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25.2: Current Research Directions - Biology

25.2: Current Research Directions - Biology


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Encoding functionality in DNA is one way synthetic biologists program cells. In fact, the number of base pairs that can be synthesized per US$ has increased exponentially, akin to Moore’s Law.

This has made the process of designing, building, and testing biological circuits much faster and cheaper. One of the major research areas in synthetic biology is the creation of fast, automated synthesis of DNA molecules and the creation of cells with the desired DNA sequence. The goal of creating a such a system is speeding up the design and debugging of making a biological system so that synthetic biological systems can be prototyped and tested in a quick, iterative process.

Synthetic biology also aims to develop abstract biological components that have standard and well-defined behavior like a part an electrical engineer might order from a catalogue. To accomplish this, the Registry of Standard Biological Parts (partsregistry.org) [4] was created in 2003 and currently contains over 7000 available parts for users. The research portion of creating such a registry includes the classification and description of biological parts. The goal is to find parts that have desirable characteristics such as:

Orthogonality Regulators should not interfere with each other. They should be independent.

Composability Regulators can be fused to give composite function.
Connectivity Regulators can be chained together to allow cascades and feedback.
Homogeneity Regulators should obey very similar physics. This allows for predictability and efficiency.

Synthetic biology is still developing, and research can still be done by people with little background in the field. The International Genetically Modified Machine (iGEM) Foundation (igem.org) [3] created the iGEM competition where undergraduate and high school students compete to design and build biological systems that operate within living cells. The student teams are given a kit of biological parts at the beginning of the summer and work at their own institutions to create biological system. Some interesting projects include:

Arsenic Biodetector The aim was to develop a bacterial biosensor that responds to a range of arsenic concentrations and produces a change in pH that can be calibrated in relation to arsenic concentration. The team’s goal was to help many under-developed countries, in particular Bangladesh, to detect arsenic contamination in water. The proposed device was intended be more economical, portable and easier to use in comparison with other detectors.

BactoBlood The UC Berkeley team worked to develop a cost-effective red blood cell substitute constructed from engineered E. coli bacteria. The system is designed to safely transport oxygen in the bloodstream without inducing sepsis, and to be stored for prolonged periods in a freeze-dried state.

E. Chromi The Cambridge team project strived to facilitate biosensor design and construction. They designed and characterised two types of parts - Sensitivity Tuners and Colour Generators – E. coli engineered to produce different pigments in response to different concentrations of an inducer. The availability of these parts revolutionized the path of future biosensor design.


High-Throughput Cellular Thermal Shift Assays in Research and Drug Discovery

Thermal shift assays (TSAs) can reveal changes in protein structure, due to a resultant change in protein thermal stability. Since proteins are often stabilized upon binding of ligand molecules, these assays can provide a readout for protein target engagement. TSA has traditionally been applied using purified proteins and more recently has been extended to study target engagement in cellular environments with the emergence of cellular thermal shift assays (CETSAs). The utility of CETSA in confirming molecular interaction with targets in a more native context, and the desire to apply this technique more broadly, has fueled the emergence of higher-throughput techniques for CETSA (HT-CETSA). Recent studies have demonstrated that HT-CETSA can be performed in standard 96-, 384-, and 1536-well microtiter plate formats using methods such as beta-galactosidase and NanoLuciferase reporters and AlphaLISA assays. HT-CETSA methods can be used to select and characterize compounds from high-throughput screens and to prioritize compounds in lead optimization by facilitating dose-response experiments. In conjunction with cellular and biochemical activity assays for targets, HT-CETSA can be a valuable addition to the suite of assays available to characterize molecules of interest. Despite the successes in implementing HT-CETSA for a diverse set of targets, caveats and challenges must also be recognized to avoid overinterpretation of results. Here, we review the current landscape of HT-CETSA and discuss the methodologies, practical considerations, challenges, and applications of this approach in research and drug discovery. Additionally, a perspective on potential future directions for the technology is presented.

Keywords: CETSA cell-based assays drug–target interaction target engagement thermal shift.


Publications

Sea-level rise vulnerability of mangrove forests on the Micronesian Island of Pohnpei

IntroductionThe mangrove forests across the Federated States of Micronesia provide critical resources and contribute to climate resilience. Locally, mangrove forests provide habitat for fish and wildlife, timber, and other cultural resources. Mangrove forests also protect Micronesian communities from tropical cyclones and tsunamis, providing a.

Thorne, Karen M. Buffington, Kevin J.

Changes in the abundance and distribution of waterfowl wintering in the Central Valley of California, 1973–2000

The Central Valley of California is one of the most important areas for wintering waterfowl in the world and the focus of extensive conservation efforts to mitigate for historical losses and counter continuing stressors to habitats. To guide conservation, we analyzed trends in the abundance and distribution (spatiotemporal abundance patterns) of.

Fleskes, Joseph P. Casazza, Michael L. Overton, Cory T. Matchett, Elliott L. Yee, Julie L.

Wildfires and global change

No single factor produces wildfires rather, they occur when fire thresholds (ignitions, fuels, and drought) are crossed. Anomalous weather events may lower these thresholds and thereby enhance the likelihood and spread of wildfires. Climate change increases the frequency with which some of these thresholds are crossed, extending the duration of.


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25.2: Current Research Directions - Biology

Recent and Historical Tsunami Events and Relevant Data

Simulated Tsunami Events

• Cascadia simulated event (Mw 9.0): Map | Event Page

Recent Tsunami Events:

• Mar. 4, 2021 -- Kermadec Islands (Mw 8.1) Map | Event Page
• Feb. 10, 2021 -- Loyalty Islands (Mw 7.7) Map | Event Page
• Oct. 19, 2020 -- Sand Point, Alaska (Mw 7.6) Map | Event Page
• Jul. 22, 2020 -- Alaska Peninsula (Mw 7.8) Map | Event Page
• Jun. 23, 2020 -- Oaxaca, Mexico (Mw 7.4) Map | Event Page
• Mar. 25, 2020 -- Kuril Islands (Mw 7.5) Map | Event Page
• Jun. 15, 2019 -- Kermadec (Mw 7.2) Map | Event Page
• Sep. 28, 2018 -- Sulawesi (Mw 7.5) Map | Event Page
• Jan. 23, 2018 -- Kodiak, Alaska (Mw 7.9) Map | Event Page
• Sep. 8, 2017 -- Pijijiapan, Mexico (Mw 8.1) Map | Event Page
• Dec. 8, 2016 -- Solomon Islands (Mw 7.8) Map | Event Page
• Nov. 13, 2016 -- New Zealand (Mw 7.8) Map | Event Page
• Sep. 1, 2016 -- New Zealand (Mw 7.1) Map | Event Page
• Apr. 16, 2016 -- Ecuador (Mw 7.8) Map | Event Page
• Mar. 2, 2016 -- Southwest of Sumatra (Mw 7.8) Map | Event Page
• Sep. 16, 2015 -- Chile (Mw 8.3) Map | Event Page
• Jul. 18, 2015 -- Solomon Islands (Mw 7.0): Map | Event Page
• Oct. 14, 2014 -- Nicaragua (Mw 7.3): Map | Event Page
• Apr. 19, 2014 -- Solomon Islands (Mw 7.5): Map | Event Page
• Apr. 18, 2014 -- Guerrero, Mexico (Mw 7.2): Map | Event Page
• Apr. 13, 2014 -- Solomon Islands (Mw 7.4): Map | Event Page
• Apr. 12, 2014 -- Solomon Islands (Mw 7.6): Map | Event Page
• Apr. 1, 2014 -- Iquique, Chile (Mw 8.2): Map | Event Page
• Oct. 25, 2013 -- Honshu, Japan (Mw 7.1): Map | Event Page
• Jun. 13, 2013 -- East Coast, US (non-seismic): Map | Event Page
• Feb. 6, 2013 -- Solomon Islands (Mw 8.0): Map | Event Page
• Dec. 7, 2012 -- Honshu (Kamaishi), Japan (Mw 7.2): Map | Event Page
• Nov 7, 2012 -- Guatemala (Mw 7.4) Map | Event Page
• Oct. 27, 2012 -- Queen Charlotte Islands (Mw 7.8): Map | Event Page
• Sep. 5, 2012 -- Costa Rica (Mw 7.6): Map | Event Page
• Aug. 27, 2012 -- El Salvador (Mw 7.3): Map | Event Page
• Apr. 11, 2012 -- Sumatra (Mw 8.6): Map | Event Page
• Jul. 6, 2011 -- Kermadec (Mw 7.6): Map | Event Page
• Mar. 11, 2011 -- Tohoku (East Coast of Honshu) (Mw 9.0): Map | Event Page
• Dec. 21, 2010 -- Bonin Islands, Japan (Mw 7.4): Map | Event Page
• Oct. 25, 2010 -- Mentawai, Indonesia (Mw 7.7): Map | Event Page
• Apr. 6, 2010 -- Sumatra (Mw 7.8): Map | Event Page
• Feb. 27, 2010 -- Chile (Mw 8.8): Map | Event Page
• Jan. 12, 2010 -- Haiti (Mw 7.0): Map | Event Page
• Jan. 3, 2010 -- Solomon Islands (Mw 7.1): Map | Event Page
• Oct. 7, 2009 -- Vanuatu (Mw 7.7) and Santa Cruz Islands (Mw 7.8): Event Page
• Sep. 29, 2009 -- Samoa (Mw 8.1): Map | Event Page
• Aug. 10, 2009 -- Andaman Islands (Mw 7.7): Map | Event Page
• Jul. 15, 2009 -- New Zealand (Mw 7.8): Map | Event Page
• Nov. 14, 2007 -- Northern Chile (Mw 7.7): Map | Event Page
• Sep. 12, 2007 -- Sumatra (Mw 8.5): Map | Event Page
• Aug. 15, 2007 -- Peru (Mw 8.0): Map | Event Page
• Apr. 1, 2007 -- Solomon Islands (Mw 8.1): Map | Event Page
• Jan. 13, 2007 -- Kuril Islands, Russia (Mw 8.1): Map | Event Page
• Nov. 15, 2006 -- Kuril Islands, Russia (Mw 8.3): Map | Event Page
• Jul. 17, 2006 -- South Java (Mw 7.7): Map | Event Page
• Mar. 28, 2005 -- Indonesia (Mw 8.6): Map | Event Page
• Dec. 26, 2004 -- Indian Ocean (Mw 9.1): Map | Event Page
• Sep. 25, 2003 -- Hokkaido (Mw 8.3): Map | Web Link Compilation
• Jun. 23, 2001 -- Peru (Mw 8.4): Map | Event Page
• Jan. 13, 2001 -- El Salvador (Mw 7.7): Map | Event Page
• Nov. 26, 1999 -- Vanuatu (Mw 7.4): Map | Data on FTP Site
• Jul. 17, 1998 -- Papua New Guinea (Mw 7.0): Map | Event Page
• Jun. 10, 1996 -- Andreanov (Mw 7.9): Map | Event Page
• Jul. 12, 1993 -- Okushiri, Japan (Mw 7.7): Map | Event Page
• Mar. 28, 1964 -- Alaska (Mw 9.2): Map | Event Page


25.2: Current Research Directions - Biology

"Rarely in basic or clinical research do we have the thrill of seeing results translated into therapies that transform lives. Such an opportunity now exists within the Stanford Institute of Neuro-innovation and Translational Neurosciences where critical discoveries in the laboratory are being translated into viable treatment strategies for patients and their families."

- Craig Heller, PhD, Director

Our mission is to help people with Down syndrome lead healthier and happier lives by rapidly and effectively applying research discoveries to useful treatments.

Families with a member with Down syndrome face many challenges and have many questions. We present on this website an extensive and curated collection of references, articles, blogs, news articles, and essays that will be valuable sources of information.

Question and Answers (Q&A) on COVID-19 have been developed to help you support your loved one with Down syndrome. These documents have been endorsed by all the United States Down syndrome organizations, the Jerome Lejeune Foundation, and Trisomy 21 Research Society.


Introduction

Stress is a broad concept that comprises challenging or difficult circumstances (stressors) or the physiological or psychological response to such circumstances (stress responses). In humans, among other species, one of the systems that responds to challenging circumstances is the immune system. Broadly, the immune system comprises cells, proteins, organs, and tissues that work together to provide protection against bodily disease and damage (see Box for explanations of relevant immunological parameters). Several facets of the human immune system have been empirically associated with stress. During acute stress lasting a matter of minutes, certain kinds of cells are mobilized into the bloodstream, potentially preparing the body for injury or infection during 𠇏ight or flight” [1]. Acute stress also increases blood levels of pro-inflammatory cytokines [2]. Chronic stress lasting from days to years, like acute stress, is associated with higher levels of pro-inflammatory cytokines, but with potentially different health consequences [3]. Inflammation is a necessary short-term response for eliminating pathogens and initiating healing, but chronic, systemic inflammation represents dysregulation of the immune system and increases risk for chronic diseases, including atherosclerosis and frailty [4]. Another consequence of chronic stress is activation of latent viruses. Latent virus activation can reflect the loss of immunological control over the virus, and frequent activation can cause wear-and-tear on the immune system [5].

Interestingly, these responses may not be the same for everyone. Those who have experienced early adversity, for example, may be more likely to exhibit exaggerated immune reactions to stress [6, 7]. Currently, the field is moving toward a greater understanding of who might be most at risk for chronic inflammation and other forms of immunological dysregulation, and why. This question is important not only for health, but also for longevity, as evidence suggests that the immunological effects of chronic stress can advance cellular aging and shorten telomere length [8].

Meta-analyses provide a look backward at this research and summarize what has been learned about the relationship between stress and human immunity since it was first studied in the 1960s [1, 2, 9]. This review describes recent, groundbreaking work on the stress-immune relation in humans, including the immunological consequences of stress in early and late life, mediators of the stress-immunity link, ecological perspectives, and how the relationship between stress and immunity is manifest in clinical populations (see Figure ).

Stress, immunity, and disease can affect each other in reciprocal ways, but these relationships can be moderated by life stage, other ecological pressures and goals, stressor duration, and protective factors such as good sleep.

Early life stress

Stress that occurs early in development (e.g., maltreatment, poverty, and other adverse experiences) has immunological consequences that can be observed both in the near and long term after the stressor occurs. Early life stress (ELS) in children associates with immunological dysregulation, including low basal levels of cytokines that control immune responses [10]. When immune cells were stimulated in vitro (e.g., with tetanus toxoid), those cells from children who experienced ELS produced more pro-inflammatory cytokines [10]. Whereas much of the extant research focuses on maltreatment or poverty, a recent study into the effects of a less-studied adversity, bullying, also suggests that chronic peer victimization predicts a steeper increase in CRP from childhood into young adulthood [11]. EBV antibody levels in a younger adult sample were also found to differ based on the type, timing, and frequency of exposure to ELS. Individuals exposed to sexual abuse more than 10 times, as well as those physically abused starting between ages 3 and 5, had elevated levels of antibodies against EBV as adults, a signal of viral reactivation [12]. In adults, a meta-analysis of ELS and inflammation found a positive association between maltreatment and several inflammatory markers, with the most robust association for circulating CRP [13]. Recent work has investigated mechanisms linking ELS to immune alterations over time (e.g., self-control, adiposity, smoking, and stress 14, 15] as well as examining inflammatory dysregulation as a pathway through which ELS affects adult disease prevalence and outcomes [16]. Finally, empirically based interventions to target immunological consequences of ELS are a necessary next step recent evidence suggests the plausibility of such interventions to improve inflammatory profiles for youth raised in low-income families [17].

Stress, immunity, and aging

As people age, they are less able to mount appropriate immune responses to stressors. These could be physical stressors, such as injury, or psychological stressors such as caregiving. In addition, psychological stress affects organisms in a manner similar to the effects of chronological age, and chronological aging coupled with chronic stress accelerates immunological aging [18]. Research has suggested that older adults are unable to terminate cortisol production in response to stress. Cortisol is ordinarily anti-inflammatory and contains the immune response, but chronic elevations can lead to the immune system becoming “resistant,” an accumulation of stress hormones, and increased production of inflammatory cytokines that further compromise the immune response [18]. Older adults often have to provide long term care for an ailing spouse or partner. Caregiving has been implicated in significantly lower antibody and cell-mediated immune responses after vaccination [19, 20]. Caregivers also experience longer wound healing times, lower lymphocyte proliferation, increased proinflammatory cytokine levels, and more reactivation of latent viruses [21].

An important direction in aging research involves an examination of telomeres. Telomere length has been used as a measure of biological aging and is associated with psychological, physiological, and social factors. Chronic stress is linked to shortened telomere length along with increased disease in older adults [22]. Socioeconomic factors such as marital status and income have been linked with telomere length: those married for longer periods of time and who make more money are biologically younger than others in their cohort [22, 23]. However, studies thus far have found this link only in Caucasians and Hispanics, but not African Americans. This suggests that low socioeconomic status (SES) may accelerate aging in some populations [23]. Interestingly, health behaviors can moderate this effect by protecting individuals from accelerated aging during stress exposure [24]. It is unclear how this moderation occurs, and more work is needed.

Collectively, recent work points to new discoveries into how biological aging and stress interact to influence the immune response. This will lead to a better understanding of mechanisms of immunosenescence caused by stress and chronological aging that are presently unclear.

Biological and behavioral mediators of the relationship between stress and immunity

How does stress get “under the skin” to influence immunity? Immune cells have receptors for neurotransmitters and hormones such as norepinephrine, epinephrine, and cortisol, which mobilize and traffic immune cells, ideally preparing the body to mount an immune response if needed [25]. Recent evidence shows that immunological cells (e.g., lymphocytes) change their responsiveness to signaling from these neurotransmitters and hormones during stress [26]. However, immunological responses are biologically and energetically costly, and over time, chronic stress produces negative systemic changes both in immune trafficking and in target tissues [6].

The linkages between stress and immunity may be mediated by specific health behaviors, psychosocial factors, or both. For instance, stress has been linked to being in troubled relationships, having negative or competitive social interactions, and feeling lonely, which have each in turn been linked to increases in pro-inflammatory responses to stress [27-29]. Other potential mediators, like getting good sleep, are increasingly being recognized as important pieces of the stress-immunity puzzle [30]. Even one night of total sleep deprivation was recently found to significantly increase neutrophil counts and decrease neutrophil function in healthy men [31].

Taken together, these examples highlight a better understanding of the factors that mediate or moderate stress's influence on immunity. This direction may serve to one day develop targeted behavioral or pharmacotherapies to those at highest risk for poor health outcomes.

Ecological immunology

Over the last several years, there has been greater attention paid to the relevance of ecological immunity to the relationship between stress and immunity. Ecological immunity is based on the premise that mounting immune responses is energetically costly and that the (mal)adaptiveness of immune responses to stress is determined by cost:benefit ratios [32-34]. In early human history many stressors were life-threatening: being eaten by a predator, being excluded by one's peer group, or being faced with starvation, to name a few. Appropriately responding to some of these stressors (e.g., predation) required activating the energetically costly fight or flight response, including immunological changes that could protect against infection secondary to wounding. However, energetic costs of the immune system during other kinds of stressors (e.g., social exclusion) that resulted in less availability of energetic resources (e.g., shared food) might have been counterproductive. Thus, downregulating immune responses might have been evolutionarily adaptive. Research in bumblebees finds that under conditions of starvation, immune responses to an immune challenge accelerated time to death from starvation, suggesting that allocating energy to the immune system under those conditions was maladaptive [35]. Although energetic resources are abundant in the modern environment, physiological evidence of these ecological tradeoffs in the ancestral environment can still be found. For example, in contemporary humans, costly endeavors such as building and maintaining a large social network or persisting on unsolvable challenges can be associated with decreases in some immune parameters [36, 37]. Taken together, these and other findings [for reviews, see 33, 38] suggest that ecological conditions and resource availability may shape immune functioning in ways that remain relatively underexplored.

Stress, immunity, and clinical health

Psychological stress has been implicated in altered immune functioning in many diseases. Stress induces chronic immune activation and altered health outcomes that resemble those seen in chronic inflammatory diseases such as RA [39, 40]. Altered immune function can lead to exacerbated symptoms of both physical and psychological illnesses. In irritable bowel syndrome, sustained cortisol activity during stress is associated with an increase in gastrointestinal symptoms [41]. High levels of proinflammatory cytokines resulting from stress have recently been implicated in the etiology of schizophrenia and schizophrenia-related brain alterations [42]. Chronic stress has been shown to enhance risk for developing autoimmune disease [e.g., 43]. Individuals with autoimmune disease also appear to have difficulty down-regulating their immune responses after exposure to stressors. In MS, neuropeptides secreted under stress (e.g., corticotropin-releasing hormone) activate glial cells in the brain to release inflammatory molecules that result in brain inflammation and worsen MS pathology [44]. Similar immune activation and symptom exacerbation is evidenced in those with other autoimmune diseases [40]. Currently, possible mechanisms by which autoimmune diseases alter individual responses to stress are being explored. This knowledge may lead to interventions that decrease stress-induced immune responses and improve outcomes in autoimmune diseases.

Conclusions and future directions

Research on the immunological effects of stress has burgeoned over the past decade following Segerstrom and Miller's meta-analysis [1]. This research has explored new avenues, including the areas reviewed here, that show particular promise for illuminating the conditions under which stress impacts the immune system. Research on stressors occurring early (i.e., childhood and adolescence) and late (i.e., aging) in the lifespan have suggested that individuals exposed to chronic stressors (e.g., abuse, caregiving) can exhibit immune dysregulation that may be persistent and severe. Stressor qualities (e.g., type, timing) as well as individual characteristics that make individuals more or less susceptible to these effects are targets for future work. Examinations of mediators and mechanisms of the stress-immune relation can also determine how and for whom exposure to stress impacts the immune response. Ecological immunology suggests that downregulating the immune response may sometimes be adaptive, and future work building from this perspective will help to further elucidate contexts in which immunosuppression may occur but progress toward superordinate goals is facilitated. Finally, research into the effects of stress on inflammation in clinical populations has demonstrated that stress exposure can increase the likelihood of developing disease, as well as exacerbating preexisting conditions. Further work in this area may help to treat or even prevent morbidity. Overall, this area of research is broad, rapidly developing, and holds promise for improving human health.

Box: Guide to some immunological parameters related to stress

Antibodies: Proteins produced by immune cells that can bind to pathogens such as viruses, bacteria, and parasites. Bound pathogens are inactivated or marked for killing by other immune cells.

Autoimmune disease: Caused when the immune system misidentifies self tissue as foreign and mounts an attack against it. Examples include rheumatoid arthritis (RA), lupus, and multiple sclerosis (MS).

C-reactive protein (CRP): A downstream product of pro-inflammatory signaling and marker of systemic inflammation.

Cell-mediated immunity: The arm of the immune system that protects against pathogens residing inside cells (e.g., viruses) and other “sick” cells such as cancer cells.

Cortisol: A steroid hormone produced by the adrenal gland with broad metabolic effects, including suppression of some facets of the immune system.

Cytokines: Proteins that coordinate immune responses. Examples include interleukins (IL). Some cytokines, such as IL-5 and IL-10, primarily control and contain immune responses. Others, such as IL-6 and tumor necrosis factor-α (TNF-α), induce inflammation.

Inflammation: Local inflammation is a part of the healing process that includes accumulation of immune cells, anti-pathogen activity, and initiation of tissue repair. Chronic, systemic inflammation, in contrast, can promote tissue damage across a number of systems.

Latent viruses: Viruses that reside in the body indefinitely after infection, often without overt disease consequences either acutely or chronically. Examples include Epstein-Barr virus (EBV) and cytomegalovirus (CMV).

Neutrophils: The first cells to infiltrate damaged or infected tissue and effect an inflammatory response.

Telomeres: The protective caps on the end of chromosomes that prevent deterioration.

Highlights

Psychological stress can dysregulate the human immune system.

Stress can impact immunity differentially across individuals and contexts.

Recent work in this area has made strides towards elucidating these differences.

Future work holds promise for reducing stress's effects on physical health.


25.2: Current Research Directions - Biology

Welcome to The Molecular Biology Institute At the Heart of the UCLA Community Founded by a Nobel Prize Winner with a Transformative Vision And Pioneer Research Faculty


Types of cortical neuroplasticity

Developmental plasticity occurs most profoundly in the first few years of life as neurons grow very rapidly and send out multiple branches, ultimately forming too many connections. In fact, at birth, each neuron in the cerebral cortex (the highly convoluted outer layer of the cerebrum) has about 2,500 synapses. By the time an infant is two or three years old, the number of synapses is approximately 15,000 per neuron. This amount is about twice that of the average adult brain. The connections that are not reinforced by sensory stimulation eventually weaken, and the connections that are reinforced become stronger. Eventually, efficient pathways of neural connections are carved out. Throughout the life of a human or other mammal, these neural connections are fine-tuned through the organism’s interaction with its surroundings. During early childhood, which is known as a critical period of development, the nervous system must receive certain sensory inputs in order to develop properly. Once such a critical period ends, there is a precipitous drop in the number of connections that are maintained, and the ones that do remain are the ones that have been strengthened by the appropriate sensory experiences. This massive “pruning back” of excess synapses often occurs during adolescence.

American neuroscientist Jordan Grafman has identified four other types of neuroplasticity, known as homologous area adaptation, compensatory masquerade, cross-modal reassignment, and map expansion.


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Watch the video: Alzheimers disease - plaques, tangles, causes, symptoms, pathology and current research (February 2023).