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Depression
Published in Henry J. Woodford, Essential Geriatrics, 2022
Depression occurs more commonly in people with dementia, perhaps affecting 20% of those with Alzheimer's disease.50 At any point in time, around 40% of people with dementia experience any of depression, anxiety or apathy symptoms.51 It may have a different neurobiological causation. Mood-related neural circuits might be interrupted by neuronal loss. For example, Alzheimer's disease often affects norepinephrinergic and serotonergic pathways of the locus coeruleus and dorsal raphe nuclei.
Improving the Old, Embracing the New: Implications of Alcohol Research for Future Practice
Published in Gary Rosenberg, Weissman Andrew, Behavioral and Social Sciences in 21st Century Health Care: Contributions and Opportunities, 2021
One of the more interesting issues in combined therapeutic approaches is how medications and verbal therapy might work together. I believe that there are three possibilities. One possibility is that each type of therapy might continue to function if the other fails as a type of “back-up.” Another, is that one therapy might increase the efficacy of the other. For example, if the drug relieves craving, the patient is not thinking about the bar downstairs while he or she is talking to the social worker, but the social worker’s effort could increase compliance with the drug-taking. What you then have is a mutually reinforcing effect of the two therapies. Finally, the most interesting possibility is that the verbal and pharmacological therapies might act on the same neural circuits. A few years ago Dr. Louis Baxter demonstrated this possibility not with respect to alcoholism, but in the treatment of obsessive-compulsive-disorder (OCD). Dr. Baxter and his colleagues compared positron emission tomography (PET) scans of patients before and after verbal therapy with PET scans of patients before and after treatment with a serotonin uptake inhibitor. In this study, the PET scans of patients who had responded to the behavioral treatment resembled changes seen in patients who had responded to the pharmacological treatment. Even though this study has limitations, these observations are striking because they indicate that successful verbal therapies and pharmacological therapies may work on the same neural systems.
Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Plasticity of neuronal circuits is the alteration of the behavior of these circuits in response to experience or injury. Plasticity could result from: modification of the response of neurons to synaptic inputs (Chapter 7), such as a change in the intrinsic excitability of neurons; the addition or removal of synaptic pathways; or modification of the strength or efficacy of synapses, the latter being referred to as synaptic plasticity. In view of the complexity of the subject, however, only some basics of synaptic plasticity will be presented in this section.
Combination of tea polyphenols and proanthocyanidins prevents menopause-related memory decline in rats via increased hippocampal synaptic plasticity by inhibiting p38 MAPK and TNF-α pathway
Published in Nutritional Neuroscience, 2022
Qian Yang, Yusen Zhang, Luping Zhang, Xuemin Li, Ruirui Dong, Chenmeng Song, Le Cheng, Mengqian Shi, Haifeng Zhao
Memory function declines with age, and is believed to deteriorate because of changes in synaptic function rather than loss of neurons [16]. It is thought that memories are formed and stored by long-term changes in the strength of synaptic connections between neurons, a process known as synaptic plasticity that can be defined as structural and functional adaptations of neuronal circuits to changes due to learning and memory. Structural plasticity refers to changes in synaptic morphology and quantity caused by repetitive synaptic activity. Long-term potentiation (LTP) is one of the important manifestations of the functional plasticity [17,18]. LTP is a long lasting enhancement of synaptic transmission induced by high frequency stimulation of presynaptic afferents into fibers, mainly for the high frequency stimulation of postsynaptic population spike (PS) the increase of the amplitude and shortened the latency of group, excitatory postsynaptic potential (fEPSP) the amplitude and slope increase the phenomenon of enhanced synaptic transmission efficiency [19]. LTP of Schaffer collateral to CA1 pyramidal neuron synapse of the hippocampus is thought to play a key role in episodic memory formation [17]. Strong antioxidant vitamin E and 17-beta estradiol (E2) treatment in different rat models prevents the LTP impairment and neuronal apoptosis as well as increases synapse density and enhances the magnitude of LTP [20,21]. In this study, we want to know if the TP and PC combination can improve memory by improving synaptic plasticity and try to explore the mechanism.
Sex- and stress-dependent effects of a single injection of ketamine on open field and forced swim behavior
Published in Stress, 2021
Paul J. Fitzgerald, Savannah K. Kounelis-Wuillaume, Ali Gheidi, Jonathan D. Morrow, Joanna L. Spencer-Segal, Brendon O. Watson
The sex differences we observed in the effect of ketamine on behavior could suggest that ketamine modulates different neural circuitry in males and females. Alternatively, it could modulate similar neural circuits but this circuitry is sexually dimorphic in its behavioral output. In either case, these findings potentially have translational relevance to our understanding of human affective disorders. These data may also suggest that any putative sex differences in the therapeutic properties of ketamine are not mediated by upstream, acute effects on HPA axis responsivity, as we found this to be similar in our male and female animals. The possibility of sex differences in the modulation of the neural circuitry underlying anxiety disorders versus MDD should be addressed in future clinical studies as it may be relevant to the clinical use of this drug (Chen et al., 2014; Coyle & Laws, 2015; Niciu et al., 2014). Our data also lend support to a growing body of evidence suggesting that the time delay between administration of ketamine and the onset and continuation of its therapeutic-like effects is of critical importance and may differ across sexes (Fitzgerald et al., 2019; Franceschelli et al., 2015).
Ethical Implications of BRAIN 2.0: Beyond Bioethics, Beyond Borders
Published in AJOB Neuroscience, 2020
A central goal of the US BRAIN Initiative is to elucidate fundamental brain function at the level of neural circuits by “identifying and characterizing the component cells, defining their synaptic connections with one another, [and] observing their dynamic patterns of activity as the circuit functions in vivo during behavior” (BRAIN 2025 Report 2014). While an important ultimate goal of the Initiative is to treat and cure disease (BRAIN Initiative 2.0 2019), it is recognized that understanding healthy brain function is a key step toward to doing so. This ambitious goal is shared by similar neuroscience initiatives across the globe. For example, the China Brain Project seeks to understand “how specific neural circuits perform their signal processing functions during cognitive processes and behaviors, [which] requires detailed information on the architecture of neural circuits at single-cell resolution and on the spatiotemporal pattern of neuronal activity” (Poo et al. 2016). These examples illustrate that the global neuroscience community—of researchers publishing in the same journals, attending meetings together and citing each other’s results—is generally in accord about the next big steps in understanding the brain.