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"Foster, Thomas C."
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Alteration in NMDA Receptor Mediated Glutamatergic Neurotransmission in the Hippocampus During Senescence
Glutamate is the primary excitatory neurotransmitter in neurons and glia. N-methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainate receptors are major ionotropic glutamate receptors. Glutamatergic neurotransmission is strongly linked with Ca2+ homeostasis. Research has provided ample evidence that brain aging is associated with altered glutamatergic neurotransmission and Ca2+ dysregulation. Much of the work has focused on the hippocampus, a brain region critically involved in learning and memory, which is particularly susceptible to dysfunction during senescence. The current review examines Ca2+ regulation with a focus on the NMDA receptors in the hippocampus. Integrating the knowledge of the complexity of age-related alterations in Ca2+ homeostasis and NMDA receptor-mediated glutamatergic neurotransmission will positively shape the development of highly effective therapeutics to treat brain disorders including cognitive impairment.
Journal Article
How to read literature like a professor : a lively and entertaining guide to reading between the lines
What does it mean when a fictional hero takes a journey? Shares a meal? Gets drenched in a sudden rain shower? Often, there is much more going on in a novel or poem than is readily visible on the surface-- a symbol, maybe, that remains elusive, or an unexpected twist on a character-- and there's that sneaking suspicion that the deeper meaning of a literary text keeps escaping you. In this practical and amusing guide to literature, Thomas C. Foster shows how easy and gratifying it is to unlock those hidden truths, and to discover a world where a road leads to a quest, a shared meal may signify a communion and rain, whether cleansing or destructive, is never just rain. Ranging from major themes to literary models, narrative devices, and form, this is the perfect companion for making your reading experience more enriching, satisfying, and fun.
Book
Effect of peripheral cellular senescence on brain aging and cognitive decline
We examine similar and differential effects of two senolytic treatments, ABT‐263 and dasatinib + quercetin (D + Q), in preserving cognition, markers of peripheral senescence, and markers of brain aging thought to underlie cognitive decline. Male F344 rats were treated from 12 to 18 months of age with D + Q, ABT‐263, or vehicle, and were compared to young (6 months). Both senolytic treatments rescued memory, preserved the blood–brain barrier (BBB) integrity, and prevented the age‐related decline in hippocampal N‐methyl‐D‐aspartate receptor (NMDAR) function associated with impaired cognition. Senolytic treatments decreased senescence‐associated secretory phenotype (SASP) and inflammatory cytokines/chemokines in the plasma (IL‐1β, IP‐10, and RANTES), with some markers more responsive to D + Q (TNFα) or ABT‐263 (IFNγ, leptin, EGF). ABT‐263 was more effective in decreasing senescence genes in the spleen. Both senolytic treatments decreased the expression of immune response and oxidative stress genes and increased the expression of synaptic genes in the dentate gyrus (DG). However, D + Q influenced twice as many genes as ABT‐263. Relative to D + Q, the ABT‐263 group exhibited increased expression of DG genes linked to cell death and negative regulation of apoptosis and microglial cell activation. Furthermore, D + Q was more effective at decreasing morphological markers of microglial activation. The results indicate that preserved cognition was associated with the removal of peripheral senescent cells, decreasing systemic inflammation that normally drives neuroinflammation, BBB breakdown, and impaired synaptic function. Dissimilarities associated with brain transcription indicate divergence in central mechanisms, possibly due to differential access. The results of the current study demonstrate that senolytic treatment reduced morphological evidence of microglial activation, decreased expression of immune response genes in the dentate gyrus, and rescued hippocampal‐dependent spatial memory. Further, senolytic intervention preserved the blood‐brain barrier integrity. Finally, senolytic treatment prevented the age‐related decline in hippocampal N‐methyl‐D‐aspartate receptor‐mediated synaptic function associated with impaired cognition.
Journal Article
Reading the silver screen : a film lover's guide to decoding the art form that moves
\"No art form is as instantly and continuously gratifying as film. When the house lights go down and the lion roars, we settle in to be shocked, frightened, elated, moved, and thrilled. We expect magic. While we're being exhilarated and terrified, our minds are also processing data of all sorts--visual, linguistic, auditory, spatial--to collaborate in the construction of meaning. Thomas C. Foster's Reading the Silver Screen will show movie buffs, students of film, and even aspiring screenwriters and directors how to transition from merely being viewers to becoming accomplished readers of this great medium. Beginning with the grammar of film, Foster demonstrates how every art form has a grammar, a set of practices and if-then propositions that amount to rules. He goes on to explain how the language of film enables movies to communicate the purpose behind their stories and the messages they are striving to convey to audiences by following and occasionally breaking these rules. In Reading the Silver Screen, readers will gain the expertise and confidence to glean all they can from the movies they love,\"--Amazon.com.
Book
Sex, senescence, senolytics, and cognition
This review focuses on sexual dimorphism in cellular senescence and senolytic treatment in relation to brain health and age-related cognitive decline. The stressors of aging, DNA damage, inflammation, and oxidative stress induce cell senescence, a hallmark of aging. Senescent cells change their function and molecular profile and are primed to release pro-inflammatory cytokines. The functional changes include the activation of cell signals to prevent cell death. The release of pro-inflammatory cytokines from peripheral senescent cells during middle age induces senescence of neighbor cells and heightens the level of systemic inflammation, contributing to neuroinflammation. In response to neuroinflammation and oxidative stress, some neurons alter their physiology, decreasing neuronal excitability and synaptic transmission. Senescent neurophysiology is protective against cell death due to excitotoxicity, at the expense of a loss of normal cell function, contributing to age-related cognitive decline. The level of peripheral cell senescence and systemic inflammation may underlie sexual dimorphism in the prevalence, symptoms, and pathogenesis of age-related diseases, including neurodegenerative diseases. Sex differences have been observed for senescence of astrocytes, microglia, and peripheral cells, including those involved in innate and adaptive immune responses. Interventions that remove senescent cells, such as senolytic drugs, can reduce or ameliorate some of the aging-related loss of function. Similarities and differences in senolytic responses of males and females depend on the system examined, the treatment regimen, the level of senescent cell burden, and the age when treatment is initiated. Estrogen impacts several of these factors and influences the transcription of genes promoting growth, proliferation, and cell survival programs in a manner opposite that of senolytic drugs. In addition, estrogen has anti-aging effects that are independent of cell senescence, including rapidly modifying senescent neurophysiology. Thus, it is important to recognize that, in addition to sex differences in cell senescence, there are other sexually dimorphic mechanisms that contribute to the aging process. The results indicate that senolytics interact with fundamental biology, including sex hormones.
Journal Article
Failure of senolytic treatment to prevent cognitive decline in a female rodent model of aging
There are sex differences in vulnerability and resilience to the stressors of aging and subsequent age-related cognitive decline. Cellular senescence occurs as a response to damaging or stress-inducing stimuli. The response includes a state of irreversible growth arrest, the development of a senescence-associated secretory phenotype, and the release of pro-inflammatory cytokines associated with aging and age-related diseases. Senolytics are compounds designed to eliminate senescent cells. Our recent work indicates that senolytic treatment preserves cognitive function in aging male F344 rats. The current study examined the effect of senolytic treatment on cognitive function in aging female rats. Female F344 rats (12 months) were treated with dasatinib (1.2 mg/kg) + quercetin (12 mg/kg) or ABT-263 (12 mg/kg) or vehicle for 7 months. Examination of the estrus cycle indicated that females had undergone estropause during treatment. Senolytic treatment may have increased sex differences in behavioral stress responsivity, particularly for the initial training on the cued version of the watermaze. However, pre-training on the cue task reduced stress responsivity for subsequent spatial training and all groups learned the spatial discrimination. In contrast to preserved memory observed in senolytic-treated males, all older females exhibited impaired episodic memory relative to young (6-month) females. We suggest that the senolytic treatment may not have been able to compensate for the loss of estradiol, which can act on aging mechanisms for anxiety and memory independent of cellular senescence.
Journal Article
How to read literature like a professor : a newly expanded, lively, and entertaining guide to reading between the lines
\"A thoroughly revised and expanded edition of Thomas C. Foster's classic guide-a lively and entertaining introduction to literature and literary basics, including symbols, themes and contexts, that shows you how to make your everyday reading experience more rewarding and enjoyable. While many books can be enjoyed for their basic stories, there are often deeper literary meanings interwoven in these texts. How to Read Literature Like a Professor helps us to discover those hidden truths by looking at literature with the eyes-and the literary codes-of the ultimate professional reader, the college professor. What does it mean when a literary hero is traveling along a dusty road? When he hands a drink to his companion? When he's drenched in a sudden rain shower? Ranging from major themes to literary models, narrative devices and form, Thomas C. Foster provides us with a broad overview of literature-a world where a road leads to a quest, a shared meal may signify a communion, and rain, whether cleansing or destructive, is never just a shower-and shows us how to make our reading experience more enriching, satisfying, and fun. This revised edition includes new chapters, a new preface and epilogue, and incorporates updated teaching points that Foster has developed over the past decade. Foster updates his classic text with ore writers and books in the contemporary pantheon, including: Angie Thomas's The Hate U Give, Emily St. John Mandel's Station Eleven, Neil Gaiman's Neverwhere, Elizabeth Acevedo's The Poet X ), Helen Oyeyemi's Mr. Fox and Boy, Snow, Bird, Sandra Cisneros's The House on Mango Street, Zora Neale Hurston's Their Eyes Were Watching God, Maggie O'Farrell's Hamnet, Madeline Miller's Circe, Pat Barker's The Silence of the Girls, and Tahereh Mafi's A Very Large Expanse of Sea\"-- Provided by publisher.
BOOK
Cognitive Reserve in Model Systems for Mechanistic Discovery: The Importance of Longitudinal Studies
The goal of this review article is to provide a resource for longitudinal studies, using animal models, directed at understanding and modifying the relationship between cognition and brain structure and function throughout life. We propose that forthcoming longitudinal studies will build upon a wealth of knowledge gleaned from prior cross-sectional designs to identify early predictors of variability in cognitive function during aging, and characterize fundamental neurobiological mechanisms that underlie the vulnerability to, and the trajectory of, cognitive decline. Finally, we present examples of biological measures that may differentiate mechanisms of the cognitive reserve at the molecular, cellular, and network level.
Journal Article