semantic Memory Impairment in Alzheimer’s Disease:
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BURTON, A. E. (2001). semantic Memory Impairment in Alzheimer’s Disease: . National Undergraduate Research Clearinghouse, 4. Available online at http://www.webclearinghouse.net/volume/. Retrieved October 23, 2017 .

semantic Memory Impairment in Alzheimer’s Disease:
ALEXANDER E. BURTON
HAMLINE UNIVERSITY DEPARTMENT OF NEUROPSYCHOLOGY

Sponsored by: MARK RODHEIMER (alexburton@c4.com)
ABSTRACT
 The purpose of this paper is to examine, validate and interpret the findings of howAlzheimer’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” inAD patients and how this can explain how semantic memory impairment happens. Next, we willinterpret the affects that semantic priming and other contextual mechanisms have had on semanticmemory and language in general in AD patients. Finally, we will examine the separateness of thetwo major language function hypotheses accounting for semantic memory impairment inAlzheimer’s disease. In closing, we will examine the relative importance of both hypotheses andtheir roles in future research development in Alzheimer’s disease.

RESEARCH
“I fear I am not in my perfect mind. 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 diseasepatients. In the past twenty years, considerable research has been conducted regarding whether ornot Alzheimer’s disease, AD for short, affects semantic memory. The majority of studies havefound 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 theirmeaning, and in essence gives meaning to our sensory experience” (Binetti 1995 in reference toSquire 1987). In explaining the semantic memory impairment found in AD patients’ language,there have stood two popular hypotheses: one hypothesis postulates that semantic memoryimpairment in AD is due to a general deterioration in semantic knowledge–the degradationhypothesis and the second hypothesis postulates that semantic memory impairment in AD is dueto 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 theother. Therefore, the semantic memory impairment commonly found among Alzheimer’s diseasepatients is due both to a semantic knowledge retrieval deficit problem and to a degradation ofsemantic 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’sDisease. This may be one of the worst symptoms of the disease and it is often observed in thepatient’s unpredictable speech. Most measures used to analyze word searching have focused onthe 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 certaindefinition. Patients have also been asked to generate the names of members within a certaincategory. As with examining other symptoms commonly found in AD, the problem has been todecipher whether or not this word-searching problem is due to a lexical access deficiency or anactual loss of stored information from semantic memory. Often, AD patients suffer a word-searching loss very early in the disease. Therefore, a lossin 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 tobe vague, repetitive, and empty of content words. Also, it is full or pronouns withoutantecedents, 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 thatover there though on that” (Bayles, 1982). Although the speech of AD patients lacks contentwords and communicates little information, it remains grammatically correct, which could beexplained by language universals. Furthermore, the frequency with which different “syntacticconstructions” 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 thedisease. Kemper, Curtiss, and Jackson (1987) examined a spontaneous speech sample and foundthat normals, non-AD elderly patients, and AD patients were very similar in their use ofprepositional phrases and subordinate clauses. The authors also found the length and grammaticalcorrectness of their speech to be similar (Kemper, Curtiss, and Jackson 1987). However, the ADpatients used many more empty words (e.g., “thing”) and other unclear referents. Manyresearchers (Bayles 1982 and Nicholas, Obler, Albert, & Helm-Estabrooks 1985) believe there isa significant lexical semantic impairment in AD but only minimal syntactic problems. In measuring the semantic deficit in AD, researchers have tested verbal fluency. Mostoften, researchers give the patient a category and then ask the patient to formulate as manymembers of that category as possible within a given time, usually sixty to ninety seconds. Thestudies have usually used two different categories: first, is a letter category–here subjects areasked to generate as many words as they think of that begin with a particular letter (e.g., “s”), andthe second type is a semantic category (e.g., four-legged animals or furniture). One of the mostdetailed 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 ofitems produced by normals. Furthermore, the AD patients also produced more inappropriateresponses (non-category responses) than did the old-aged normal controls. Another importantfinding 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 notappear 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 generatedsignificantly fewer words than did normal controls with semantic categories; whereas with lettercategories, the two groups did equally well. However, Rosen (1983) found the opposite–the ADpatients were more impaired in verbal fluency tasks with letter categories than with semanticcategories. 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 authorsfound that the normal subjects, on average, named three or four items from each of a number ofcontrasting subcategories, such as fruits or meats. However, they found that Alzheimer patientsnamed fewer items, and on average, AD patients produced only a single item from eachsubcategory (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 aresponse (e.g., “vegetables”). Ober et al. reasoned that if AD patients’ decreased verbal fluencywas due solely to a slowing in the rate at which they searched their memory, then they shouldhave gotten through fewer subcategories, but they should have generated the same number ofitems 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 thenormal controls (Ober et al. 1986). An impairment in naming objects is commonly found among patients with aphasia (Benson1985). 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 normalsubjects in their thirties and normal subjects in their seventies. However, patients with AD havesignificant impairments in naming objects; many researchers have shown that the magnitude ofthis 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 semanticallyrelated objects (e.g., calling a carrot a vegetable) or other objects within a category (e.g., calling acomputer a television) (Kirshner, Webb, & Kelly 1984). These findings strengthen the degradationof semantic memory. The retrieval deficit hypothesis has also been strengthened by Kirshner’sstudies–he found that the degree of the naming deficit in demented patients varied with thefrequency of the name in language. The less the name was used, the less success dementedpatients 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 (astandard protocol evaluation test), were affected by phonemic cues sixty percent of the time; thesecues helped AD patients name an object which they had failed to name when only showed apicture of the object (Martin and Fedio 1983). Lastly, there is one result suggesting the namingproblem of AD patients has more than one source. Barker and Lawson (1968) found that whenAD patients were allowed to handle an object or to see it in use, they had more success ingenerating its name. Barker and Lawson (1968) also found, like Kirshner et al. (1984), that thesuccess of object naming in demented patients varied with the frequency of the object’s name inthe 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 namingdeficit in dementia may be the result of both an impairment in lexical access and from some sort ofobject identification problem (Barker and Lawson 1968).


NEXT RESEARCH
Another method used in testing the ability of AD patients to search their lexicon requiresthe 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 placewhere books are kept for use but not for sale”) for both abstract and concrete words (Rissenberand Glanzer 1987). They found no difference in naming accuracy between normal old and youngsubjects. However, they also found that the AD patients not only produced significantly fewerwords 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 concreteand abstract words. Therefore, the contrast in word-searching aptitude between abstract andconcrete words could be due to the demented patients having more problems in comprehendingthe definitions used to describe abstract words. The authors implied that these results show alexical retrieval problem in AD patients that is especially severe for abstract words (Rissenbergand Glanzer 1987). A different study showed contrasting results; Huff, Mack, Mahlmann, &Greenberg (1986), in examining a similar task as just described, interpreted their results asshowing 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 thistask, 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 askedto say yes or no to a sentence of the form “Is the tool used to pound nails called a hammer?” ADpatients successfully understood the names of items they had failed to name in the earlierexperiment, 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 retrievaldeficit 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 benoted that the majority of studies are forcefully subjective; most studies are designed to prove onehypothesis right or wrong. The findings all vary, and their interpretative postulations vary evenmore. After reviewing these past studies on the ability of AD patients to search for words, it isvery obvious that AD patients suffer an impairment of word-searching ability. As with otheraspects of semantic memory impairment in AD, there is an uncertainty of whether this problem isa result from solely the loss of a retrieval mechanism or from a general semantic memory loss. Themajority of research, on word-searching ability in Alzheimer’s disease, supports the hypothesis ofthe 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 deficithypothesis. Therefore, one cannot conclude that word finding problems in AD are solely the resultof either a semantic memory storage impairment or a semantic memory access impairment. As aresult of numerous studies interpreting word-searching problems in AD by one hypothesis or theother, one can reasonably attribute word-searching problems in AD to both an impairment inlexical 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 foundationaldeficiency in the semantic memory impairment commonly found in AD. Most models of semanticmemory include the presence of semantic associations that represent both perceptual and abstractknowledge about a perceived, symbolized idea. Patients with AD are hypothesized to have lostthese associations that make up the meaning of perceived, symbolized ideas; however, as withother symptoms commonly found among patients with AD, it is not known whether or not thisimpairment of idea-meaning is due to a general semantic memory degradation or a lexical retrievaldeficit. This loss of perceived, symbolized ideas in AD has been believed to underlie impairmentsin other “cognitive domains” such as understanding language (Bayles 1987). The primary concernin explaining this loss of perceived, symbolized meaning-idea is whether the idea-meaning is trulylost or is only difficult to retrieve under certain conditions. Also, researchers have attempted toexplain whether all aspects of idea-meaning are influenced in a similar manner or whether onlycertain elements are impaired (Bayles 1987). Both “expressive” (WAIS vocabulary) and“receptive” (Peabody Picture Vocabulary Test) vocabulary tests scores decline proportionatelywith 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 inAD, have not been entirely explained by either the degradation of semantic memory hypothesis orthe 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 specificinformation about a certain idea, they gradually lose knowledge of the specific, semanticcharacteristics 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 characteristicsof semantic information are needed to distinguish between closely related semantic ideas–such asmembers of the same semantic category. Therefore, this loss could be responsible for theproblems that demented patients have in naming (Huff et al., 1986). Flicker’s (1987) AD subjectshad 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 itdoes the degradation one. Grober, Buschke, Kawas, and Fuld (1985) concluded that “conceptualattributes” 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 atarget word and asked them to pick out from among many other words those that were related tothe initial one. Demented patients were very accurate (95% correct in comparison with 98% fornormal controls) on this particular task. The authors implied that AD patients remember semanticcharacteristics of some idea-meanings (Grober, Buschke, Kawas, and Fuld 1985). However, theauthors also found that the characteristics the AD subjects did miss could have been veryimportant characteristics to the idea-meaning, just as the characteristics could have been notimportant to the idea-meaning. This hypothesis was supported by a second experiment. In thisexperiment, the subjects were given an initial word and three characteristics that varied in theirrelative importance to the idea-meaning of the initial word (e.g., for the concept “airplane”, thewords “fly”, “radar”, and “luggage”). The demented patients did not do well. Therefore, theseresults again suggest that although Alzheimer’s patients retain knowledge about the semanticcharacteristics of idea-meanings, they have trouble retrieving this information by a self-directedsearch (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 characteristictesting, and asked to say the first word that comes to mind. In these studies, semantic structure isrevealed in the pattern of associations generated. It is believed that stimulation of theseassociations spreads to related idea-meaning. Associations are usually described as being“paradigmatic” or “syntagmatic” (Gewirth, Shindler, and Hier 1984). Paradigmatic associationsare words from the same grammatical category as the initial word and they are related to it inmeaning (e.g., synonyms, antonyms). Syntagmatic associations, however, are words, from adiffering category than the initial word (Gewirth, Shindler, and Hier 1984). The authors examinedthe “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 semanticcorrelations are much more greatly affected by AD than are syntactic associations. Many researchers disagree on whether or not AD patients suffer a category knowledgedeficit. The majority of studies, until recently have suggested that category knowledge is intact inAD patients. According to Martin and Fedio (1983) when given a group of different words, ADpatients are able to categorize the words and name the categories (Martin and Fedio 1983). Huffet al. (1986) found that when AD patients were showed a picture from a certain category, theywere 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–thatcategory knowledge is affected by AD. Most studies supporting this theory have found that ADpatients are unable to categorize living things but they are able to categorize living things. In thesestudies, 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 thingssuch as furniture, vehicles, and other artifacts (Warrington and Shallice 1984). These findingshave become controversial because correctly explaining them would be correctly explaining thestructure the of semantic memory in the brain. The common interpretation is that semanticmemory is organized by taxonomic category (Pietrini et al., 1988). A different explanation is thatliving and nonliving things depend unequally on the amount of knowledge. Here, the authorssuggested that living things are classified by visual and sensory perceptions whereas nonlivingthings are classified by what the object does or what the object is used for (Warrington andShallice 1984). Deterioration of visual characteristics would impair the knowledge of livingthings, 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, thesubjects were asked to name the pictures, whereas in the verbal association task, subjects wererequired to say whether or not a picture and a word were related. On both tasks, patientsperformed 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 andMcClelland 1991). Yet, as with other aspects of AD, the uncertainty remains whether or not thisproblem 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 thephonemic-category and semantic-category tasks could lead to better understanding semanticmemory impairment in AD. They argued that if problems with the semantic-category fluency taskswere affected by the degradation of semantic memory in AD patients, then the impairment on thistask 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 memoryimpairment in AD, then the authors argued that phonemic-category fluency tasks and semantic-category fluency tasks should show parallel declines. The researchers investigated theses twofluency 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 resultsfrom fluency tasks. The authors found that the ability of patients with AD to generate bothsemantic and phonemic categories declines in parallel throughout the course of the disease(Salmon, Heindel, & Lange 1999). These results are consistent with several other studiesincluding Butters et al. (1987). Salmon et al. (1999) concluded that because AD patients, whencompared to normal controls, show more difficulties in semantic memory tasks than phonemicones, 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 ADpatients’ 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 foundsimilar results, and because most researchers agree that a loss in semantic category fluency tasksis a defining characteristic of a general degradation of semantic memory, semantic memoryimpairment in AD is the result of a general degradation of semantic memory.


THE EFFECTS OF SEMANTIC PRIMING
Semantic Priming in Alzheimer’s Disease: The Effects of Context in AD

Throughout the past twenty years, numerous studies have examined semantic memory inAD by looking at the effect that semantic priming has on behavior. The majority of studies havefound that the normal elderly show positive influences from semantic priming. The controversialissue, regarding semantic priming effects, has been whether or not AD patients show positiveeffects from semantic priming. Many researchers have postulated that if AD patients showpositive effects from semantic priming, then the semantic memory impairment commonly foundamong AD patients is due to a semantic memory retrieval deficit. Therefore, researchers interprettheir results based on this idea–that positive priming effects in AD patients can be directlycorrelated to a retrieval deficit problem. However, as we will see, the results are fairlydispersed–overall there is no tendency one way or the other; some studies show positive and somestudies show no priming effects. Even though the inconclusive nature of these studies does notprovide 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. Inthis hypothesis, ideas are reflections of interconnected relationships, such as membership of acommon category (e.g., pencil-pen), functional relationships (e.g., pencil-write), and propertyrelationships (e.g., pencil-point). When an idea is presented, it is believed that there is anautomatic spread of activation (Balota and Duchek 1991). Experimental support for such a spreadof 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 lexicaldecision or name a word aloud) a target word (‘cat’) when it follows a related word (‘dog’) thanwhen it follows an unrelated word (‘pen’). The semantic priming effect has been at the center ofconsiderable work in word recognition research and has been one of the hallmark indicators ofspreading activation within a semantic memory network” (Balota and Duchek 1991). In manystudies, researchers have found that AD subjects show more semantic priming than normalcontrols; 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 negativepriming when compared to normal controls (Albert & Milberg 1989). Thus, due to theinconclusive nature of these results, one cannot attribute semantic memory in AD to a particularform of semantic priming. Even though many studies, and many authors, support the retrievaldeficit hypothesis, there have been almost equal numbers of opposing results. Therefore, in orderto examine the effects that context has on AD patients, one must look at other semanticcontextual studies in AD. Many studies examining semantic memory impairment in AD have focused on thesubjects’ ability to carry out a lexical search. In these studies, a sentence is given to the ADpatients with the final word missing. It is up to the AD patients to fill in the missing word, and thetime and accuracy is measured. In these tasks, the AD patients use syntactic and semanticcontextual mechanisms to carry out their search (Cohen and Faulkner 1983). The sentences varyin the amount of contextual information available to the AD patients. Some sentences were veryspecific–few words would fill the blank (e.g., “Mother poured the milk into a ”), whereas othersentences were less specific (e.g., They went to see the smart ”). The amount of contextualinformation available affected both the time and accuracy of sentence completion (Cohen andFaulkner 1983). These authors found that AD patients were more affected by the contextualinformation available than were normals. The authors also found that sentence completionaccuracy was directly proportional to the degree of directed context within a sentence (Cohen andFaulkner 1983). Thus, it can be deduced from these studies that AD patients are susceptible to thedegree of contextual information within a sentence, and that sentence completion in AD patientsis greatly influenced by framework. Also, in testing the effects of semantic contextual information, AD subjects are examinedby methods of sentence correction tasks. In testing this issue, Kempler et al. (1987) has tested thedegree 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 syntacticones, then the ability of AD patients to correct sentences with semantic errors should be lowerthan their ability to correct sentences with syntactic errors. The sentences had errors that wereeither phonetic, syntactic, or semantic. The authors found that AD patients were worse thannormals, 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. Instudying this, researchers use words that have similar sounds but differentmeanings–“homophones”. Kempler et al. (1987) compared the affects of semantic contexts onAD patients’ ability to make sense out of these similar sounding but different meaning words. Thesubject were asked to write down a series of spoken words, the last word was a homophone. Theother words provided either a semantic (e.g., church, music, “hymn”) or a syntactic context (“tohim” vs. “a hymm”). As with the sentence correction task just described, the hypothesis was thatif AD patients do have semantic deficit, they should be less successful in using a semantic contextthan using a syntactic one to make sense of homophones (Kempler et al., 1987). The authorsfound that the AD patients were less responsive than were the normal controls. However, theauthors found that AD patients made substantially more errors with semantically related tasksthan with just syntactically related tasks (Kempler et al., 1987). Therefore, these resultscontradict the previous results. In this sense, explaining the degree of semantic memoryimpairment in AD patients, by modes of semantic context, is nondirectional. It is obvious that there have been semantic priming effects in patients with Alzheimer’sdisease. However, these semantic priming studies have only found that semantic primingpresented to AD patients only affects the general processing of words, not the degree of lexicalaccess. The results of the sentence completion task show that context can facilitate a lexicalsearch itself in AD patients. However, the context of this search must be very specific. If there isless specific contextual information within a sentence, AD patients are less susceptible, thannormal controls, to semantic priming. Depending on the paradigmatic interpretations used inexamining these studies, one can conclude, from the given information, that semantic memory inAD is affected somewhat by semantic priming. However, from another perspective, we have seenthat these results support the general degradation hypothesis. Therefore, according to past studiesregarding semantic priming effects in AD, one can propose that semantic memory impairment inAD is due both to a degradation of semantic memory and to a deterioration of a semantic memoryretrieval mechanism.

A Compilation of Hypotheses: AD Theories Merge As we have seen, AD affects both the retrieval and knowledge functions. The uncertaintyremains whether or not the two are the same or if they are two separate entities. In comparingsemantic memory impairment in different forms of dementia, researchers, through medicaltechniques 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 ofthe language function. As we have seen, AD affects both semantic memory retrieval and semanticknowledge language functions; we have now just seen proof that these are two separate languageentities. Therefore, reasoning from the study just mentioned, one could argue that AD affects bothsemantic memory retrieval and semantic memory knowledge functions. The two controversial, opposing hypotheses in explaining semantic memoryimpairment in AD–the degradation and retrieval deficit hypotheses–have both shown supportiveevidence. We have seen evidence supporting the retrieval hypothesis and almost disproving thesemantic memory degradation hypothesis, and we have seen the reverse. On the one hand, someresearchers believe that semantic memory impairment in AD is due to a retrieval deficit ofsemantic memory. They believe that the storage for this memory is relatively intact, but that theretrieval mechanisms are damaged. On the other hand, some researchers believe that there is agradual deterioration of the organization and content of semantic memory as the diseaseprogresses. Many of the studies above provide contrasting results in that they support onehypothesis 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 alsobeen a debate of whether or not the these two language functions are separate entities. Thearguments made in this regard postulate that if knowledge and retrieval mechanisms are veryclosely related, than the results seen–those supporting both hypotheses–should explain theconnectedness and synchrony of the two. However, as we have seen with the last study, the twohave been proved to be separate language function entities. Therefore, due to the positive resultssupporting both hypotheses, and since both functions have been proved to be separate, one canconclude that semantic memory impairment in AD is due to a general degradation of knowledgeand 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 shouldacknowledge that AD has a profound impact on both language functions. Further research,development, and corrective measures should regard this. In conclusion, the highly inconclusiveand nondirectional interpretations resulting from studies on semantic memory impairment in ADcan be correlated to the uncertainty of how exactly memory works. Either way, great strides intreating and better understanding AD should be better met by noting the conclusions made in thispaper–that AD affects both language functions, retrieval and general knowledge, and that thesetwo semantic memory language functions are separate.

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