The purpose of this paper is to examine, validate and interpret the findings of how

Alzheimer’s disease affects semantic memory functions. We will examine many past studies

chronological order. We will first analyze findings regarding the inability of Alzheimer’s disease

patients to generate words. We will then examine studies regarding the loss of “idea-meaning” in

AD patients and how this can explain how semantic memory impairment happens. Next, we will

interpret the affects that semantic priming and other contextual mechanisms have had on semantic

memory and language in general in AD patients. Finally, we will examine the separateness of the

two major language function hypotheses accounting for semantic memory impairment in

Alzheimer’s disease. In closing, we will examine the relative importance of both hypotheses and

their roles in future research development in Alzheimer’s disease.

Methinks I should know you and know this man,

Yet I am doubtful; for I am mainly ignorant

What a place this is, and all the skill I have

Remembers not these garments, nor I know not where I did lodge last night.”

(William Shakespeare, King Lear, Act 4, Scene 7)

King Lear’s words accurately encapsulate the language difficulties of Alzheimer’s disease

patients. In the past twenty years, considerable research has been conducted regarding whether or

not Alzheimer’s disease, AD for short, affects semantic memory. The majority of studies have

found that AD does affect semantic memory. “Semantic memory is part of the long-term memory,

and contains the permanent representation of our knowledge of concepts, of words and their

meaning, and in essence gives meaning to our sensory experience” (Binetti 1995 in reference to

Squire 1987). In explaining the semantic memory impairment found in AD patients’ language,

there have stood two popular hypotheses: one hypothesis postulates that semantic memory

impairment in AD is due to a general deterioration in semantic knowledge–the degradation

hypothesis and the second hypothesis postulates that semantic memory impairment in AD is due

to a lexical access problem–the retrieval deficit hypothesis. Most studies have not been able to

prove solely one hypothesis or the other; however, there are many studies that support one or the

other. Therefore, the semantic memory impairment commonly found among Alzheimer’s disease

patients is due both to a semantic knowledge retrieval deficit problem and to a degradation of

semantic memory in general. Furthermore, many authors believe the two are closely related.

However, the two are separate language functions.

Word-Generating Impairment

A loss in word-searching ability is commonly found among patients with Alzheimer’s

Disease. This may be one of the worst symptoms of the disease and it is often observed in the

patient’s unpredictable speech. Most measures used to analyze word searching have focused on

the potential of patients to successfully search their lexicon for specific words. For example,

subjects have been asked to describe pictures and generate a word that correlates with a certain

definition. Patients have also been asked to generate the names of members within a certain

category. As with examining other symptoms commonly found in AD, the problem has been to

decipher whether or not this word-searching problem is due to a lexical access deficiency or an

actual loss of stored information from semantic memory.

Often, AD patients suffer a word-searching loss very early in the disease. Therefore, a loss

in word-finding ability has been characterized as an early sign for the disease. In examining this,

researchers ask AD patients to describe an object or a picture. The speech of AD patients tends to

be vague, repetitive, and empty of content words. Also, it is full or pronouns without

antecedents, empty phrases (“something like that”), indefinite terms (“things”, “stuff”), and

semantically related but incorrect words (e.g., calling a stool a chair) (Nicholas, Obler, Albert &

Helm-Estabrooks, 1985). For example, a patient describing a bathtub might say “Well I see now,

yeah, well you go into the bathtub and you don’t have any problems here or there. You got that

over there though on that” (Bayles, 1982). Although the speech of AD patients lacks content

words and communicates little information, it remains grammatically correct, which could be

explained by language universals. Furthermore, the frequency with which different “syntactic

constructions” are used is the same in normal and AD patients (Kemper, Curtiss, & Jackson,

1987). Later in the disease, syntactic errors, although not overly significant, are seen in the

disease. Kemper, Curtiss, and Jackson (1987) examined a spontaneous speech sample and found

that normals, non-AD elderly patients, and AD patients were very similar in their use of

prepositional phrases and subordinate clauses. The authors also found the length and grammatical

correctness of their speech to be similar (Kemper, Curtiss, and Jackson 1987). However, the AD

patients used many more empty words (e.g., “thing”) and other unclear referents. Many

researchers (Bayles 1982 and Nicholas, Obler, Albert, & Helm-Estabrooks 1985) believe there is

a significant lexical semantic impairment in AD but only minimal syntactic problems.

In measuring the semantic deficit in AD, researchers have tested verbal fluency. Most

often, researchers give the patient a category and then ask the patient to formulate as many

members of that category as possible within a given time, usually sixty to ninety seconds. The

studies have usually used two different categories: first, is a letter category–here subjects are

asked to generate as many words as they think of that begin with a particular letter (e.g., “s”), and

the second type is a semantic category (e.g., four-legged animals or furniture). One of the most

detailed examinations of verbal fluency has been by Ober, Dronkers, Koss, Delis, and Friedland

(1986). They found that even mildly demented patients generated only one half the number of

items produced by normals. Furthermore, the AD patients also produced more inappropriate

responses (non-category responses) than did the old-aged normal controls. Another important

finding is that the “average category response (Ober, Dronkers, Koss, Delis, and Friedland 1986)

made by AD patients was not different than that of the normal controls. Ober et al. (1986)

highlighted that whatever the cause of the decreased verbal fluency in AD patients, it does not

appear to affect the “dominance or frequency structure” of the categories Ober, Dronkers, Koss,

Delis, and Friedland 1986). However, Butters et al. (1987) concluded that AD patients generated

significantly fewer words than did normal controls with semantic categories; whereas with letter

categories, the two groups did equally well. However, Rosen (1983) found the opposite–the AD

patients were more impaired in verbal fluency tasks with letter categories than with semantic

categories. A different fluency task was used by Martin and Fedio (1983) and by Ober et al.

(1986). In these studies, the subject was asked to name items found in a supermarket. The authors

found that the normal subjects, on average, named three or four items from each of a number of

contrasting subcategories, such as fruits or meats. However, they found that Alzheimer patients

named fewer items, and on average, AD patients produced only a single item from each

subcategory (Martin and Fedio 1983 and Ober et al. 1986). In some cases, Ober et al. (1986)

found that AD patients, when asked to name items, would give the subcategory name itself as a

response (e.g., “vegetables”). Ober et al. reasoned that if AD patients’ decreased verbal fluency

was due solely to a slowing in the rate at which they searched their memory, then they should

have gotten through fewer subcategories, but they should have generated the same number of

items for each subcategory (Ober et al 1986). But this was not what the authors found; instead,

according to the authors, AD patients’ category search appeared more random than that of the

normal controls (Ober et al. 1986).

An impairment in naming objects is commonly found among patients with aphasia (Benson

1985). Normal aging affects relatively small changes in the accuracy of naming objects (LaBarge,

Edwards, & Knesevich, 1986). In a “cross sectional study”, Nicholas, Obler, Albet, & Helm-

Estabrooks (1985) showed only a nine percent difference in object naming scores between normal

subjects in their thirties and normal subjects in their seventies. However, patients with AD have

significant impairments in naming objects; many researchers have shown that the magnitude of

this impairment is directly proportional to the magnitude of the disease (Kirshner, Webb, & Kelly,

1984). Kirshner found that naming errors in AD patients tended to be the names of semantically

related objects (e.g., calling a carrot a vegetable) or other objects within a category (e.g., calling a

computer a television) (Kirshner, Webb, & Kelly 1984). These findings strengthen the degradation

of semantic memory. The retrieval deficit hypothesis has also been strengthened by Kirshner’s

studies–he found that the degree of the naming deficit in demented patients varied with the

frequency of the name in language. The less the name was used, the less success demented

patients had in generating the name of an object (Kirshner, Webb, & Kelly 1984). Furthermore,

Martin and Fedio (1983) found that AD patients, when taking the Boston Naming Test (a

standard protocol evaluation test), were affected by phonemic cues sixty percent of the time; these

cues helped AD patients name an object which they had failed to name when only showed a

picture of the object (Martin and Fedio 1983). Lastly, there is one result suggesting the naming

problem of AD patients has more than one source. Barker and Lawson (1968) found that when

AD patients were allowed to handle an object or to see it in use, they had more success in

generating its name. Barker and Lawson (1968) also found, like Kirshner et al. (1984), that the

success of object naming in demented patients varied with the frequency of the object’s name in

the language (Barker and Lawson 1968). They found that these two effects did not “interact”.

They implied that these two factors affect different cognitive operations and that the naming

deficit in dementia may be the result of both an impairment in lexical access and from some sort of

object identification problem (Barker and Lawson 1968).

the subject to produce the name of a specific word that fits a given definition–otherwise known as

“naming to definition”. Rissenberg and Glanzer (1987) gave definitions to subjects (e.g., “A place

where books are kept for use but not for sale”) for both abstract and concrete words (Rissenber

and Glanzer 1987). They found no difference in naming accuracy between normal old and young

subjects. However, they also found that the AD patients not only produced significantly fewer

words when they were given a definition, but they were much worse with the abstract words

(Rissenberg and Glanzer 1987). The authors noted that they did not use equally difficult concrete

and abstract words. Therefore, the contrast in word-searching aptitude between abstract and

concrete words could be due to the demented patients having more problems in comprehending

the definitions used to describe abstract words. The authors implied that these results show a

lexical retrieval problem in AD patients that is especially severe for abstract words (Rissenberg

and Glanzer 1987). A different study showed contrasting results; Huff, Mack, Mahlmann, &

Greenberg (1986), in examining a similar task as just described, interpreted their results as

showing that in addition to a retrieval deficit, AD patients may also suffer from a loss of “lexical-

semantic information about the defined referents” (Huff, Mahlmann, & Greenberg 1986). In this

task, the subject was given an incomplete sentence (e.g., “A tool used to pound nails is called

”). Huff et al. (1986) found that AD patients consistently failed to name the name the same items.

However, the authors then gave the subjects a multiple choice task. Here, the subject was asked

to say yes or no to a sentence of the form “Is the tool used to pound nails called a hammer?” AD

patients successfully understood the names of items they had failed to name in the earlier

experiment, suggesting that at least part of their naming impairment was due to a retrieval failure.

At this point it should be noted that throughout the majority of studies we have visited thus far,

every method of measuring semantic memory impairment seems to have a double sided paradigm;

one paradigm proves the degradation hypothesis and the other paradigm supports the retrieval

deficit paradigm–this depends on the angle of approach. In some cases, as we have just seen,

researchers cannot solely attribute their results to one hypothesis or another. It should also be

noted that the majority of studies are forcefully subjective; most studies are designed to prove one

hypothesis right or wrong. The findings all vary, and their interpretative postulations vary even

more.

After reviewing these past studies on the ability of AD patients to search for words, it is

very obvious that AD patients suffer an impairment of word-searching ability. As with other

aspects of semantic memory impairment in AD, there is an uncertainty of whether this problem is

a result from solely the loss of a retrieval mechanism or from a general semantic memory loss. The

majority of research, on word-searching ability in Alzheimer’s disease, supports the hypothesis of

the degradation of stored semantic memory. However, many studies have interpreted word-

searching problems in AD as being a reflection of a deficit in lexical access–the retrieval deficit

hypothesis. Therefore, one cannot conclude that word finding problems in AD are solely the result

of either a semantic memory storage impairment or a semantic memory access impairment. As a

result of numerous studies interpreting word-searching problems in AD by one hypothesis or the

other, one can reasonably attribute word-searching problems in AD to both an impairment in

lexical access and a more general semantic memory impairment.

Loss of Perceived, Symbolized Ideas

Many AD researchers believe a loss in the meaning of ideas to be the foundational

deficiency in the semantic memory impairment commonly found in AD. Most models of semantic

memory include the presence of semantic associations that represent both perceptual and abstract

knowledge about a perceived, symbolized idea. Patients with AD are hypothesized to have lost

these associations that make up the meaning of perceived, symbolized ideas; however, as with

other symptoms commonly found among patients with AD, it is not known whether or not this

impairment of idea-meaning is due to a general semantic memory degradation or a lexical retrieval

deficit. This loss of perceived, symbolized ideas in AD has been believed to underlie impairments

in other “cognitive domains” such as understanding language (Bayles 1987). The primary concern

in explaining this loss of perceived, symbolized meaning-idea is whether the idea-meaning is truly

lost or is only difficult to retrieve under certain conditions. Also, researchers have attempted to

explain whether all aspects of idea-meaning are influenced in a similar manner or whether only

certain elements are impaired (Bayles 1987). Both “expressive” (WAIS vocabulary) and

“receptive” (Peabody Picture Vocabulary Test) vocabulary tests scores decline proportionately

with the increase of dementia (Bayles 1987). However, as with the majority of symptoms that

characterize AD, major changes in vocabulary tests, as with other aspects of idea-meaning loss in

AD, have not been entirely explained by either the degradation of semantic memory hypothesis or

the retrieval deficit hypothesis (Norton 1997).

In studying knowledge of idea-meaning, numerous researchers (Huff et al., 1986; Martin

& Fedio 1983) have postulated that even though patients with dementia may hold specific

information about a certain idea, they gradually lose knowledge of the specific, semantic

characteristics that compose an idea’s meaning (its physical features and functions) (Martin &

Fedio 1983; Huff et al., 1986). These two studies have suggested that the specific characteristics

of semantic information are needed to distinguish between closely related semantic ideas–such as

members of the same semantic category. Therefore, this loss could be responsible for the

problems that demented patients have in naming (Huff et al., 1986). Flicker’s (1987) AD subjects

had problems in describing the use of a certain object; however, these same subjects could choose,

from a wide assortment of options–the items that would be useful in a certain situation (e.g.,

cooking dinner) (Flicker 1987). This study supports the retrieval deficit hypothesis more than it

does the degradation one. Grober, Buschke, Kawas, and Fuld (1985) concluded that “conceptual

attributes” are not lost in demented patients but that the structure of these “attributes” is impaired

(Grober, Buschke, Kawas, and Fuld 1985). In one particular experiment they gave subjects a

target word and asked them to pick out from among many other words those that were related to

the initial one. Demented patients were very accurate (95% correct in comparison with 98% for

normal controls) on this particular task. The authors implied that AD patients remember semantic

characteristics of some idea-meanings (Grober, Buschke, Kawas, and Fuld 1985). However, the

authors also found that the characteristics the AD subjects did miss could have been very

important characteristics to the idea-meaning, just as the characteristics could have been not

important to the idea-meaning. This hypothesis was supported by a second experiment. In this

experiment, the subjects were given an initial word and three characteristics that varied in their

relative importance to the idea-meaning of the initial word (e.g., for the concept “airplane”, the

words “fly”, “radar”, and “luggage”). The demented patients did not do well. Therefore, these

results again suggest that although Alzheimer’s patients retain knowledge about the semantic

characteristics of idea-meanings, they have trouble retrieving this information by a self-directed

search (Grober, Buschke, Kawas, and Fuld 1985).

Word correlation is another method that has been used to examine the structure of idea-

meaning in AD. Typically, the subject is given an initial word, as with idea-meaning characteristic

testing, and asked to say the first word that comes to mind. In these studies, semantic structure is

revealed in the pattern of associations generated. It is believed that stimulation of these

associations spreads to related idea-meaning. Associations are usually described as being

“paradigmatic” or “syntagmatic” (Gewirth, Shindler, and Hier 1984). Paradigmatic associations

are words from the same grammatical category as the initial word and they are related to it in

meaning (e.g., synonyms, antonyms). Syntagmatic associations, however, are words, from a

differing category than the initial word (Gewirth, Shindler, and Hier 1984). The authors examined

the “associations” that demented subjects made to a group of words. They found that

“paradigmatic associations” decreased proportional to the severity of the disease. However,

“syntagmatic associations” remained constant throughout the severity of the disease (Gewirth,

Shindler, and Hier 1984). From these studies, it can be reasonably inferred that semantic

correlations are much more greatly affected by AD than are syntactic associations.

Many researchers disagree on whether or not AD patients suffer a category knowledge

deficit. The majority of studies, until recently have suggested that category knowledge is intact in

AD patients. According to Martin and Fedio (1983) when given a group of different words, AD

patients are able to categorize the words and name the categories (Martin and Fedio 1983). Huff

et al. (1986) found that when AD patients were showed a picture from a certain category, they

were able to decide which category the picture belonged to (e.g., “Is this a piece of furniture?”)

(Huff et al. 1986). However, studies conducted more recently imply contrasting ideas–that

category knowledge is affected by AD. Most studies supporting this theory have found that AD

patients are unable to categorize living things but they are able to categorize living things. In these

studies, investigators have found that AD patients have trouble naming or defining living things,

including animals and plants, and that AD patients do much better categorizing nonliving things

such as furniture, vehicles, and other artifacts (Warrington and Shallice 1984). These findings

have become controversial because correctly explaining them would be correctly explaining the

structure the of semantic memory in the brain. The common interpretation is that semantic

memory is organized by taxonomic category (Pietrini et al., 1988). A different explanation is that

living and nonliving things depend unequally on the amount of knowledge. Here, the authors

suggested that living things are classified by visual and sensory perceptions whereas nonliving

things are classified by what the object does or what the object is used for (Warrington and

Shallice 1984). Deterioration of visual characteristics would impair the knowledge of living

things, and nonvisual knowledge of living things (Farah and McClelland 1991). Silveri et al.

(1991) tested the categorizing ability of AD patients. They used two different methods to test this,

a “confrontation naming task” and a “verbal associates recognition” task. In the naming task, the

subjects were asked to name the pictures, whereas in the verbal association task, subjects were

required to say whether or not a picture and a word were related. On both tasks, patients

performed worse with the living things. The authors concluded that even in early stages of AD,

patients have less of an ability to categorize living things than nonliving things (Farah and

McClelland 1991). Yet, as with other aspects of AD, the uncertainty remains whether or not this

problem is due to a general degradation of semantic memory or to a retrieval deficit problem.

Salmon, Heindel, and Lange (1999) postulated that comparing the factors that affect the

phonemic-category and semantic-category tasks could lead to better understanding semantic

memory impairment in AD. They argued that if problems with the semantic-category fluency tasks

were affected by the degradation of semantic memory in AD patients, then the impairment on this

task will progress at a higher rate than the impairment in the phonemic-category fluency tasks

(Salmon, Heindel, & Lange 1999). In contrast, if a retrieval deficit is the only semantic memory

impairment in AD, then the authors argued that phonemic-category fluency tasks and semantic-

category fluency tasks should show parallel declines. The researchers investigated theses two

fluency tasks in AD patients over a course of three years with four annual examinations. This

“longitudinal” examination allowed for semantic memory impairment to be compared with results

from fluency tasks. The authors found that the ability of patients with AD to generate both

semantic and phonemic categories declines in parallel throughout the course of the disease

(Salmon, Heindel, & Lange 1999). These results are consistent with several other studies

including Butters et al. (1987). Salmon et al. (1999) concluded that because AD patients, when

compared to normal controls, show more difficulties in semantic memory tasks than phonemic

ones, they suffer from a general degradation of semantic memory as the disease worsens (Salmon,

Heindel, & Lange 1999). Norton et al. (1997) also supported this notion. They found that AD

patients’ performance on the “Number Information Test” declined as the disease progresses

(Norton et al. 1997). Thus, it can be concluded that because the majority of studies have found

similar results, and because most researchers agree that a loss in semantic category fluency tasks

is a defining characteristic of a general degradation of semantic memory, semantic memory

impairment in AD is the result of a general degradation of semantic memory.

Throughout the past twenty years, numerous studies have examined semantic memory in

AD by looking at the effect that semantic priming has on behavior. The majority of studies have

found that the normal elderly show positive influences from semantic priming. The controversial

issue, regarding semantic priming effects, has been whether or not AD patients show positive

effects from semantic priming. Many researchers have postulated that if AD patients show

positive effects from semantic priming, then the semantic memory impairment commonly found

among AD patients is due to a semantic memory retrieval deficit. Therefore, researchers interpret

their results based on this idea–that positive priming effects in AD patients can be directly

correlated to a retrieval deficit problem. However, as we will see, the results are fairly

dispersed–overall there is no tendency one way or the other; some studies show positive and some

studies show no priming effects. Even though the inconclusive nature of these studies does not

provide undoubtfull proof, the interpretations and analyses of them must be accounted for.

Numerous studies have been based on a certain network theory of semantic memory. In

this hypothesis, ideas are reflections of interconnected relationships, such as membership of a

common category (e.g., pencil-pen), functional relationships (e.g., pencil-write), and property

relationships (e.g., pencil-point). When an idea is presented, it is believed that there is an

automatic spread of activation (Balota and Duchek 1991). Experimental support for such a spread

of activation has come from the studies of semantic priming. “The effect [semantic priming effect]

refers to the finding that subjects are faster and more accurate to recognize (e.g., make a lexical

decision or name a word aloud) a target word (‘cat’) when it follows a related word (‘dog’) than

when it follows an unrelated word (‘pen’). The semantic priming effect has been at the center of

considerable work in word recognition research and has been one of the hallmark indicators of

spreading activation within a semantic memory network” (Balota and Duchek 1991). In many

studies, researchers have found that AD subjects show more semantic priming than normal

controls; still, many studies show that semantic priming has little or no effects on AD patients

(Glosser 1998). Furthermore, Albert and Milberg, 1989 found that AD patients have negative

priming when compared to normal controls (Albert & Milberg 1989). Thus, due to the

inconclusive nature of these results, one cannot attribute semantic memory in AD to a particular

form of semantic priming. Even though many studies, and many authors, support the retrieval

deficit hypothesis, there have been almost equal numbers of opposing results. Therefore, in order

to examine the effects that context has on AD patients, one must look at other semantic

contextual studies in AD.

Many studies examining semantic memory impairment in AD have focused on the

subjects’ ability to carry out a lexical search. In these studies, a sentence is given to the AD

patients with the final word missing. It is up to the AD patients to fill in the missing word, and the

time and accuracy is measured. In these tasks, the AD patients use syntactic and semantic

contextual mechanisms to carry out their search (Cohen and Faulkner 1983). The sentences vary

in the amount of contextual information available to the AD patients. Some sentences were very

specific–few words would fill the blank (e.g., “Mother poured the milk into a ”), whereas other

sentences were less specific (e.g., They went to see the smart ”). The amount of contextual

information available affected both the time and accuracy of sentence completion (Cohen and

Faulkner 1983). These authors found that AD patients were more affected by the contextual

information available than were normals. The authors also found that sentence completion

accuracy was directly proportional to the degree of directed context within a sentence (Cohen and

Faulkner 1983). Thus, it can be deduced from these studies that AD patients are susceptible to the

degree of contextual information within a sentence, and that sentence completion in AD patients

is greatly influenced by framework.

Also, in testing the effects of semantic contextual information, AD subjects are examined

by methods of sentence correction tasks. In testing this issue, Kempler et al. (1987) has tested the

degree with which AD patients can recognize and correct errors in sentences (Kempler et al.

1987). The authors argued that if semantic functions in AD are affected, compared to syntactic

ones, then the ability of AD patients to correct sentences with semantic errors should be lower

than their ability to correct sentences with syntactic errors. The sentences had errors that were

either phonetic, syntactic, or semantic. The authors found that AD patients were worse than

normals, but that this was not enough evidence to make important conclusions (Kempler et al.

1987).

Another important aspect of semantic context is to make sense out of a certain word. In

studying this, researchers use words that have similar sounds but different

meanings–“homophones”. Kempler et al. (1987) compared the affects of semantic contexts on

AD patients’ ability to make sense out of these similar sounding but different meaning words. The

subject were asked to write down a series of spoken words, the last word was a homophone. The

other words provided either a semantic (e.g., church, music, “hymn”) or a syntactic context (“to

him” vs. “a hymm”). As with the sentence correction task just described, the hypothesis was that

if AD patients do have semantic deficit, they should be less successful in using a semantic context

than using a syntactic one to make sense of homophones (Kempler et al., 1987). The authors

found that the AD patients were less responsive than were the normal controls. However, the

authors found that AD patients made substantially more errors with semantically related tasks

than with just syntactically related tasks (Kempler et al., 1987). Therefore, these results

contradict the previous results. In this sense, explaining the degree of semantic memory

impairment in AD patients, by modes of semantic context, is nondirectional.

It is obvious that there have been semantic priming effects in patients with Alzheimer’s

disease. However, these semantic priming studies have only found that semantic priming

presented to AD patients only affects the general processing of words, not the degree of lexical

access. The results of the sentence completion task show that context can facilitate a lexical

search itself in AD patients. However, the context of this search must be very specific. If there is

less specific contextual information within a sentence, AD patients are less susceptible, than

normal controls, to semantic priming. Depending on the paradigmatic interpretations used in

examining these studies, one can conclude, from the given information, that semantic memory in

AD is affected somewhat by semantic priming. However, from another perspective, we have seen

that these results support the general degradation hypothesis. Therefore, according to past studies

regarding semantic priming effects in AD, one can propose that semantic memory impairment in

AD is due both to a degradation of semantic memory and to a deterioration of a semantic memory

retrieval mechanism.

A Compilation of Hypotheses: AD Theories Merge

As we have seen, AD affects both the retrieval and knowledge functions. The uncertainty

remains whether or not the two are the same or if they are two separate entities. In comparing

semantic memory impairment in different forms of dementia, researchers, through medical

techniques and practices, have found that the two are unrelated. For example, Weingartner et al.

(1993) found that “benzodiazepines”, more specifically:

“Triazolam, given in increasing doses led to a “dose dependent change in

recent memory without impairing access to knowledge memory. Triazolam,

administered orally in doses of 0.5 mg to fifteen young healthy normals,

induced a 78% decrease in free recall. In contrast, elderly normal controls

treated with a cholinergic antagonist, such as scopolamine, demonstrate

cognitive changes that simulate a dementia similar to that found in AD

rather than an amnestic-like disorder. Following treatment with

scopolamine, recent memory impairments are associated with impairments

in accessing semantic memory as evidenced by decreased ability to generate

exemplars of closed categories of information”. (Weingartner et al. 1993)

Thus, semantic memory access and general knowledge have been shown to be separate entities of

the language function. As we have seen, AD affects both semantic memory retrieval and semantic

knowledge language functions; we have now just seen proof that these are two separate language

entities. Therefore, reasoning from the study just mentioned, one could argue that AD affects both

semantic memory retrieval and semantic memory knowledge functions.

The two controversial, opposing hypotheses in explaining semantic memory

impairment in AD–the degradation and retrieval deficit hypotheses–have both shown supportive

evidence. We have seen evidence supporting the retrieval hypothesis and almost disproving the

semantic memory degradation hypothesis, and we have seen the reverse. On the one hand, some

researchers believe that semantic memory impairment in AD is due to a retrieval deficit of

semantic memory. They believe that the storage for this memory is relatively intact, but that the

retrieval mechanisms are damaged. On the other hand, some researchers believe that there is a

gradual deterioration of the organization and content of semantic memory as the disease

progresses. Many of the studies above provide contrasting results in that they support one

hypothesis or the other. In some cases, neither hypothesis was supported, and in some cases, as

many biological studies have found, we conclude that AD affects both functions. There has also

been a debate of whether or not the these two language functions are separate entities. The

arguments made in this regard postulate that if knowledge and retrieval mechanisms are very

closely related, than the results seen–those supporting both hypotheses–should explain the

connectedness and synchrony of the two. However, as we have seen with the last study, the two

have been proved to be separate language function entities. Therefore, due to the positive results

supporting both hypotheses, and since both functions have been proved to be separate, one can

conclude that semantic memory impairment in AD is due to a general degradation of knowledge

and to a retrieval-of-knowledge deficit. Instead of treating these functions as completely related,

and instead of trying to solely account for one hypothesis or the other, researchers should

acknowledge that AD has a profound impact on both language functions. Further research,

development, and corrective measures should regard this. In conclusion, the highly inconclusive

and nondirectional interpretations resulting from studies on semantic memory impairment in AD

can be correlated to the uncertainty of how exactly memory works. Either way, great strides in

treating and better understanding AD should be better met by noting the conclusions made in this

paper–that AD affects both language functions, retrieval and general knowledge, and that these

two semantic memory language functions are separate.

Author Contact Information:Rodheimer

Manuscript Submitted 1/4/01 6:55:11 PM
Manuscript Last Edited 1/4/01 7:19:21 PM
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