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Biomedical subjects

M F Folstein

Publications and source records attributed to M F Folstein.

At least 73 records · Page 4Linked to original sources
PubMed1989

Alzheimer's dementia: performance on parallel forms of the dementia assessment battery.

Fifty-four patients with Alzheimer's disease performed on the Dementia Assessment Battery that comprised of finger tapping, forward digit span, naming, verbal memory, visual memory, Token Test, digit cancellation, word-list generation, symbol-digit substitution, and copying geometric designs. Four forms of the battery were administered at weekly intervals. The equivalence of the forms, the relative difficulty of the tests, retest reliability, and factorial composition of the battery are presented. Performance improved with repetition. Impairments in visuo-spatial and verbal abilities were independent of each other. The fragility of the patients' working memory was identified as a main cause for their poor recall. The importance of "component analysis" in individual assessment is illustrated.

Aged↗
PubMed1989

Depression and Alzheimer's disease.

In his classic case, Alzheimer described cognitive symptoms such as amnesia, aphasia, and apraxia and noncognitive symptoms such as delusions and agitation. Recent studies have suggested that depression also occurs in Alzheimer's disease. In this study, 144 patients who met criteria for Alzheimer's disease were examined for depression on a modified version of the Present State Examination. The prevalence rate of major depression was 17%. The depressed Alzheimer's disease patients were more cognitively impaired and more disabled than the nondepressed patients. Studies are needed to clarify the etiology and treatment of depression in Alzheimer's disease.

Aged↗
PubMed1989

Dementia of depression among patients with neurological disorders and functional depression.

Cognitive performance on the Mini-Mental State Examination (MMSE) was assessed in depressed patients (diagnosis of major depression) with cerebrovascular lesions, with Parkinson's disease, or with functional depression (no known brain lesions). Controls for patients with brain lesions or Parkinson's disease were nondepressed patients with the same conditions. Controls for functionally depressed patients were age-matched normal individuals. Depressed patients had significantly lower total MMSE scores than their nondepressed counterparts, but depression did not have an effect on cognitive performance across the three disease groups. The only significant difference between depressed and nondepressed patients shared by all three groups was poorer performance by depressed patients on the delayed-recall task. The findings suggest that major depression may lead to a specific pattern of cognitive deficits independent of coexisting brain pathology.

Brain Damage, Chronic↗
PubMed1989

Major depression in Down's syndrome.

Five patients with trisomy 21 (Down's syndrome (DS], referred to us for evaluation of dementia, were instead found to have major depression. All had shown cognitive and behavioural deterioration and this had led to a mistaken diagnosis of Alzheimer's disease in two. We outline and contrast the features of major depression and Alzheimer's disease in DS, and suggest that electroconvulsive therapy is an effective treatment for major depression in DS.

Adolescent↗
PubMed1989

The new genetics of bipolar affective disorder: clinical implications.

Underrecognition and undertreatment of affective disorders (i.e., major depressive disorder and bipolar affective disorder) constitute a serious public health problem in this country. The recent availability of sufficient mapped restriction fragment length polymorphism (RFLP) probes to cover the human genome and of improved methods of genetic linkage analysis make the definition of the genetic basis of bipolar affective disorders (and recurrent depressions) feasible within the foreseeable future. However, the degree of genetic heterogeneity involved might make the use of tightly linked RFLPs for diagnostic testing, as has been done for Huntington's disease or cystic fibrosis, impractical. Assuming multiple disease loci, then widely applicable and useful "molecular" diagnostic tests will await the cloning of the disease genes or identification of pathogenic gene products. In addition, the combination of genetic heterogeneity and a substantial degree of assortative mating (i.e., people with affective disorders marrying each other) in families with these disorders could make the search for linked loci a "bottleneck" in the path toward developing such diagnostic tests. Recently, three disease loci have been tentatively identified on chromosome 6, 11, and X.

Bipolar Disorder↗
PubMed1989

Neuropathology of aminergic nuclei in Alzheimer's disease.

In order to comprehensively evaluate pathological involvement of the locus coeruleus (LC) and cortically projecting raphe nuclei in Alzheimer's disease (AD), we have recently completed a study (Zweig, et al., 1988) in which numbers of neurons containing neuromelanin within the LC and large nucleolus-containing neurons within the dorsal raphe nucleus (DR) and the central superior (raphe) nucleus (CSN) were determined in 25 cases of AD and 12 age-matched controls. Numbers of neurofibrillary tangles (NFTs) within these regions were also counted. Pathological results were compared with clinical data, including psychiatric evaluations, available for 21 of the AD cases. Neuronal loss in AD cases was most severe within LC at mid level (p less than .01) and within DR, caudally (p less than .05). Counts of NFTs within LC were also highest at mid level (p less than .05) in comparison with caudal level). Neuronal loss was not demonstrated within CSN, although NFTs were abundant within this nucleus. At individual levels, neuronal and NFT counts did not correlate. Relative severity of neuronal loss or NFTs was usually consistent from level to level within nuclei; internuclear correlations were weaker. Cases of AD complicated by depression had significantly fewer neurons at mid LC and rostral CSN levels than nondepressed cases (p less than .05). There was also a trend (nonsignificant) suggesting increased neuronal loss at all levels of LC and DR in depressed cases. Neuronal loss correlated negatively with age, particularly within LC. NFT counts correlated negatively with duration of illness, particularly within DR. As all but 3 individuals had severe dementia, NFT counts may reflect rate of progression of disease. Neuronal loss and NFTs frequently occur in the LC and cortically projecting raphe nuclei in AD (Curcio and Kemper, 1984, Hirano and Zimmermann, 1962, Ishii, 1966, Marcynuik et al., 1986, Yamamoto and Hirano, 1985, Bondareff and Mountjoy, 1986, Iverson et al., 1983, Mann et al., 1985, Tabaton et al., 1986). We have recently completed a comprehensive evaluation of pathological involvement of the LC, the DR, and the CSN in a series of aged controls and AD patients for whom detailed clinical information, including psychiatric evaluations, were available (Zweig et al., 1988). This report summarizes the findings of that study.

Aged↗
PubMed1988

Differential cognitive impairment in Alzheimer's disease and Huntington's disease.

The differentiation between cortical and subcortical dementias requires that the cognitive characteristics of dementias attributable to different causes be discriminable. For large samples of Alzheimer's disease and Huntington's disease patients, distinct cognitive profiles were obtained on the Mini-Mental State Exam. The profile differences were independent of severity of dementia and were sufficiently robust to classify patients as Alzheimer's disease or Huntington's disease with 84% accuracy. The qualitative differences in cognitive functioning may also be typical of other cortical and subcortical dementias.

Aged↗
PubMed1988

The neuropathology of aminergic nuclei in Alzheimer's disease.

Neuronal loss and the presence of neurofibrillary tangles (NFTs) within aminergic nuclei were examined in a series of patients with Alzheimer's disease (AD). Neuromelanin-containing neurons within the locus ceruleus and large nucleolus-containing neurons within the dorsal raphe nucleus and the central superior (raphe) nucleus were counted in 25 patients with AD and in 12 age-matched control subjects. Numbers of NFTs were quantified in the same regions. Counts were compared with clinical data, including psychiatric evaluations, available for 21 of the patients with AD. Within the locus ceruleus in the patients with AD, abnormalities were more severe at mid level than at caudal or rostral levels (p less than 0.01). Within the dorsal raphe nucleus, neuronal loss was most severe caudally (p less than 0.05). NFTs, but not neuronal loss, were demonstrated within the central superior nucleus. Neuronal and NFT counts did not correlate at individual levels; the relative severity of both pathological processes was consistent from level to level within nuclei but was less consistent between nuclei. Neuronal loss correlated inversely with age, particularly within the locus ceruleus. Duration of disease correlated inversely with counts of NFTs, particularly within the dorsal raphe nucleus, implying a correlation between NFT counts and rate of progression of disease as all but 3 patients had severe dementia. Significantly, patients with AD complicated by major depression had fewer neurons at the mid level of the locus ceruleus and at the rostral level of the central superior nucleus in comparison with nondepressed patients. There was a trend suggesting greater loss of neurons at all levels of the locus ceruleus and dorsal raphe nucleus in depressed individuals.

Adult↗
PubMed1988

Semantic activation and implicit memory in Alzheimer disease.

Patients with Alzheimer disease (AD) invariably display pronounced deficits in verbal memory when retention is tested explicitly. The present study examined the possibility that tasks which require memory only implicitly would be performed normally. Moderately demented patients with probable AD were severely impaired in free recall of a word list. On a subsequent word association test, the AD patients were less likely than normals to give items from the recall list as their word associations. The results suggest that implicit verbal memory, as well as explicit memory, is impaired in AD. While the magnitude of the activation effect was significantly reduced in AD patients, it was uncorrelated with recall performance or a measure of global cognitive functioning. Memory activation may thus depend on neural circuitry outside the traditional (i.e. temporo-limbic) memory system.

Aged↗
PubMed1988

Interobserver reliability of a "Standardized Psychiatric Examination" (SPE) for case ascertainment (DSM-III).

The authors describe the Standardized Psychiatric Examination (SPE), a new method for conducting psychiatric examinations in both clinical and research settings that preserves the clinical method. The SPE provides a consistent replicable format for eliciting and recording psychiatric history, signs, and symptoms without perturbing the patient-clinician interaction. By means of the SPE, the clinician can formulate diagnoses using DSM-III or ICD-9 criteria and yet generate CATEGO profiles derived from the Present State Examination, 9th edition. Psychiatrists using the SPE demonstrated high interrater reliability in ascertaining individual psychopathological symptoms (Kappa range, 0.55 to 1.0) and in making DSM-III diagnoses (Kappa range, 0.79 to 1.0) among a sample of study subjects (N = 43) drawn from both a psychiatric inpatient population and a large community sample of nonpatients from the Epidemiological Catchment Area (ECA) study. The implications of the SPE for clinical practice and for research are discussed.

Catchment Area, Health↗
PubMed1987

beta-Amyloid gene is not present in three copies in autopsy-validated Alzheimer's disease.

Recently, it has been suggested that Alzheimer's disease is associated with a duplication of the amyloid precursor protein gene localized to chromosome 21q21. In this study, a cloned DNA probe (B2.3), complementary to the sequence coding the beta-amyloid peptide, and DNA polymorphisms adjacent to this sequence were used to determine the number of copies of the beta-amyloid gene in DNA isolated from human blood and brain. Individuals with trisomy 21 (Down syndrome) who were heterozygous for the polymorphisms showed a gene-dosage effect, with one allele exhibiting twice the autoradiographic intensity as the other. Heterozygous individuals with Alzheimer's disease and controls showed equal intensities of the two allelic bands, suggesting that there are only two copies of the beta-amyloid gene in these individuals. In individuals with Alzheimer's disease and in controls who were homozygous for these polymorphisms, the number of copies of the beta-amyloid gene was determined by comparing the autoradiographic intensity of beta-amyloid alleles to that of DNA fragments detected by a reference probe. No difference was detected between these two groups.

Alzheimer Disease↗
PubMed1987

Voluntary movement dysfunction in Huntington's disease and tardive dyskinesia.

Psychiatric patients with tardive dyskinesia (TD) may be difficult to distinguish from those with Huntington's Disease (HD), who frequently have psychiatric symptoms. This study compared 14 patients with HD with 21 patients (15 schizophrenics and 6 with affective disorder), matched for involuntary movements, using a quantitated neurological examination and other objective and semi-objective tests. The HD group was significantly more impaired on measures of voluntary movement and saccadic eye movements. When the psychiatric group was subdivided, voluntary motor impairment was most marked in schizophrenics with both TD and parkinsonism. The implications of these findings are discussed.

Antipsychotic Agents↗
PubMed1987

Huntington disease in Maryland: clinical aspects of racial variation.

In a Maryland survey of Huntington disease, the prevalence in blacks was unexpectedly high and equal to that in whites. Age at onset was earlier in blacks, and their clinical features, at all ages at onset, were similar to those seen in juvenile-onset Huntington disease. Blacks had more severe bradykinesia and abnormalities of eye movement and less frequent psychiatric disorder, particularly depression.

Adolescent↗
PubMed1986

Familial aggregation in Alzheimer dementia--I. A model for the age-dependent expression of an autosomal dominant gene.

An autosomal dominant genetic etiology has been proposed for Alzheimer Dementia (AD), but many cases appear to be sporadic. Evaluation of the possible genetic transmission of AD from its familial aggregation requires consideration of (1) the proportion of index cases with genetic disease, and (2) the consequences of typically very late onset. To investigate these factors, a provisional biomathematical genetic model was developed from the empirical age-specific incidence of AD in relatives. Based upon the premise of an autosomal dominant AD gene in proband families, the modeling technique provides estimates of the proportion of genetic index cases (as opposed to phenocopies) and the parameters of age-dependent gene expression. With appropriate parameters the model accurately reflects the age-specific familial risk of AD, suggesting the appropriateness of its underlying assumptions. The estimated proportions of genetic index cases suggest that heritable disease constitutes a majority of AD. In cases ascertained by the presence of aphasia or apraxia the estimated proportion of genetic cases is 100%. The greatest likelihood of gene expression is in the ninth decade, however, suggesting that most genetically predisposed relatives will die from other causes before developing AD.

Age Factors↗
PubMed1986

Familial aggregation in Alzheimer dementia--II. Clinical genetic implications of age-dependent onset.

A biomathematical genetic model for the age-specific risk of Alzheimer Dementia (AD) was applied to two problems in the clinical genetics of this disorder. In a test of the ability of a clinical marker specifically to identify genetic AD, cases grouped by the phenotype of amnesia with aphasia or apraxia (aaa) were shown to have familial risk that suggested a pure genetic illness, and differed significantly (p = 0.006) from cases without this phenotype. The model was also used in a Bayesian paradigm to assess the probability that individual cases had hereditary disease, given their family history. Here the results were surprisingly ambiguous: Even with no affected relatives, there is a substantial likelihood that many AD cases may have a genetic illness. Hence, one cannot reliably classify individual cases as "familial" or "sporadic" from family history alone. The phenotype of aaa (or other suitable marker) appears to be more reliable than the degree of manifest familial aggregation as an indicator of genetic AD.

Age Factors↗