scholarly journals Brain-derived estrogen and neural function

Author(s):  
Darrell W. Brann ◽  
Yujiao Lu ◽  
Jing Wang ◽  
Quanguang Zhang ◽  
Roshni Thakkar ◽  
...  
Keyword(s):  
Author(s):  
Gabriela Soto Laveaga

In my brief response to Terence Keel’s essay “Race on Both Sides of the Razor,” I focus on something as pertinent as alleles and social construction: how we write history and how we memorialize the past. Current DNA analysis promises to remap our past and interrogate certainties that we have taken for granted. For the purposes of this commentary I call this displacing of known histories the epigenetics of memory. Just as environmental stimuli rouse epigenetic mechanisms to produce lasting change in behavior and neural function, the unearthing of forgotten bodies, forgotten lives, has a measurable effect on how we act and think and what we believe. The act of writing history, memorializing the lives of others, is a stimulus that reshapes who and what we are. We cannot disentangle the discussion about the social construction of race and biological determinism from the ways in which we have written—and must write going forward—about race. To the debate about social construction and biological variation we must add the heft of historical context, which allows us to place these two ideas in dialogue with each other. Consequently, before addressing the themes in Keel’s provocative opening essay and John Hartigan’s response, I speak about dead bodies—specifically, cemeteries for Black bodies. Three examples—one each from Atlanta, Georgia; Rio de Janeiro, Brazil; and Mexico—illustrate how dead bodies must enter our current debates about race, science, and social constructions. 


Author(s):  
Dale Purves

Brains as Engines of Association seeks an operating principle of the human brain and is divided into four parts. The first part (“What Nervous Systems Do for Animals”) is intended to set the stage for understanding the emergence of neural systems as promoting what all organisms must accomplish: survival and reproduction. The second part (“Neural Systems as Engines of Association”) lays out the general argument that biological sensing systems face a daunting problem: they cannot measure the parameters of the world in the way physical instruments can. As a result, nervous systems must make and update associations (synaptic connections) on the basis of empirical success or failure over both evolutionary and individual time. The third part (“Evidence that Neural Systems Operate Empirically”) reviews evidence accumulated over the past 20 years that supports this interpretation in vision and audition, the sensory systems that have been most studied from this or any other perspective. Finally, the fourth part (“Alternative Concepts of Neural Function”) considers the pros and cons of other interpretations of how brains operate. The overarching theme is that the nervous systems of humans and every other animal operate on the basis associations between stimuli and behavior made by trial and error over species and lifetime experience.


2021 ◽  
Vol 22 (15) ◽  
pp. 8196
Author(s):  
Dorit Trudler ◽  
Swagata Ghatak ◽  
Stuart A. Lipton

Neurodegenerative diseases affect millions of people worldwide and are characterized by the chronic and progressive deterioration of neural function. Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), represent a huge social and economic burden due to increasing prevalence in our aging society, severity of symptoms, and lack of effective disease-modifying therapies. This lack of effective treatments is partly due to a lack of reliable models. Modeling neurodegenerative diseases is difficult because of poor access to human samples (restricted in general to postmortem tissue) and limited knowledge of disease mechanisms in a human context. Animal models play an instrumental role in understanding these diseases but fail to comprehensively represent the full extent of disease due to critical differences between humans and other mammals. The advent of human-induced pluripotent stem cell (hiPSC) technology presents an advantageous system that complements animal models of neurodegenerative diseases. Coupled with advances in gene-editing technologies, hiPSC-derived neural cells from patients and healthy donors now allow disease modeling using human samples that can be used for drug discovery.


2021 ◽  
Vol 11 (7) ◽  
pp. 889
Author(s):  
Anton D. Filev ◽  
Denis N. Silachev ◽  
Ivan A. Ryzhkov ◽  
Konstantin N. Lapin ◽  
Anastasiya S. Babkina ◽  
...  

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.


1994 ◽  
Vol 107 (4) ◽  
pp. 1226
Author(s):  
A Rühl ◽  
I Khan ◽  
MG Blennerhassett ◽  
SM Collins
Keyword(s):  

2010 ◽  
Vol 48 ◽  
pp. 263-274 ◽  
Author(s):  
Tania L. Roth ◽  
Eric D. Roth ◽  
J. David Sweatt

Rapid advances in the field of epigenetics are revealing a new way to understand how we can form and store strong memories of significant events in our lives. Epigenetic modifications of chromatin, namely the post-translational modifications of nuclear proteins and covalent modification of DNA that regulate gene activity in the CNS (central nervous system), continue to be recognized for their pivotal role in synaptic plasticity and memory formation. At the same time, studies are correlating aberrant epigenetic regulation of gene activity with cognitive dysfunction prevalent in CNS disorders and disease. Epigenetic research, then, offers not only a novel approach to understanding the molecular transcriptional mechanisms underlying experience-induced changes in neural function and behaviour, but potential therapeutic treatments aimed at alleviating cognitive dysfunction. In this chapter, we discuss data regarding epigenetic marking of genes in adult learning and memory formation and impairment thereof, as well as data showcasing the promise for manipulating the epigenome in restoring memory capacity.


2010 ◽  
Vol 5 (4) ◽  
pp. 391-400 ◽  
Author(s):  
Denise C. Park ◽  
Chih-Mao Huang

There is clear evidence that sustained experiences may affect both brain structure and function. Thus, it is quite reasonable to posit that sustained exposure to a set of cultural experiences and behavioral practices will affect neural structure and function. The burgeoning field of cultural psychology has often demonstrated the subtle differences in the way individuals process information—differences that appear to be a product of cultural experiences. We review evidence that the collectivistic and individualistic biases of East Asian and Western cultures, respectively, affect neural structure and function. We conclude that there is limited evidence that cultural experiences affect brain structure and considerably more evidence that neural function is affected by culture, particularly activations in ventral visual cortex—areas associated with perceptual processing.


Sign in / Sign up

Export Citation Format

Share Document