Estrogen Alters Spine Number and Morphology in Prefrontal Cortex of Aged Female Rhesus Monkeys

Hao, Jiandong; Rapp, Peter R.; Leffler, Abba E.; Leffler, Shoshana R.; Janssen, William G.M.; Lou, Wendy; McKay, Heather; Roberts, Jeffrey A.; Wearne, Susan L.; Hof, Patrick R.; Morrison, John H.

doi:10.1523/jneurosci.3440-05.2006

Cited by 235 publications

(202 citation statements)

References 69 publications

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“…She points to both in vivo and in vitro laboratory studies for supporting evidence, bolstered by the clinical trials referenced above and by others. Hao et al (2006) offer similar arguments to explain the WHIMS results.…”

Section: Cognitive Function and Performancesupporting

confidence: 56%

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: Cognitive Function and Performancesupporting

confidence: 56%

Can endocrine disruptors influence neuroplasticity in the aging brain?

Weiss

2007

NeuroToxicology

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“…First, we could not rule out the possibility that potential downregulation of the spinophilin gene expression contributes to our quantitative observations in spines. Second, in the absence of electron microscopy data, it is not possible to exclude that the observed changes in spinophilin immunoreactivity may partly reflect concurrent changes in spine size as suggested in a recent study in macaque monkeys [26]. Third, it was not possible to identify separately cortical layers II-VI in spinophilin-labeled area 9 with the precision required for stereologic analysis.…”

Section: Discussionmentioning

confidence: 96%

Stereologic estimates of total spinophilin-immunoreactive spine number in area 9 and the CA1 field: Relationship with the progression of Alzheimer's disease

Akram

Christoffel

Rocher

et al. 2008

Neurobiology of Aging

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The loss of presynaptic markers is thought to represent a strong pathologic correlate of cognitive decline in Alzheimer's disease (AD). Spinophilin is a postsynaptic marker mainly located to the heads of dendritic spines. We assessed total numbers of spinophilin-immunoreactive puncta in the CA1 and CA3 fields of hippocampus and area 9 in 18 elderly individuals with various degrees of cognitive decline. The decrease in spinophilin-immunoreactivity was significantly related to both Braak neurofibrillary tangle (NFT) staging and clinical severity but not Aβ deposition staging. The total number of spinophilin-immunoreactive puncta in CA1 field and area 9 were significantly related to MMSE scores and predicted 23.5% and 61.9% of its variability. The relationship between total number of spinophilin-immunoreactive puncta in CA1 field and MMSE scores did not persist when adjusting for Braak NFT staging. In contrast, the total number of spinophilin-immunoreactive puncta in area 9 was still significantly related to the cognitive outcome explaining an extra 9.6% of MMSE and 25.6% of the Clinical Dementia Rating scores variability. Our data suggest that neocortical dendritic spine loss is an independent parameter to consider in AD clinicopathologic correlations.

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“…The results of the study suggest that estrogen has a protective sparing role in cortical regions during aging that may provide cognitive benefit, as well as protection from neurodegenerative disorders. Finally, estrogen has also been shown to enhance dendritic spine density in the prefrontal cortex of young and aged monkeys and in young rats [279][280][281], which may explain the prefrontal cognitive enhancing effects of estrogen. As a whole, these findings provide support for the prefrontal cortex being considered, along with the hippocampus, as a potential key target for estrogen actions on cognition.…”

Section: The Hippocampus and Prefrontal Cortex As Important Sites Of mentioning

confidence: 99%

Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

et al. 2007

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Estrogen is an important hormone signal that regulates multiple tissues and functions in the body. This review focuses on the neurotrophic and neuroprotective actions of estrogen in the brain, with particular emphasis on estrogen actions in the hippocampus, cerebral cortex and striatum. Sex differences in the risk, onset and severity of neurodegenerative disease such as Alzheimer's disease, Parkinson's disease and stroke are well known, and the potential role of estrogen as a neuroprotective factor is discussed in this context. The review assimilates a complex literature that spans research in humans, non-human primates and rodent animal models and attempts to contrast and compare the findings across species where possible. Current controversies regarding the WHI (Women's Health Initiative) study, its ramifications, concerns and the new studies needed to address these concerns are also addressed. Signaling mechanisms underlying estrogen-induced neuroprotection and synaptic plasticity are reviewed, including the important concepts of genomic versus nongenomic mechanisms, types of estrogen receptor involved and their subcellular targeting, and implicated downstream signaling pathways and mediators. Finally, a multicellular mode of estrogen action in the regulation of neuronal survival and neurotrophism is discussed, as are potential future directions for the field.

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Estrogen Alters Spine Number and Morphology in Prefrontal Cortex of Aged Female Rhesus Monkeys

Cited by 235 publications

References 69 publications

Can endocrine disruptors influence neuroplasticity in the aging brain?

Can endocrine disruptors influence neuroplasticity in the aging brain?

Stereologic estimates of total spinophilin-immunoreactive spine number in area 9 and the CA1 field: Relationship with the progression of Alzheimer's disease

Neurotrophic and neuroprotective actions of estrogen: Basic mechanisms and clinical implications

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