Age at onset, duration, and severity of dementia were evaluated in 165 patients with a clinical diagnosis of Alzheimer's disease. Rate of progression of dementia was determined in 77 patients by repeated administration of the Blessed Dementia Scale (BDS). The distribution of age at onset among patients was bimodal, with a division at about age 65. Duration of dementia at the time of initial examination was shorter, and rate of progression on follow-up examination was more rapid in senile-onset (age 65 or greater) than in presenile-onset (before age 65) cases. Considerable overlap among values for the two patient groups was observed for both variables, indicating that age at onset is not a strong predictor of rate of progression of dementia in patients with Alzheimer's disease.
Few investigators have studied whether the behavioral effects of brain insult in adulthood are stable after the period of maximum recovery. We addressed this issue in a 30-year longitudinal study of 84 veterans of World War II, 57 with penetrating head injury (HI) and 27 with peripheral nerve injury (PNI), matched with respect to age, premorbid intelligence, and premorbid education. Each subject was examined during the 1950s and during the 1980s; each examination included the largely verbal Army General Classification Test (AGCT) (with Vocabulary, Arithmetic, and Block Counting subscales) and the Hidden Figures Test (which measures figure-ground discrimination). HI exacerbated decline in performance over time, irrespective of lesion site or cognitive test. HI and PNI subjects differed significantly (p less than 0.05) in AGCT Total and Arithmetic change scores, and means were in the same direction for all other measures. In analyses contrasting subjects in each of the eight lesion groups to PNI subjects, those with left parietal lobe injuries showed significantly greater decline from the 1950s to the 1980s on the Vocabulary and Arithmetic subscales of the AGCT, as did those with left temporal lobe injuries on the Arithmetic subscale, whereas subjects with right parietal lobe injuries showed significantly greater decline on the Hidden Figures Test. We hypothesize that the observed reduction of cognitive capacities late in life was due to some combination of HI in young adulthood, secondary effects of the injury occurring with time, effects of stress on remaining brain tissue caused by functioning for decades in a compromised state, and changes in the brain occurring with age. Although the HI subjects were not demented, follow-up studies must assess whether exacerbated decline is a harbinger of dementia.
In order to develop a test of naming ability that is sensitive to changes in performance on repeated testing, but is unbiased by practice effects, the 85 items of the Boston Naming Test (BNT) were divided into two 42-item forms. Both forms were given to 15 healthy adult subjects, 24 patients with a clinical diagnosis of Alzheimer's disease, and 17 patients with other brain lesions. The reliability of the BNT was high as measured by coefficient alpha and interitem correlations. Performance on the two forms of the test was similar as indicated by mean scores and by correlations between scores. The BNT score includes uncued (spontaneous) and cued responses. When uncued responses were analyzed separately, the reliability and equivalence of the forms remained strong. Using uncued scores therefore does not alter the psychometric properties of the test, and considerably reduces administration time. The modification of the BNT described here should be useful in studies in which repeated measurements are obtained for the purpose of detecting changes in naming ability.
Visual AbstractDevelopmental cell death eliminates half of the neurons initially generated in the mammalian brain, and occurs perinatally in many species. It is possible that the timing of neuronal cell death is developmentally programmed, and only coincidentally associated with birth. Alternatively, birth may play a role in shaping cell
Significance StatementThe importance of neuronal cell death for brain development has been recognized for decades, but it is unknown what regulates its timing, or accounts for differences in the amount of cell death between brain regions. In many species, including mice, developmental cell death occurs perinatally. We find that advancing birth by 1 d in mice advances patterns of cell death, but does not advance overall forebrain (FB) growth. Because humans across the world routinely alter birth timing, usually to advance birth, our findings may have implications for current obstetric practices. Birth timing also affects the magnitude of cell death in a region-specific manner, suggesting that birth has important, previously unrecognized, effects on brain development. January/February 2020, 7(1) ENEURO.0517-19.2020 1-11Research Article: New Research death. To test these competing hypotheses, we experimentally advanced or delayed birth by 1 d in mice (within the normal range of gestation for the species) and examined effects on the temporal pattern and magnitude (amount) of neuronal cell death, using immunohistochemical detection of activated caspase-3 as a cell death marker. In order to detect effects of subtle changes in birth timing, we focused on brain areas that exhibit sharp postnatal peaks in cell death. We find that advancing birth advances peak cell death, supporting the hypothesis that birth triggers cell death. However, a delay of birth does not delay cell death. Thus, birth can advance cell death, but if postponed, a developmental program governs. Advancing or delaying birth also caused region-specific changes in the overall magnitude of cell death. Our findings shed light on the longstanding question of what controls the timing and magnitude of developmental neuronal cell death, and position birth as an orchestrator of brain development. Because humans across the world now routinely alter birth timing, these findings may have implications for current obstetric practices.
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