preserved conceptual priming in ad

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1 Preserved Conceptual Priming in Alzheimer’s Disease Carla A. R. Martins and Toby J. Lloyd-Jones University of Kent, UK Correspondence to: Carla Alexandra Rodrigues Martins, 5, Vivienne Court, Peat Moors, Headington, Oxford, OX3 7HG, Tel. 07743379194, Email: [email protected]. Running page heading: Conceptual priming in Alzheimer’s disease.

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Page 1: Preserved Conceptual Priming in AD

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Preserved Conceptual Priming in Alzheimer’s Disease

Carla A. R. Martins and Toby J. Lloyd-Jones

University of Kent, UK

Correspondence to: Carla Alexandra Rodrigues Martins, 5, Vivienne Court, Peat Moors,

Headington, Oxford, OX3 7HG, Tel. 07743379194, Email: [email protected].

Running page heading: Conceptual priming in Alzheimer’s disease.

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Abstract

We assess Alzheimer’s disease (AD) and healthy older adult control (HC) group

performance on: (1) a conceptual priming task, in which participants had to make a

semantic decision as to whether a degraded picture of an object encountered previously

belonged to the category of living or non-living things; and (2) a recognition memory

task. The AD group showed a dissociation between impaired performance on the

recognition task and preserved priming for semantic decisions to degraded pictures. We

argue that it is not whether priming is conceptual or perceptual that is important for the

observation of priming in AD, rather it is the nature of the response that is required (cf.,

Gabrieli, et al., 1999).

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Introduction

Explicit memory, as measured by tests of conscious recollection of a previous

episode (e.g., recognition or recall tasks) deteriorates as a function of age (e.g. Mitchell

& Brown, 1988) and is dramatically impaired in individuals with Alzheimer’s disease

(AD; e.g. Fleischman, et al., 1995; Keane, Gabrieli, Growdon & Corkin, 1994; Keane

et al., 1991; Koivisto, Portin & Rinne, 1996). In contrast implicit memory, the

unconscious or unintentional retrieval of memories measured usually through ‘repetition

priming’ (i.e., the facilitation of performance for studied compared with unstudied

stimulus) can be preserved in AD.

Patients with AD can show normal priming on a range of implicit tasks, for

instance: mirror reading (e.g., Deweer, et al., 1994); word and pseudoword

identification (e.g., Fleischman et al., 1995; Keane et al., 1994; Keane et al., 1991;

Koivisto et al., 1996); picture naming (e.g., Gabrieli, Francis, Grosse & Wilson, 1991;

Park & Gabrieli, 1995; Gabrieli et al., 1999); and picture-fragment identification (e.g.,

Gabrieli, Keane, Stager, Kjelgaard, et al., 1994). Nevertheless, impaired priming has

been also observed in tasks such as category-exemplar generation (e.g. Monti et al.,

1996; Vaidya et al., 1999) and word-association (e.g. Salmon, Shimamura, Butters &

Smith, 1988; Carlesimo, Fadda, Marfia & Caltagirone, 1995)

This diversity of preserved and impaired priming in AD has led to the suggestion

that the dissociation reflects a distinction between perceptual and conceptual implicit

memory processes (Keane et al., 1991; Gabrieli et al., 1994; Fleischman & Gabrieli,

1998). That is, AD patients may display intact priming in perceptually driven-tasks,

which draw on processes concerned with the visual, auditory or tactual form of a target

stimulus. However, impaired or no priming will be found in conceptually-driven tasks

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which draw on processes concerned with the content or meaning of a target stimulus

(Keane et al., 1991; Fleischman & Gabrieli, 1998).

This functional distinction between perceptual and conceptual priming in AD is

supported by converging evidence from normal participants (e.g. Blaxton, 1989), and

evidence of a corresponding anatomical separation between neural systems that may

mediate the two kinds of implicit memory (e.g., Blaxton, 1999). However, the picture is

complicated by the fact that AD patients also exhibit dissociations between perceptual

priming tasks. For instance, priming can be intact in tests such as word-identification

and picture naming, but impaired in word-stem completion and degraded picture and

word naming (see Fleischman & Gabrieli, 1998, for a review). Furthermore,

dissociations between conceptual priming tasks have also been reported for AD

patients. For instance, a dissociation between intact category-exemplar verification and

impaired category-exemplar production (Vaidya et al., 1997; 1999; Gabrieli et al.,

1999).

These results suggest that a distinction between perceptual and conceptual

priming alone is insufficient to account for all AD implicit memory deficits.

Identification versus production

Accordingly, Gabrieli et al. (1999) have suggested a distinction in the cognitive

and neural organization of implicit memory which is based on the dissociation between

identification and production forms of knowledge retrieval. Gabrieli et al. (1999) found

intact priming in AD patients for perceptual (i.e., picture-naming) and conceptual (i.e.

category-exemplar identification) tasks that required an identification response, while

performance was impaired on perceptual (i.e., word-stem completion) and conceptual

(i.e., category-exemplar production) tasks which required the generation or production

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of a response. More precisely, a distinction is made between identification tasks which

instruct participants to identify presented stimuli, and production tasks which instruct

participants to use a presented cue to guide retrieval of a response. This distinction is

related to the different attentional demands of each task, which can be affected by AD

whereby the division of attention may have a selective effect on response production but

not on identification. It is suggested that production is more demanding on study phase

attentional resources than identification, due to response competition at test (Vaydia et

al., 1997): the identification task, by definition, lacks response competition because the

stimulus is provided at test, while in most production tasks response competition

involves multiple legitimate responses. It is possible that effects of Alzheimer’s disease

do not impair conceptual implicit memory processes in general, but rather selectively

impair word production processes that are called upon in many of these tests (Lazzara,

Yonelinas & Ober, 2001).

The Present Study

The present study examined AD performance on explicit and implicit tests of

memory which involved the manipulation of nonverbal material, namely intact and

fragmented pictures of common objects. Explicit memory was measured using a picture

recognition test, and implicit memory was measured via priming of a semantic decision

task. In the semantic decision task, complete pictures were presented during a study

phase, and fragmented pictures were presented during the test phase. Participants were

required to identify whether the fragmented picture was a living or nonliving thing,

without being required to produce the name of the object (for details of picture

fragmentation stimuli, see Snodgrass, Smith, Feenan & Corwin, 1987, and Snodgrass &

Corwin, 1988).

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Very few studies examining implicit memory performance in AD have used

fragmented pictures as stimuli. Some of these studies used identical fragmented pictures

at both study and test (e.g., Bondi & Kaszniak, 1991; Gabrieli et al., 1994), whereas

other studies have used complete pictures at study and fragmented pictures at test (e.g.

Heindel, Salmon, Schults, Walicke & Butters, 1989). The evidence arising from these

studies is mixed: some investigations show impaired priming of fragmented picture

naming (e.g. Bondi & Kaszniak, 1991) while others show preserved priming of

fragmented picture naming. For instance, Gabrieli et al. (1994) examined the repetition

priming performance of AD patients on the Gollin Incomplete-Pictures task and found

intact priming in AD on incomplete picture identification.

One contributing factor to these contrasting findings may be the nature of

‘perceptual closure’; the process whereby an observer fills in missing portions of a

stimulus so as to complete an image and produce an identifiable object (Snodgrass &

Kinjo, 1998). Perceptual closure is an important process influencing priming effects in

picture fragment identification. Snodgrass and Feenan (1990) propose that optimal

priming arises from a situation that produces the closure experience and contains the

minimum amount of information necessary to support the closure. Supporting this idea,

they found that a moderately fragmented study picture produced more priming than

either a very fragmented or an intact picture.

On the basis of previous findings we predict that the AD group will show

impaired performance on the recognition memory test relative to a healthy older adult

control (HC) group. In contrast, the AD group will show intact priming, within the

normal range, on the semantic decision task. The logic is that although the semantic

decision task is conceptual, it requires an identification rather than a production

response, and it is this dimension rather than the perceptual-conceptual dimension that

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is most important for priming to be observed in AD (Fleischman, Gabrieli et al., 1995;

Koivisto et al., 1996; Fleischman & Gabrieli 1998; Park & Gabrieli et al., 1998; Vaidya

et al., 1999). To maximise the possibility of finding priming, we used stimuli that were

moderately fragmented at test (Snodgrass & Feenan, 1990). Alternatively, if the AD

group show no or impaired priming in the semantic decision task, it will suggest that

perceptual-conceptual dimension of the task is more important than the nature of the

response.

As a subsidiary issue we examined whether altering the nature of the study task

would influence priming. If priming occurs only when the tasks at study and test are

identical, that is when both are semantic decisions, such priming may be the result of

task-specific encoding processes. Alternatively, if equivalent priming effects on

semantic decisions at test are obtained for both semantic decision and naming tasks at

study, then we can be assured that such priming effects are the result of retrieval rather

than encoding-based processes or an identical match between encoding and retrieval

processes (cf., Maki & Knopman, 1996).

Experiment

Method

Participants

An AD and HC group participated in this experiment (see Table 1). The AD

group consisted of 16 participants in all, 9 males and 7 females ranging in age from 67

to 85 years (M = 75.6; SD = 5.86) and in years of education from 0 to 17 years (M =

6.1; SD = 4.18). The AD participants were recruited from the Psychiatric Hospital of

Magalhães Lemos and from the Clinic of Neurology of Dr. Manuel Laranjeira at Porto

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in Portugal. All patients were evaluated by a neurologist, psychiatrist and psychologist

who gathered information concerning patients’ medical history, neuropsychological

testing (i.e., the mini-mental state exam; MMSE, Folstein et al., 1975) and

neuroimaging examinations. Patients met the clinical criteria of the NINCDS-ADRDA

(McKhann, Folstein, Katzman, Price & Stadlan, 1984) and DSM-IV (1994) for a

diagnosis of AD. Camcog scores (Roth, Huppert, Mountijoy & Tym, 1998) ranged from

30 to 68 (M = 51.4; SD = 10.31) and the MMSE scores ranged from 10 to 20 (M =

16.2; SD = 3.14) suggesting that patients were within the mildly to severely cognitive

impairment.

The HC group consisted of 16 participants in all, 7 males and 9 females, raging

in age from 64 to 85 years (M = 73.5; SD = 6.26) and years of education ranging from 0

to 17 years (M = 4.8; SD = 4.13). These controls were recruited from a nursing home at

Porto (Portugal) – Lar do Comércio – and from an elderly voluntary group in the

Lordelo do Ouro Church, at Porto (Portugal). The inclusion criteria for normal

participants were that the MMSE scores be within the cut-off scores for no cognitive

impairment according to the level of education of participants for the Portuguese

population (Guerreiro et al, 1993): no education ≥ 15; 1 to 11 years of education ≥ 22

and more than 11 years of education ≥ 27. The MMSE Scores ranged from 22 to 29 (M

= 25.6; SD = 2.68).

The two groups did not differ significantly on age (t (30) = 0.99; p = n.s.) or

education (t (30) = 0.85; p = n.s.) but differed significantly on MMSE scores (t

(28.424) = – 8.643) (see Table 1).

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----------------------

Table 1 about here

-----------------------

Material

The material consisted 60 pictures of common objects selected from the

Snodgrass and Vanderwart (1980) norms. Half were living things and half were non-

living things. The pictures were fragmented according to the algorithm developed by

Snodgrass et al. (1987). Briefly, fragmented pictures were created on the Apple

Macintosh Computer and original drawings from the 260 pictures in Snodgrass and

Vanderwart (1980) were reduced so as to fit within a 246 x 246 pixel square (8.3 x 8.3

cm) on the computer screen. These pictures were then digitised using the Thunderscan

digitiser and saved as a MacPaint File. Through a set of procedures written in Microsoft

Basic, pictures were subject to fragmentation. In order to delete cumulatively, and to

ensure that each successive fragmentation level has fewer fragments than the next lower

level 16 x 16 blocks were identified that contained information. The fragmentation

program lays out a grid of 16 x 16 blocks, determines which blocks contain black

pixels, and stores the locations of these critical blocks. The program then randomly

selects increasing proportions of critical blocks to be erased according to an exponential

function (number of remaining blocks (level) = number of total blocks [1 – aEXP (8-

level)]), to produce eight levels of fragmented images per stimulus. The level of

fragmentation selected for this study was level 3; a medium level that would not prove

too difficult for patients and controls. All items were presented one at the time on single

cards (10 cm x 7.5 cm) with the picture centred on the card.

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Design

The experiment consisted of 4 phases, sequentially presented to each participant:

(1) a study phase which was either a semantic decision task or a naming task; (2)

neuropsychological evaluation (i.e. Camcog and MMSE); (3) a semantic decision task

(in which priming was measured); and (4) a recognition memory test.

The pictures presented in the study phase of the semantic decision task were

intact, and those presented in semantic decision test phase were fragmented. Similarly,

for recognition test the pictures presented in the recognition phase were fragmented.

The original list of 60 objects was divided into 3 lists each of 20 pictures. Participants

would encounter one of these lists as the study list, then the same list again plus a new

list as the unprimed items in the semantic decision test phase. For the recognition task,

the unprimed items in the semantic decision task served as the study list (and thus as

‘old’ items in the recognition test), and another new list acted as the unstudied ‘new’

items for the recognition test. To ensure that the study phases of both the implicit

semantic decision task and the recognition task were similar, participants were also

asked to name an intact version of each picture following their semantic decision to the

fragmented picture. This was to enable recognition performance to be as efficient as

possible and to provide the maximum possibility of successful recognition performance

for the AD group, who we had predicted would find recognition particularly difficult.

The lists of objects were rotated across participants, and within participant

groups, so that no object was encountered more than once for each participant and both

implicit and explicit tasks were carried out by each participant. This design yields the

following variables: (1) for the study phase, Group (AD vs. HC participants) and Study

Task (semantic decision task vs naming task), which are between-subject measures; (2)

for the semantic decision test phase, Group (AD vs. HC), Study Task (semantic decision

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vs. naming) and Priming (Unprimed vs. Primed), where priming is a repeated measure;

and finally (3) for the recognition test phase, the main variable was Group (AD vs. HC).

Note, we also included Study Task (semantic decision task vs naming task) as a variable

for the recognition test phase to ensure there was no influence on recognition

performance of having carried out either of these tasks in particular during the initial

study phase prior to the semantic decision test phase.

Due to a procedural error in operationalization of the design, the full stimulus

rotation procedure was carried out for only half the participants within each group,

whereas for the remaining half all the participants in that group received the same three

lists (i.e., study list A, semantic decision lists A and B, recognition lists B and C). To

assess whether this influenced the results we added this group difference as a within AD

and HC group variable to the statistical analyses.

The dependent variable for the naming and semantic decision tasks was

percentage correct. For the recognition test, the measures were hits, false alarms, and a

corrected recognition score (calculated as hits minus false alarms).

Procedure

Each participant was tested individually in a single experimental session that

was scheduled to last approximately 45 minutes. In the initial study phase participants

were presented with intact pictures displayed one at the time on separate cards which

participants were asked either to categorize as living or non-living, or to name. There

was no time limit for the answer to be provided, but participants were instructed to

answer as quickly and accurately as possible. After a short delay of 15 minutes during

which the neuropsychological test was conducted, the semantic decision test phase

began. As in the study phase, pictures were presented one at the time on separate cards,

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and participants were asked to categorize the fragmented picture as living or non-living.

After each response, participants were shown the corresponding intact picture and asked

to name it. There was no time limit for the answer to be provided, but participants were

instructed to answer as quickly as possible. Finally, the recognition task was

administered 10 minutes after the semantic decision task. In this task participants were

asked to perform a yes or no recognition judgement to fragmented pictures. Participants

were instructed to respond “yes” to a picture if they had previously encountered the

object and “no” if they had not.

Results

Recognition

The average hits and false alarms for the AD group were 14.9 (SD = 4) and 13.6

(SD = 4.6) respectively, compared with 15.7 (SD = 3.5) and 3.4 (SD = 3.4) respectively,

for the HC group.

AD patients and HC participants did not differ significantly in terms of hits,

t(30) = -6.10, p = n.s., but there was a significant difference for false alarms between the

two groups with more false alarms for the AD group, t(30) = 7.10, p ≤ 0.001 (see Table

2).

Corrected recognition scores (i.e., hits minus false alarms) were also computed

for each participant. The mean corrected recognition score was 0.6 (SD = 0.15) for AD

patients, and 0.43 (SD = 0.35) for HC participants (see Table 2). AD patients exhibited

a significant recognition memory impairment in comparison to the HC group. A two

factor analysis of variance (ANOVA) computed on corrected recognition scores with

group (AD vs HC) and study task (semantic decision vs naming) as a between-subject

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variables reveals a main effect of group with AD patients significantly less accurate at

recognizing previously seen pictures, F(1,28) = 15.5, p < 0.001. However, there was no

effect of study task, F (1,28) = 0.48; p = n.s., and no interaction between group and

study task, F(1,28) = 2.02, p = n.s..

To examine whether there were any differences between the groups for the

initial study phase, t-tests were also carried out on corrected recognition scores. There

was no significant difference between: (1) AD patients that performed a semantic

decision task at study (M = 0.03, SD = 0.13) and AD patients that performed a naming

task at study (M = 0.09, SD = 0.18), t(14) = -0.09, p = ns; and (2) NC participants that

performed a semantic decision task at study (M = 0.5, SD = 0.3) and NC participants

that performed a naming task at study (M = 0.3, SD = 0.4), t(14) = 1.16, p = ns.

----------------------

Table 2 about here

-----------------------

Semantic decision task

Study phase

The mean percentage correct responses were analysed in a two factor ANOVA

with group and study task as between-subject variables. There was a main effect of

group, with fewer correct for the AD than the HC group, F(1,28) = 62.76, p ≤ 0.001.

AD and HC group means were 77.5 (SD = 2.4) and 100 (SD = 2.41), respectively.

However, there was no effect of study task, F(1,28) = 7.031, p = 0.700, and no

interaction between group and study task, F(1,28) = 2.04, p = 0.164 (see Table 3).

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----------------------

Table 3 about here

----------------------

Test phase

The data was analysed using a mixed ANOVA, with group (AD vs HC) and

study task (semantic decision vs naming) as between-subjects variables and priming

(primed vs. unprimed) as the within-subjects variable. There was a main effect of

Group, with AD less accurate than NC, F(1,28) = 20.03, p ≤ 0.001. There was also a

main effect of priming, with greater accuracy for primed as compared with unprimed

conditions, F(1,28) = 140.23, p ≤ 0.001, Finally, there was also a marginal group x

priming interaction, revealing a trend towards a greater priming for the AD patients

relative to NC participant, F(1,28) = 3.76, p ≤ 0.1, (see Table 4). There was no effect of

study task, F(1,28) = 0.92, p = 0.35.

When we add a grouping variable to account for different groups of participants

receiving either rotated or unrotated lists of items (see Design section) the findings are

unchanged. There was no main effect of rotation, F(1,24) = 0.09, p = n.s.; and there was

no interaction between rotation condition and subject group F(1,24) = 0.04, p = n.s. The

main effect of Group remained, F(1, 24) = 17.8, p < 0.01, as did the main effect of

priming, F(1,24) = 131.5, p < 0.005. The group x priming interaction approached

significance, F(1,24) = 3.52, p = 0.07.

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----------------------

Table 4 about here

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Discussion

Although severely impaired in recognition, AD patients exhibited normal

priming with fragmented pictures in a semantic decision task. This is consistent with

intact conceptual priming in AD patients, when an identification response is required

(e.g., Gabrieli et al., 1999). It is also consistent with normal priming in AD of

fragmented picture processing, which has only been observed previously in picture

naming (e.g., Ergis, Van der Linden & Deweer, 1995; Gabrieli et al., 1994). Thus,

perceptual closure, the process whereby an observer fills in missing portions of a

stimulus so as to complete an image and produce an identifiable object, is preserved in

AD.

Nevertheless, the present results are inconsistent with two previous studies in

particular. First, Verfaellie et al. (1996) found preserved priming for undegraded

pictures, but impaired priming for degraded pictures for AD patients in a naming task.

They argue that impaired priming of naming degraded pictures arises because

processing such pictures requires explicit memorial retrieval strategies which are

impaired in AD. In the Verfaille and colleagues study priming was impaired when

degraded pictures were presented in both study and test phases of the experiment. It is

possible therefore that preserved priming is observed here because pictures were only

degraded at test. However, this is unlikely to be the case as Heindel et al. (1989) found

impaired priming of picture naming with undegraded pictures presented at study and

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degraded pictures presented at test. Rather, we suggest that explicit retrieval strategies

may contaminate implicit picture processing performance when a naming rather than a

forced two-choice categorization response is required. Naming is more difficult than

forced two-choice categorization as in the former case a single unique label has to be

attached to the stimulus, and in the latter a more general label is applied. This added

difficulty for naming may lead to explicit retrieval strategies normally being used to

benefit performance.

Second, Lazzara, Yonelinas and Ober (2001) assessed conceptual priming in AD

with a semantic decision task in which participants were required to make judgements

about the size of the objects (e.g., ‘Does the word basket represent an item that can be

larger or smaller than a shoebox?’). Conceptual priming was impaired in AD patients

relative to the control group. The reason for the disparity between the Lazarra et al.,

study and the data presented here may be either: (1) the degree of semantic impairment

in the AD groups; or (2) the extent to which the tasks used in each study require

semantic processing.

AD patients can have degraded semantic processes. For instance, recently

Giffard et al. (2002) have suggested that from the onset of Alzheimer’s dementia

semantic representations deteriorate progressively with specific features affected first

(e.g., for tiger – stripes). Differentiating between concepts becomes more difficult as

distinguishing features are lost. In a similar vein, AD patients (and other brain-damaged

groups) have been shown to have category-specific semantic memory deficits, whereby

they perform worse on living as compared with non-living things (see e.g., Whatmough

& Chertkow, 2002, for a recent review). One possible reason for the living things deficit

is that AD patients may have lost perceptual features of objects which are particularly

important for processing living things, while the functional features (such as how an

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object is used) which are more salient for non-living things remain intact. There may

also be longitudinal changes where a larger number of intercorrelated perceptual

attributes contributing to the conceptual representation of living things make them less

vulnerable in the early stages of AD, but the collapse of this correlational structure

exaggerates deficits for living things with advanced disease (Gonnerman et al., 1997,

although see Garrard, Patterson, Watson & Hodges, 1998). Returning to the present

study, it may be that the present AD group was less impaired semantically, or

alternatively that the decision as to whether an object is living or non-living is not as

sensitive to semantic processing as a comparative judgement as to an object’s size.

One final point to make is that although priming was essentially normal, the AD

group showed a trend towards a greater priming than the HC group. This is most likely

due to poorer initial baselines, as prior research suggests that the magnitude of priming

increases as a function of absolute baseline performance (e.g., Ostergaard, 1994).

However, following Park et al. (1998) who found a similar result (although for naming),

it may be that because AD patients have difficulty in semantically processing pictures,

prior processing may have disproportionately enhanced the retrieval of semantic

knowledge of those items that are usually difficult or indeed unable to be retrieved by

patients. This suggestion is also supported by studies of ‘hyperpriming’ (i.e., greater

priming for patients relative to controls) in semantic priming tasks where such priming

is observed for items for which semantic processing is impaired (e.g., Chertknow, Bub

& Seidenberg, 1989; although see e.g., Bell, Chenery & Ingram, 2001, and Giffard et

al., 2001, for alternative accounts of hyperpriming).

In sum, a dissociation between perceptual and conceptual implicit memory

processes alone is not sufficient to explain implicit memorial performance in AD

patients observed here. Rather, the nature of the response that is required (i.e., an

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identification or production response) is likely to be important as well (e.g., Gabrieli et

al., 1999). An alternative suggestion is that impaired priming in AD is a consequence of

the ‘hyperspecificity’ in their processing abilities (Maki & Knopman, 1996). According

to this view, AD patients exhibit normal priming only when processing operations are

identical between study and test phases of the experiment. The reason for this is that as

they are unable to convert information between different operations involved in the

different phases of the study. However were this the situation here, we would have

expected greater priming for the semantic decision-semantic decision group, as

compared to the naming-semantic decision group. This was not the case. Rather, in line

with Gabrieli et al. (1999), we suggest that impaired attentional resources in AD can

have important consequences for the unconscious or unintentional retrieval of long-term

memories.

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References

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental

disorders (4th Ed). Washington D.C.

Bell, E. E., Chenery, H. J., & Ingram, J. C. L. (2001). Semantic priming in Alzheimer’s

dementia: evidence for dissociation of automatic and attentional processes. Brain and

Language, 76, 130-144.

Bondi, M. W., & Kaszniak, A. W. (1991). Implicit and explicit memory in Alzheimer’s

disease and Parkinson’s disease. Journal of Clinical and Experimental

Neuropsychology, 13, 339-358.

Blaxton, T. A. (1989). Investigating dissociations among memory measures: support for

a transfer-appropriate processing framework. Journal of Experimental Psychology:

Learning, Memory and Cognition, 15, 657-668.

Blaxton, T. (1999). Combining disruption and activation techniques to map conceptual

and perceptual memory processes in the human brain. In J.K. Foster and M. Jelicic

(Eds.), Memory: Systems, Process or Function? (pp.104-129). Oxford: Oxford

University Press.

Carlesimo, G. A., Fadda, L., Marfia, G. A., & Caltagirone, C. (1995). Explicit memory

and repetition priming in dementia: evidence for a common basic mechanisms

underlying conscious and unconscious retrieval deficits. Journal of Clinical and

Experimental Neuropsychology, 17, 44-57.

Page 20: Preserved Conceptual Priming in AD

20

Chertknow, H., Bub, D., & Seindenberg, M. (1989). Priming and semantic memory loss

in Alzheimer’s disease. Brain and Language, 36, 420-446.

Deweer, B., Ergis, A. M., Fossati, P. Pillon, B., Boller, F., Agid, Y., & Dubois, B.

(1994). Explicit memory, procedural learning and lexical priming in Alzheimer’s

disease. Cortex, 30, 113-126.

Ergis, A. M., Van der Linden, M., & Deweer, B. (1995). Cross-form priming in normal

aging and mild dementia of the Alzheimer type. Cortex, 31, 699-710.

Fleischman, D. A., & Gabrieli, J. D. E. (1998). Repetition priming in normal aging and

Alzheimer’s disease: a review of findings and theories. Psychology and Aging, 13, 88-

119.

Fleischman, D. A., Gabrieli, J. D. E., Reminger, S., Rinaldi, J., Morrell, F., & Wilson,

R. (1995). Conceptual priming in perceptual identification for patients with Alzheimer’s

disease and a patient with right occipital lobectomy. Neuropsychology, 9, 187-197.

Folstein, M.F., Folstein, S.E., & McHugh, P.R. (1975). Mini-Mental State Examination:

a practical methods for grading the cognitive state of patients for the clinician. Journal

of Psychiatric Research, 12, 189-198.

Gabrieli, J. D. E., Francis, W. S., Grosse, D., & Wilson, R. S. (1991). Intact repetition

priming for time to name pictures in patients with Alzheimer’s disease: dissociations

Page 21: Preserved Conceptual Priming in AD

21

from recognition memory and from word-completion priming. Society for Neuroscience

Abstracts, 17, 3.

Gabrieli, J. D. E., Keane, M. M., Stager, B. Z., Kjelgaard, M. M., Corkin, S., &

Growdon, J. H. (1994). Dissociations among structural-perceptual, lexical-semantic and

event-fact memory systems in Alzheimer’s disease, amnesic and normal subjects.

Cortex, 30, 75-103.

Gabrieli, J. D. E., Vaidya, C. J, Stone, M., Francis, W. S., Thompson-Schill, S. L.,

Fleischman, D. A., Tinklenberg, J. R., Yesavage, J., & Wilson, R. S. (1999).

Convergent behavioural and neuropsychological evidence for a distinction between

identification and production forms of repetition priming. Journal of Experimental

Psychology: Learning, Memory and Cognition, 128, 479-498.

Garrard, P., Patterson, K., Watson, P.C., & Hodges, J.R. (1998). Category-specific

semantic loss in dementia of Alzheimer’s type: Functional-anatomical correlations from

cross-sectional analyses. Brain, 121, 633-646.

Giffard, B., Desgranges, B., Nore-Mary, F., Lalavée, C., de la Sayette, V., Pasquier, F.

& Eustache, F. (2001). The nature of semantic memory deficits in alzheimer’s disease:

new insights from hyperpriming effects. Brain, 124, 1522-1532.

Giffard, B., Desgranges, B., Nore-Mary, F., Lalavée, C., de la Sayette, V., Pasquier, F.

& Eustache, F. (2002). The dynamic time course of semantic memory impairment in

Page 22: Preserved Conceptual Priming in AD

22

Alzheimer’s disease: clues from hyperpriming and hypopriming effects. Brain, 125,

2044-2057.

Gonnerman, L.M., Andersen, E.S., Devlin, J.T., Kempler, D., & Seidenberg, M.S.

(1997). Double dissociation of semantic categories in Alzheimer’s disease. Brain &

Language, 57, 254-279.

Guerreiro, M. (1993). Adaptação portuguesa do MMSE (Portuguese Adaptation of

MMSE). Laboratório de Estudos do Centro de Estudos de Egas Moniz. Hospital de Sta.

Maria.

Heindel, W. C., Salmon, D. P., Shults, C. W., Walicke, P. A., & Butters, N. (1989).

Neuropsychological evidence for multiple implicit memory systems: a comparison of

Alzheimer’s, Huntington’s and Parkinson’s disease patients. The Journal of

Neuroscience, 9, 582-587.

Keane, M. M., Gabrieli, J. D. E., Growdon, J. H., & Corkin, S. (1991). Evidence for a

dissociation between perceptual and conceptual priming in Alzheimer’s disease.

Behavioural Neuroscience, 105, 326-342.

Keane, M. M., Gabrieli, J. D. E., Growdon, J. H., & Corkin, S. (1994). Priming in

perceptual identification of pseudowords is normal in Alzheimer’s disease.

Neuropsychologia, 32, 343-356.

Koivisto, M., Portin R., & Rinne, J. O. (1996). Perceptual priming in Alzheimer’s and

Parkinson’s diseases. Neuropsychologia, 34, 449-457.

Page 23: Preserved Conceptual Priming in AD

23

Lazzara, M. M., Yonelinas, A. P., & Ober, B. A. (2001). Conceptual implicit memory

performance in Alzheimer’s disease. Neuropsychology, 15, 483-491.

Maki, P. M., & Knopman, D. S. (1996). Limitations of the distinction between

conceptual and perceptual implicit memory: a study of Alzheimer’s disease.

Neuropsychology, 10, 464-474.

McKhann, G., Drachman, D., Folstein, M., Katzman, R., Proce, D., & Stadlan, E. M.

(1984). Clinical diagnosis of Alzheimer’s disease: Report of the NINCDS-ADRDA

work group. Neurology, 34, 939-944.

Mitchell, D. B., & Brown, A. S. (1988). Persistent repetition priming in picture naming

and its dissociation from recognition memory. Journal of Experimental Psychology:

Learning, Memory and Cognition, 14, 213-222.

Monti, L. A., Gabrieli, J. D. E., Reminger, S. L., Rinaldi, A., Wilson, R. S., &

Fleischam, D. A. (1996). Differential effects of aging and Alzheimer’s disease on

conceptual implicit and explicit memory. Neuropsychology, 10, 101-112.

Ostergaard, A. L. (1994). Dissociations between word priming effects in normal

subjects and patients with memory disorders: multiple memory systems or retrieval?

The Quarterly Journal of Experimental Psychology, 47A, 331-364.

Page 24: Preserved Conceptual Priming in AD

24

Park, S. M., Gabrieli, J. D. E., Reminger, S. L., Monti, L. A., Fleischman, D. A.,

Wilson, R. S., Tinklenberg, J. R., & Yesavage, J. A. (1998). Preserved priming across

study-test picture transformations in patients with Alzheimer’s disease.

Neuropsychology, 12, 340-352.

Park, S.M., & Gabrieli, J.D.E. (1995). Perceptual and nonperceptual components of

implicit memory for pictures. Journal of Experimental Psychology: Learning, Memory

and Cognition, 21, 1583-1594.

Salmon, D. P., Shimamura, A. P., Butters, N., & Smith, S. (1988). Lexical and semantic

priming deficits in patients with Alzheimer’s disease. Journal of Clinical and

Experimental Neuropsychology, 17, 325-334.

Snodgrass, J. G., & Feenan, K. (1990). Priming effects in pictures fragment completion:

support for the perceptual closure hypothesis. Journal of Experimental Psychology:

General, 119, 276-296.

Snodgrass, J. G., & Kinjo, H. (1998). On the generality of the perceptual closure effects.

Journal of Experimental Psychology: Learning, Memory and Cognition, 24, 645-658.

Snodgrass, J. G., Smith, B., Feenan, K., & Corwin, J. (1987). Fragmenting pictures on

the Apple Macintosh computer for experimental and clinical applications. Behaviour

Research Methods, Instruments and Computers, 19, 270-274.

Page 25: Preserved Conceptual Priming in AD

25

Snodgrass, J.G., & Vanderwart, M. (1980). A standardized set of 260 pictures: norms

for name agreement, image agreement, familiarity and visual complexity. Journal of

Experimental Psychology: Human Learning and Memory, 6, 174-215.

Vaidya, C. J., Gabrieli, J. D. E., Keane, M. M., Monti, L. A., Gutérrez-Rivas, H., &

Zarella, M. M. (1997). Evidence for multiple mechanisms of conceptual priming on

implicit memory tests. Journal of Experimental Psychology: Learning, Memory and

Cognition, 23, 1324-1243.

Vaidya, C. J., Gabrieli, J. D. E., Monti, L. A., Tinklenberg, J. R., & Yesavage, J. A.

(1999). Dissociation between two forms of conceptual priming in Alzheimer’s disease.

Neuropsychology, 13, 516-524.

Verfaellie, M., Gabrieli, J. D. E., Vaidya, C. J., Croce, P. & Reminger, S. L. (1996).

Implicit memory for pictures in amnesia: role of etiology and priming task.

Neuropsychology, 10, 517-528.

Whatmough, C., & Chertkow, H. (2002). Category-specific recognition impairments in

Alzheimer’s disease. In E.M.E. Forde and G.W. Humphreys (Eds), Category-Specificity

in Brain and Mind (pp. 181-210). Psychology Press.

Zec, R.F. (1993). Neuropsychological functioning in Alzheimer’s disease. In R.W.

Parks; R. F. Zec & R. S. Wilson (Eds), Neuropsychology of Alzheimer’s disease and

other dementias (pp. 3-80). New York: Oxford University Press.

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Table 1

Descriptive Characteristics for Alzheimer’s Disease (AD) and Healthy Older Adult

Control (HC) Participants.

Group Age Years of education Neuropsychological test

AD (n = 16)

Mean

S D

HC (n = 16)

Mean

SD

75.6

5.86

73.5

6.26

6.1

4.8

4.8

4.13

CAMCOG & MMSE

51.4/16.2

10.30/3.41

MMSE

25.5

2.68

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Table 2

Percentages of Hits and False Alarms, and Corrected Recognition Scores for

Recognition

Hits False Alarms Corrected Recognition Scores

AD

Mean

SD

14.9

4

13.6

4.6

0.6

0.15

HC

Mean

SD

15.7

3.5

3.4

3.4

0.43

0.35

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Table 3

Mean Percentage Correct for Semantic Decision and Naming as Study Tasks

Groups Task

Semantic Decision Naming

AD

Mean

SD

77.5

2.4

81.9

2.41

HC

Mean

SD

100

2.41

97.5

2.41

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Table 4

Mean Primed and Unprimed Scores for AD and HC Groups for Semantic Decision

as the Test Task With Naming and Semantic Decision as Study Tasks

Naming at Study Semantic decision at Study

Primed Unprimed Primed Unprimed

AD

Mean

SD

89.4

6.23

69.4

6.23

90.6

4.17

70.6

4.17

HC

Mean

SD

95.6

4.17

79.4

14.5

96.2

3.54

83.7

5.18