Neuron numbers and dendritic extent in normal aging and Alzheimer's disease

Coleman, Paul D.; Flood, Dorothy G.

doi:10.1016/0197-4580(87)90127-8

Cited by 734 publications

(290 citation statements)

References 174 publications

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“…These studies also documented the dynamics of synapse and spine formation, ceaseless activities that continue even during advanced age (Kempermann et al, 2003). They showed that the aging brain still retained the ability to compensate for the progressive decline in dendritic spine density observed in anatomical studies (Coleman and Flood, 1987;Duan et al, 2003).…”

Section: Neurogenesis In the Adult Brainmentioning

confidence: 91%

Can endocrine disruptors influence neuroplasticity in the aging brain?

Weiss

2007

NeuroToxicology

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Only within the last two decades has the adult mammalian brain been recognized for its ability to generate new nerve cells and other neural structures and in essence to rewire itself. Although hippocampal structures have received the greatest scrutiny, other sites, including the cerebral cortex, also display this potential. Such processes remain active in the aging brain, although to a lesser degree. Two of the factors known to induce neurogenesis are environmental enrichment and physical activity. Gonadal hormones, however, also play crucial roles. Androgens and estrogens are both required for the preservation of cognitive function during aging and apparently help counteract the risk of Alzheimer's disease. One overlooked threat to hormonal adequacy that requires close examination is the abundance of environmental endocrine-disrupting chemicals that interfere with gonadal function. They come in the form of estrogenic mimics, androgen mimics, anti-estrogens, antiandrogens, and in a variety of other guises. Because our brains are in continuous transition throughout the lifespan, responding both to environmental circumstances and to changing levels of gonadal steroids, endocrine-disrupting chemicals possess the potential to impair neurogenesis, and represent a hazard for the preservation of cognitive function during the later stages of the life cycle.

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Section: Neurogenesis In the Adult Brainmentioning

confidence: 91%

Can endocrine disruptors influence neuroplasticity in the aging brain?

Weiss

2007

NeuroToxicology

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“…With our computerized method for definition of cerebellar pixels, the demarcation of the cerebellum was comparable to that obtained with CT. Although Purkinje cell den sity is reduced in certain parts of the cerebellum during normal aging (Coleman and Flood, 1987), normal aging does not affect cerebellar glucose con sumption (Kushner et al, 1987). Finally, the mean blood flow in the cerebellum as measured by the 133Xe inhalation method in our subjects did not de cline with age.…”

Section: Methodological Considerationsmentioning

confidence: 99%

^99mTc-d,l-HMPAO and SPECT of the Brain in Normal Aging

Waldemar

Hasselbalch²,

Andersen³

et al. 1991

J Cereb Blood Flow Metab

129

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Summary: Single photon emission computed tomography (SPECT) with 99mTc-d,l-hexamethylpropyleneamine ox ime (99mTc-d,I-HMPAO) was used to determine global and regional CBF in 53 healthy subjects aged 21-83 years. For the whole group, global CBF normalized to the cer ebellum was 86.4% ± 8.4 (SD). The contribution of age, sex, and atrophy to variations in global CBF was studied using stepwise mUltiple regression analysis. There was a significant negative correlation of global CBF with sub jective ratings of cortical atrophy, but not with ratings of ventricular size, Evans ratio, sex, or age. In a subgroup of 33 subjects, in whom volumetric measurements of atro phy were performed, cortical atrophy was the only sig nificant determinant for global CBF, accounting for 27% of its variance. Mean global CBF as measured with the Tomographic measurement of regional CBF (rCBF) in humans was made possible several years ago with the development of a brain-dedicated dy namic single photon emission computed tomogra phy (SPECT) system designed for inhalation or in jection of the diffusible tracer \33Xe (Stokely et ai., 1980). This technique offers easy, repetitive, and quantitative measurements with a spatial and tem poral resolution sufficient for studying cerebrovas cular disease.The recent development of tracers that are re tained in the brain for several hours and, if ideal, "trapped" in proportion to regional blood flow has

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“…The one exception to this is the report by Smith et al (2004) of cell loss in prefrontal area 8A in the same subjects where these authors report no loss of neurons in adjacent area 46. While it is always impossible to prove the null hypothesis that neurons are not lost and to exclude the possibility raised by Coleman and Flood (1987) that neuron loss may be limited to very specific areas as the observation of Smith et al (2004) suggests, it seems quite unlikely that cell loss in the cortex is a major factor in normative aging. This assertion is supported by increasing numbers of studies that have confirmed the stability of neuron numbers in normal aging in rodents where cell loss had also been claimed Gallagher 1996, 2002) and in human brain from subjects given careful neuropsychological examination to exclude even the earliest stages of AD (Gomez-Isla et al 1996).…”

Section: The Non-human Primate As a Model Of Normative Agingmentioning

confidence: 99%

Age-related changes in human and non-human primate white matter: from myelination disturbances to cognitive decline

Kohama

Rosene

Sherman

2011

AGE

121

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The cognitive decline associated with normal aging was long believed to be due primarily to decreased synaptic density and neuron loss. Recent studies in both humans and non-human primates have challenged this idea, pointing instead to disturbances in white matter (WM) including myelin damage. Here, we review both cross-sectional and longitudinal studies in humans and non-human primates that collectively support the hypothesis that WM disturbances increase with age starting at middle age in humans, that these disturbances contribute to age-related cognitive decline, and that age-related WM changes may occur as a result of free radical damage, degenerative changes in cells in the oligodendrocyte lineage, and changes in microenvironments within WM.

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Neuron numbers and dendritic extent in normal aging and Alzheimer's disease

Cited by 734 publications

References 174 publications

Can endocrine disruptors influence neuroplasticity in the aging brain?

Can endocrine disruptors influence neuroplasticity in the aging brain?

^99mTc-d,l-HMPAO and SPECT of the Brain in Normal Aging

Age-related changes in human and non-human primate white matter: from myelination disturbances to cognitive decline

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