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Biomedical subjects

S Corkin

Publications and source records attributed to S Corkin.

87 records · Page 5Linked to original sources
PubMed1983

Parental age as a risk factor in Alzheimer's disease.

Because of the associations between Alzheimer's disease and Down's syndrome, advanced maternal and paternal age, which are risk factors for Down's syndrome, have been proposed as risk factors for Alzheimer's disease. Parental age data were obtained from a group of patients with Alzheimer's disease and compared with comparable data for a group of nondemented subjects matched for age and socioeconomic level. As a way of detecting a familial causative factor in Alzheimer's disease, life-span data were also collected for parents of patients and control subjects. The results indicated that patients with Alzheimer's disease and nondemented control subjects did not differ in the mean ages of their parents at the time of the patients' or subjects' births, nor did parental age correlate significantly with age at onset of disease. Moreover, the parents of patients with Alzheimer's disease did not differ in mean age at death from the parents of nondemented control subjects.

Aged↗
PubMed1983

Selective olfactory deficits in case H.M.

A variety of olfactory capacities were evaluated in H.M., a patient with bilateral medial temporal lobe resection. He demonstrated normal performance on a battery of tests of odour detection, discrimination of intensity, and adaptation. In striking contrast, H.M. was unable to discriminate or identify odours in same-different discriminations and in matching-to-sample tasks. Although he could name common objects using visual or tactile cues, he could not identify them by smell. These results indicate that the perceptual phenomena of odour detection and discrimination are dissociable by cerebral damage, and that structures in the medial temporal lobe play a critical role in odour discrimination.

Brain Diseases↗
PubMedDate not supplied

Mood, performance, and pain sensitivity: changes induced by food constituents.

We examined the behavioral effects of the dietary constituents tryptophan and tyrosine on human mood, sensorimotor performance and pain sensitivity. Tryptophan and tyrosine are neurotransmitter precursors present in varying amount in protein-containing foods. Tryptophan (50 mg/kg) increased subjective drowsiness and fatigue but unlike many hypnotics did not impair sensorimotor performance. Tryptophan also decreased human pain sensitivity in a manner that was more specific than certain analgesic drugs.

Adolescent↗
PubMedDate not supplied

Piracetam combined with lecithin in the treatment of Alzheimer's disease.

Nootropics, a new class of drugs believed to activate mental functions, have been proposed as a treatment for clinical disorders in which cognition is impaired. We therefore administered the nootropic drug piracetam, alone and in combination with phosphatidylcholine (PC), to 18 patients with Alzheimer's disease (AD), and measured the effects of treatment on a broad range of cognitive functions. Piracetam was administered according to three double-blind crossover protocols and a replication study that differed in piracetam dose (2.4 to 9.9 g/day) and whether PC (18 g/day) was administered concurrently. The drug was well tolerated, and there were not toxic side effects. Plasma choline levels rose significantly during piracetam and PC administration; monoamine metabolites in cerebrospinal fluid were unaffected by treatment. Piracetam, either alone or in combination with PC, did not significantly affect cognition in the AD group as a whole, nor did it improve test performance in any single patient.

Aged↗
PubMedDate not supplied

Incomplete achromatopsia in Alzheimer's disease.

We report that patients with Alzheimer's disease (AD) have a selective deficit in blue hue discrimination, as assessed with three clinical measures of color vision. The Farnsworth D-15 Test, the Lanthony New Color Test, and the City University Color Vision Test were administered to 32 patients with AD (ranging in dementia severity from mild to severe) and 32 age-matched normal control subjects (NCS). Of the AD patients, 11 who were representative of the larger group for age, education level, and dementia severity received a complete neuro-ophthalmological examination that ruled out obvious disorders of the anterior visual structures. AD patients made significantly more tritan (blue) errors than NCS on all three color vision tests but did not make more protan (red) or deutan (green) errors on two of the three tests. The results support the conclusion that there is a deficit in color discrimination in AD that is specific to blue hues, and oppose the hypothesis that AD does not deleteriously affect the color-opponent visual channel. In the absence of obvious damage to anterior visual structures, the likely substrates for the observed deficit are peristriate and inferotemporal visual cortices, which are subject to significant neuropathology in AD.

Aged↗
PubMedDate not supplied

Broad-band visual capacities are not selectively impaired in Alzheimer's disease.

Histological examination of the optic nerves of Alzheimer's disease (AD) patients has revealed a selective degeneration of large axon ganglion cells. This morphological abnormality raises the possibility of a selective impairment of broad-band channel visual function. To test this hypothesis, we administered visual psychophysical tests associated with either the color-opponent or the broad-band retinocortical channel to 14 AD patients and 29 elderly control subjects (ECS). In previous studies in monkeys, these tests had been sensitive to the effects of either parvocellular or magnocellular LGN lesions. In the present study, the color-opponent channel was assessed by tests of texture and color discrimination; the broad-band channel was assessed by tests of flicker and motion detection. Logistic regression analysis indicated that all tests collectively discriminated diagnostic groups at a borderline level of significance (p = 0.09). ANOVA also indicated a trend towards overall depressed function for AD patients on some capacities tested. Analyses comparing the prevalence of deficits in the AD and ECS groups showed that a significantly greater number of AD patients than ECS had deficits on texture discrimination, blue-violet discrimination, and 4.72 degrees/s motion detection. No individual subject demonstrated a selective impairment of broad-band channel function. The visual deficits in AD did not resemble those caused by lesions of magnocellular LGN in monkeys, indicating that the visual impairment in AD is not a functional reflection of damage limited to the broad-band channel.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Intact implicit memory for novel patterns in Alzheimer's disease.

Repetition priming is a kind of implicit memory (learning without awareness) that does not depend on the medial temporal-lobe system. For example, the amnesic patient H.M., who underwent bilateral medial temporal-lobe resection, shows intact priming with novel patterns, suggesting that perceptual priming with nonverbal material does not depend on areas critical for explicit memory. A logical candidate for the neural substrate that supports this kind of priming is the peristriate cortex, an area that is relatively spared in Alzheimer's disease (AD). We therefore predicted that AD subjects would be unimpaired on pattern priming. Subjects copied each of six target figures onto dot patterns. After performing a 3-min distractor task, they were given the same dot patterns (without lines) and asked to draw the first figure that came to mind by connecting the dots with straight lines. Subsequently, in a test of recognition (explicit) memory, subjects viewed each of the six patterns of dots that they had copied previously and were asked to indicate which of four possible completions corresponded to the figure that they had copied 3 min earlier. The AD and control groups achieved comparable priming scores, but AD subjects were significantly impaired in recognizing the patterns explicitly. Our finding of intact pattern priming in AD provides, for the first time, evidence that pattern priming depends on the peristriate cortex.

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