phonological loop
deficits also showed accompanying CES dysfunction
(Belleville et al., 1996).
Collette et al. (1999b) examined subjects with mild
AD and normal elderly controls and found that AD
subjects had a decreased PSE and WLE and were also
impaired on tests of central executive function
(alphabet span and dual task paradigms). However,
when case severity was taken into account, as measured
by span performance, only those subjects with a low
span had phonological loop deficits, whilst subjects
with high span generally had an intact phonological
loop but showed impairment on CES tasks. The
authors therefore concluded that the earliest deficits in
WM may be due to impairments of the central
executive, with phonological loop deficits occurring
only in more severely demented patients. There was
some heterogeneity between AD subjects, however,
with three subjects showing deficits of the phonological
loop but no difficulties on the tasks assessing the CES.
(Collette et al., 1999b).
In a recent study, Peters et al. (2007) assessed
subjects with mild AD and compared them to elderly
and young healthy controls. AD subjects demonstrated
a similar PSE and WLE to those of control groups,
suggesting that the phonological loop is preserved in
the early stages of AD. Central executive function,
assessed using a dual task paradigm, was significantly
impaired in AD subjects, again suggesting that in the
early stages of AD the phonological loop is intact,
however the CES is impaired, which may be
responsible for deficits seen on some verbal WM
tasks. (Peters et al., 2007).

Table 3 Studies of phonological loop in AD

Study Subjects Severity of AD (scale used if not MMSE) Tasks Results AD (vs. EC)

(Miller, 1972) 14 AD Presenile dementia PSE Impaired

14 EC No comment on severity
(Morris, 1984) 17 AD MOD PSE Intact
17 EC (Moderately severe anterograde WLE Intact
amnesia and moderately disorientated)
(Morris, 1987b) 14 AD MILD CAE Intact
14 EC (WAIS, clinical evidence)
(Morris, 1987a) 21 AD MILD Articulation rate Intact
21 EC (WAIS, clinical evidence)
(Hulme et al., 1993) 14 AD MILD Speech rate Impaired
14 EC (relatively early stage of dementia,
Clifton assessment procedure)
(Belleville et al., 1996) 20 AD MILD (n 9), MOD (n 8) WLE Impaired
12 EC MODSEV (n 3)
12 YC (Reisberg global deterioration scale) PSE Intact
(Collette et al., 1999b) 20 AD MILD (MMSE 21.80 (4.75)) WLE Impaired
20 EC PSE Impaired
(Peters et al., 2007) 20 AD MILD (MMSE < 24) PSE Intact
20 EC WLE Intact
20 YC

AD: Alzheimers disease; EC: elderly controls; YC: young controls; MMSE: mini mental state examination (score (SD)); MIN: minimal; MOD: moderate;
SEV: severe; PSE: phonological similarity effect; WLE: word length effect; CAE: concurrent articulation effect.

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126
In summary, the available evidence suggests that in
the early stages of AD the phonological loop is intact
and becomes impaired when the disease has progressed
to the mild to moderate stage. Longitudinal studies
specifically looking at the function of the phonological
loop and its subcomponents would be helpful in
clarifying the effects of disease progression. Although
the tasks described above seek to selectively test
subcomponents of the phonological loop, it is
impossible to entirely remove the contribution of
attentional and executive processes. Therefore any
impairment of central executive function may still
cause deficits in those tasks used to predominantly
investigate subsidiary system function.
Visuospatial sketchpad. Logie (1995) proposed that
the VSS is comprised of distinct visual and spatial
components, a visual temporary store where visual
information is represented and a spatial temporary
subsystem which rehearses the contents of the visual
store and can be used to plan movement (Logie, 1995).
In order to investigate visual WM, a visual patterns
task has been devised (Della Sala et al., 1999) which
involves exposing subjects to a pattern for a few
seconds before removing it and asking subjects to
reproduce it. Della Sala (1999) reported two subjects
who were able to perform this task normally, but were
impaired on the Corsi blocks task, and a subject who
had the reverse impairment pattern (Della Sala et al.,
1999).
Further evidence for the distinction of visual and
spatial components in the VSS comes from selective
interference (Hecker and Mapperson, 1997). Spatial
WM is impaired by a concurrent movement discrimi-
nation task but not by a colour discrimination task,
whereas visual object memory shows the opposite
pattern of interference (Tresch et al., 1993). This
double dissociation provides evidence for the existence
of separate visual and spatial stores and also for
separate rehearsal mechanisms for visual and spatial
information, both independent of the central executive
(Klauer and Zhao, 2004).
In terms of visual WM, there is some evidence that
basic features (e.g. colour, shape, orientation) are
independently stored in a set of parallel feature specific
stores (Wheeler and Treisman, 2002). It is assumed
that these features can be bound together by a
mechanism that integrates various components of an
object for storage in WM, using attentional resources.
This concept overlaps with the proposed functioning
of a further component of the WM modelthe
episodic buffer (Baddeley, 2000; Repovs and Baddeley,
2006).
Copyright # 2009 John Wiley & Sons, Ltd.
J. D. Huntley and R. J. Howard
VSS functioning in AD
As reviewed above, and in Table 2, visuospatial memory
span tasks, such as the Corsi block tapping task, have
been used to show impairment in visuospatial WM in
AD. Such impairment, however, is thought to reflect
potential deficits in the functioning of both the VSS
and central executive.
Macpherson et al. (2007) have recently found that
AD subjects are impaired on the visual patterns task
suggesting VSS impairment in AD. Function within the
VSS has also been assessed using the immediate recall
stage of a delayed matching to sample task in AD
patients. It is not clear, however, whether deficits on
this task seen in subjects with AD are due to specific
VSS impairment. Money et al. (1992) reported a deficit
in an AD group irrespective of whether the stimuli
were shown simultaneously (therefore only requiring
matching) or sequentially (requiring use of memory
processes). It is therefore possible that the impairment
was due to a perceptual deficit rather than an impaired
VSS (Money et al., 1992).
Due largely to the difficulties inherent in designing
tasks suitable for AD patients that satisfactorily separate
a passive visuospatial subsidiary storage system from
more active executive processes, it has not been clearly
established whether the VSS itself is specifically
impaired in AD.
Episodic buffer. Baddeley (2000) extended the WM
model to include a further subcomponent, the episodic
buffer. This was in response to various experimental
findings, for example, that grouping or chunking of
information, which requires integration of informa-
tion from LTM, improves recall and that articulatory
suppression has only limited effects on tasks involving
visually presented information (Baddeley, 2000).
Given the complexity of the cognitive processes
ascribed to the episodic buffer, it is not surprising that
it is difficult to identify clear ways of examining its
function. The processes involved in the grouping or
chunking of information have been explored (Bor
et al., 2003; Bor et al., 2004). Attempts to separate the
automatic binding that occurs in normal perception
from the more active and demanding integrative
processes that are assumed to play such an important
role in the episodic buffer, would be informative
(Baddeley, 2000). Tasks have been designed that assess
a subjects ability to maintain verbal, object and spatial
information in WM, either separately or combined, by
presenting objects in various locations on a grid and
assessing the ability to integrate and recall both object
and spatial features. This approach has been used to
Int J Geriatr Psychiatry 2010; 25: 121132.
Working memory in early Alzheimers disease
investigate normal individuals (Prabhakaran et al.,
2000), the effects of age (Mitchell et al., 2000), schizo-
phrenia (Burglen et al., 2004) and transient global
amnesia (Quinette et al., 2006) on the integrative
abilities of the episodic buffer.
Episodic buffer function in AD
There is some evidence that individuals with AD are
impaired in the integration and organisation of
relevant information. Peters et al. (2007) reported
that AD subjects were impaired on a task requiring
integration of auditory and visual information (Peters
et al., 2007). Grober et al. (1985) investigated the ability
to rank information by concept in subjects with AD
and found that they had difficulty organising material
(Grober et al., 1985). The ability of AD subjects to
group or chunk information on a word list learning
task has also been examined. AD subjects were
impaired in their ability to use inherent associations
between words, which resulted in a lack of chunking
behaviour (Carlesimo et al., 1998). In a recent study,
mild AD (mean MMSE 20.3) and very mild AD (mean
MMSE 26.39) subjects were examined in their ability to
use organisational skills to cluster semantically similar
words together and improve recall. This ability to
strategically organise information was interpreted as a
marker of episodic buffer function. Both elderly
controls and very mild AD subjects were able to use
inherent organisational structures in the word list task
to improve performance, however mild AD subjects
were not. This was interpreted as reflecting relatively
preserved episodic buffer function in very mild AD,
which becomes impaired as the disease progresses to
the mild stage (Germano et al., 2008). The strategic
organisation of information and use of relationships
and associations between stimuli to support learning
and recall in subjects with AD, involves many cognitive
steps and goes beyond WM research. However, it has
been suggested that the inability to strategically
integrate information into a coherent, meaningful
episodic representation may reflect impairment of the
episodic buffer in AD, which in turn may be involved
in the episodic memory deficits seen in AD (Germano
and Kinsella, 2005).
Central executive. The main functions of the CES have
been proposed to be co-ordination of the subsidiary
systems, focusing, switching and dividing attention,
inhibition and updating and manipulation of infor-
mation (Baddeley, 1996; Collette and Van der Linden,
2002). The CES therefore provides many attentional
and executive functions within WM and a criticism of
Copyright # 2009 John Wiley & Sons, Ltd.
127
the CES in Baddeleys WM model has been its lack of
specificity. A wide range of different tasks have been
used to assess attention and executive function and
evidence for general attentional and executive deficits
in AD has been well reviewed elsewhere (Perry and
Hodges, 1999; Baddeley et al., 2001; Amieva et al.,
2004). Executive tasks often assess multiple cognitive
processes, some of which are incidental to their stated
purpose (Burgess, 1997) and are therefore difficult to
interpret. Factor analysis techniques have been used to
identify key subprocesses underlying performance on a
range of executive tasks and have concluded that
executive functions are marked by both unity and
diversity of function (Miyake et al., 2000) and therefore
no underlying factor can be considered completely
independent (Collette and Van der Linden, 2002).
It has been repeatedly asserted, however, that a
major role of the CES is co-ordination of the subsidary
systems and therefore testing dual task performance
provides a specific marker of CES function within WM
(Baddeley et al., 1997). We have therefore concentrated
on dual task paradigms that assess divided attention
and tasks that assess manipulation of information in
WM (alphabet span) as markers of CES function in
AD.
CES function in AD
Using alphabet span tasks, patients with mild AD have
been found to have impaired central executive function
(Collette et al., 1999b; Belleville et al., 2003). Belleville
et al. (2007) studied mild AD patients, MCI subjects
and elderly controls and found that AD patients, but
not MCI subjects, were impaired on an alphabet span
task, suggesting that there is an impairment in the
manipulation of information in WM in mild AD but
not in MCI (Belleville et al., 2007).
Dual task performance has been consistently
reported as impaired in AD (Baddeley et al., 1986;
Baddeley et al., 1991; Collette et al., 1999a; Baddeley
et al., 2001; Logie et al., 2004; Sebastian et al., 2006;
MacPherson et al., 2007; Peters et al., 2007). Although
it was an initial finding that performance on Brown-
Peterson paradigms was sensitive to the degree of
processing demands required (Morris, 1986; Morris
and Kopelman, 1986), there is evidence that impaired
dual task performance in AD reflects a specific deficit
in dividing attention in AD, rather than the result of a
more general processing speed deficit (Baddeley et al.,
2001) or effect of task difficulty (Baddeley et al., 1991;
Logie et al., 2004).
The studies reviewed in Table 4 suggest that there is
a deficit in dividing attention as measured using
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128 J. D. Huntley and R. J. Howard

Table 4 Studies of CES in AD (divided attention and alphabet span tasks)

Study Subjects Severity of AD (scale used if not MMSE) Tasks Results AD

(vs. EC)

(Corkin, 1982) 18 AD MILD (n 1) BrownPeterson task Impaired

15 EC MOD (n 8)
5 Global amnesia SEV (n 9)
(WAIS and clinical/functional evidence)
(Kopelman, 1985) 16 AD MILDMOD BrownPeterson task Impaired
16 EC (NART, IQ, Wechsler logical memory)
16 Korsakoff
(Baddeley et al., 1986) 28 AD MILDMOD Dual task Impaired
28 EC (Ravens matrices, token test, orientation
20 YC task, everyday coping ability)
(Dannenbaum et al., 1988) 15 AD MILDMOD BrownPeterson task Impaired
15 EC (Mattis dementia rating scale)
15 depressed
(Kopelman, 1991) 6 AD MILDMOD BrownPeterson task Impaired
6 Korsakoff (Ravens matrices, logical memory, (using Corsi blocks)
6 EC object learning, IQ)
(Baddeley et al., 1991) 15 AD MILDMOD Dual task Impaired
18 EC (Ravens matrices, token test, orientation
task, everyday coping ability)
(Greene et al., 1995) 33 AD MIN (n 17, MMSE 26.2 (2.2)) Dual task Intact
30 EC MILD (n 16, MMSE 20.3 (3.3)) Impaired
(Collette et al., 1999b) 20 AD MILD (MMSE 21.80 (4.75)) Alphabet span Impaired
20 EC Dual task Impaired
(Perry and Hodges, 2000) 12 AD MIN (MMSE 26.2 (1.6) at baseline) Dual task Intact at
20 EC MILD (MMSE 23.3 (2.4) at year 1) baseline
Impaired
at year 1
(Perry et al., 2000) 31 AD MIN (n 17 MMSE 26.08 (1.6)) Dual task Intact
77 EC MILD (n 14 MMSE 20.4 (2)) Impaired
(Baddeley et al., 2001) 36 AD MILD (MMSE 19.94 (1.78)) Dual task Impaired
36 EC
36 YC
(Belleville et al., 2003) 23 AD MILD (MMSE 22.57 (1829)) Alphabet span Impaired
23 EC
15 YC
(Logie et al., 2004) 8 AD MILD (MMSE 21.9 (2.3)) Dual task Impaired
8 EC
8 YC
(Sebastian et al., 2006) 27 AD MILD (MMSE 20.37 (2.20)) Dual task Impaired
27 EC
30 YC
(Peters et al., 2007) 20 AD MILD (MMSE < 24) Dual task Impaired
20 EC
20 YC
(MacPherson et al., 2007) 15 AD MILD (MMSE 22.1 (1.8)) Dual task Impaired
20 EC
20 YC
(Belleville et al., 2007) 28 MCI MCI (MMSE 28.36 (1.98)) Alphabet span AD impaired
19 AD Adapted MCI intact
29 EC MILD (MMSE 24.65 (3.6)) BrownPeterson AD/MCI
task impaired

AD: Alzheimers disease; EC: elderly controls; YC: young controls; MMSE: mini mental state examination (score (SD)); MIN: minimal; MOD: moderate;
SEV: severe; WAIS: Wechsler adult intelligence scale; MID: multi infarct dementia. NART: national adult reading test, MCI: mild cognitive impairment.

Copyright # 2009 John Wiley & Sons, Ltd. Int J Geriatr Psychiatry 2010; 25: 121132.
Working memory in early Alzheimers disease
BrownPeterson and dual task paradigms in mild and
moderate AD and that this worsens over the course of
the disease. However, there are conflicting reports of
the presence of impairments at the minimal AD/MCI
stage. Greene et al. (1995) tested groups of minimal AD
subjects and mild AD subjects on a divided attention
task and found that, although the minimal AD group
did show some impairment, only mild AD patients
were significantly impaired on divided attention tasks
(Greene et al., 1995). Perry et al. (2000) investigated
subjects with minimal AD, mild AD and elderly
controls using forward and backward digit spans and a
dual task paradigm. There was no significant difference
in dual task performance between the minimal AD and
control groups, however the mild AD subjects were
significantly impaired (Perry et al., 2000).
Perry and Hodges (2000), in a longitudinal study of
minimal AD patients, examined dual task performance
at baseline (mean MMSE 26.2) and at 1 year (mean
MMSE 23.3) compared with controls and found no
significant difference at baseline but a significant
difference after 1 year (Perry and Hodges, 2000). Peters
et al. (2007) investigated a group of mild AD subjects
and young and elderly controls on a dual task
paradigm and found that AD subjects were signifi-
cantly impaired compared to elderly controls (Peters
et al., 2007). Belleville et al. (2007) used alphabet span
and dual task paradigms on early AD patients, MCI
subjects and elderly controls. Both the AD and MCI
groups were significantly impaired compared to the
controls on the dual task and, whilst MCI subjects were
not significantly impaired on the alphabet span task, a
third did show some impairment, with disease severity
positively correlated with deficits on both tasks
(Belleville et al., 2007).
These results strongly suggest that early AD subjects
show impairment in the ability to perform two tasks
simultaneously and to manipulate information main-
tained in WM. Both of these are considered to be
functions of the central executive, independent of
storage deficits or processing speed (Peters et al., 2007).
It is clear these deficits are present at an early stage of
the disease and it has been suggested that dual task
impairment may be a useful diagnostic marker for early
AD (Belleville et al., 2007) although there are conflic-
ting reports of the presence of impairment at an earlier
minimal AD or MCI stage.
Neurological correlates of working memory
A number of studies of verbal WM using PET have
localised the PSS to the left supramarginal gyrus and
the ARM to left hemisphere speech areas, such as
Copyright # 2009 John Wiley & Sons, Ltd.
129
Brocas area and premotor cortex, both in normal
subjects (Paulesu et al., 1993; Salmon et al., 1996) and
in AD (Collette et al., 1997).
Functional imaging studies have implicated several
locations involved in the operation of the VSS, inclu-
ding areas in frontal, posterior parietal and occipital
cortex (Jonides et al., 1993; Smith and Jonides, 1998).
There is also evidence that premotor and right superior
parietal cortex may mediate spatial storage and
rehearsal, while inferior parietal areas mediate object
storage (Smith and Jonides, 1998; Wager and Smith,
2003). Although a wide range of brain areas are
activated in WM tasks, the localisation of areas
underlying basic verbal and visuospatial WM is likely
to contribute to variability in performance on verbal
and nonverbal WM tasks in AD. There is some
evidence of asymmetry of regional hypometabolism, as
demonstrated by PET, at mild-moderate stages of the
disease, with left hypometabolism associated with
impairment on verbal compared to visuospatial tasks
in AD (Haxby et al., 1990; Zahn et al., 2004). A further
observation is that individuals with early onset AD
have more pronounced left sided hypometabolism of
frontal and parietal areas, compared to late onset AD
patients, and this has been associated with impaired
verbal WM performance (Kalpouzos et al., 2005).
Therefore, although general patterns of verbal and
visuospatial WM impairment can be seen in early AD,
factors such as age of onset and asymmetry of cortical
pathology are likely to contribute to the heterogeneity
of WM deficits reported at the early stage of the disease.
Although the CES is a theoretical concept, several
studies have attempted to identify the neurological
basis of CES function. Using alphabet span tasks,
several groups have found activation in dorsolateral
prefrontal cortex (PFC) and left parietal cortex during
the manipulation of information in WM (Collette
et al., 1999a; DEsposito et al., 1999; Postle et al., 1999).
Dual task paradigms have also been examined. An
early fMRI study identified activation in dorsolateral
PFC and anterior cingulate gyrus when tasks were
performed together but not when performed separ-
ately, interpreted as reflecting CES functioning
(DEsposito et al., 1995). However, subsequent studies
have reported no additional activations during dual
task co-ordination, with dual task performance
associated with activation in a network of frontal
and parietal areas already activated by single tasks
(Klingberg, 1998; Adcock et al., 2000; Bunge et al.,
2000). This suggests that the dual task co-ordination
role of the CES relies on interactions between cerebral
areas already activated in single tasks rather than on the
recruitment of additional cortical areas.
Int J Geriatr Psychiatry 2010; 25: 121132.
130
Key Points

Phonological loop function is intact at the
preclinical and early stages of AD.

Central executive function is impaired in mild AD
and may be affected during the preclinical stage.

Further research into central executive and
episodic buffer function at the earliest stages of
AD is required.
The N back task has also been used in fMRI studies
as a test of WM, and activations have been found in a
range of areas including dorsolateral PFC, inferior
frontal cortex, anterior cingulate and posterior parietal
cortex (Cohen et al., 1997; Owen et al., 2005).
Therefore it seems likely that the function of the CES
as measured by alphabet span, dual task and N back
tasks involves a network of prefrontal, frontal and
parietal areas.
In AD, there is evidence of regional frontal lobe
degeneration and hypoperfusion (Waldemar et al.,
1994), however, there is increasing evidence that AD
pathology is associated with breakdown of effective
connectivity between neuronal systems (Delbeuck
et al., 2003). Neuroimaging connectivity studies also
provide evidence for disconnection in AD (Grady et al.,
2001) and this may play a key role in the deficits
observed in the CES (Collette et al., 1999c).
SUMMARY
There is considerable evidence that the central
executive is affected at an early stage of AD, with
subsidiary systems affected later, as the disease
becomes moderately severe. The evidence that central
executive function shows some impairment at the very
early stages of the disease makes investigation of this
component an important part of the assessment of
subjects at early stages of AD. Future research into the
extent of central executive impairment at the earliest
stages of the disease, combined with further longi-
tudinal studies, needs to be carried out. Tasks to assess
the proposed functions of the episodic buffer and
specific tests of the VSS suitable for AD subjects need to
be developed and validated.
Learning more about these processes and how they
are affected in AD may enable the development of
management strategies, both pharmacological and
non-pharmacological, to overcome some of the effects
of the cognitive impairments faced by individuals
suffering from AD.
Copyright # 2009 John Wiley & Sons, Ltd.
J. D. Huntley and R. J. Howard
Declaration of Interest
None.
Acknowledgements
We thank Richard Brown and two anonymous
reviewers for helpful comments on an earlier draft.
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