All events, All years

The development and molecular mechanisms of crystal-forming cells

Lecture
Date:
Wednesday, February 1, 2023
Hour: 10:00 - 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Dvir Gur
|
Departments of Molecular Genetics

My adventures in the rat interactive foraging facility (RIFF)

Lecture
Date:
Tuesday, January 31, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eli Nelken
|
ELSC-The Hebrew University of Jerusalem

We developed an arena (called colloquially the RIFF) for jointly studying behavior and neural activity in freely-behaving rats. The RIFF operates as a state machine, allowing us to implement a large number of different behaviors as Markov Decision Processes and therefore to analyze much of the data within the theoretical framework of reinforcement learning. In the studies I will show here, we recorded neural activity from auditory cortex while rats performed auditory-guided behavior. We observed an intricate interplay between behavior and neural activity that was much richer than we expected.

Naturalistic approaches for studying social interactions, communication and language at cellular scale

Lecture
Date:
Tuesday, January 24, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Ziv Williams
|
Center for Nervous System Repair Harvard Medical School, Boston MA

Social interactions are remarkably dynamic, requiring individuals to understand not only how their behavior may affect others but also how others may respond in return. In humans, social interactions are also often dominated by processes such as language and theory of mind which allow us to communicate complex thoughts and beliefs. Understanding the basic cellular processes that underlie social behavior or by which individuals communicate, however, has remained a challenge. Here, I describe naturalistic approaches developed in animals and humans that aim of investigating these questions. First, by developing an ethologically based group task in three-interacting rhesus macaques, I describe representations of other’s behavior by neurons in the prefrontal cortex, reflecting the other’s identities, their interactions, actions, and outcomes. I also show how these cells collectively represent the interaction between specific group members and how they enable mutually beneficial social behavior. Second, by recording from neurons in the human prefrontal cortex during language-based tasks, I describe neurons that reliably encode information about others’ beliefs across richly varying scenarios and that distinguish self- from other-belief-related representations. By further following their encoding dynamics, I also describe how these cells represent the contents of the others’ beliefs and predict whether they are true or false. Finally, I describe how these cell ensembles track linguistic information during natural speech processing and how language can be used to ask specific questions about the single-cellular constructs that underlie social reasoning. Together, these studies reveal cellular mechanisms for interactive social behavior in animals and humans and highlight the prospective use of naturalistic approaches in social neuroscience.

Rapid learning (and unlearning) in the human brain

Lecture
Date:
Thursday, January 19, 2023
Hour: 14:00 - 15:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Nitzan Censor
|
School of Psychological Sciences & Sagol School of Neuroscience Tel Aviv University

A plethora of studies have pointed to sensory plasticity in the adult visual system, documenting long-term improvements in perception. Such perceptual learning is enabled by repeated practice, inducing use-dependent plasticity in early visual areas and their readouts. I will discuss results from our lab challenging the fundamental assumption in low-level perceptual learning that only 'practice makes perfect', indicating that brief reactivations of visual memories induce efficient rapid perceptual learning. Utilizing behavioral psychophysics, brain stimulation and neuroimaging, we aim to reveal the neurobehavioral mechanisms by which brief exposure to learned information modulates brain plasticity and supports rapid learning processes. In parallel, we investigate how these learning mechanisms operate across domains, for example by testing the hypothesis that similar inherent mechanisms may also result in maladaptive consequences, when brief reactivations occur spontaneously as intrusive enhanced memories following negative events. Unraveling the mechanisms of this new form of rapid learning could set the foundations to enhance learning in daily life when beneficial, and to downregulate maladaptive consequences of negative memories.

Is behaviour a developmental trait?

Lecture
Date:
Wednesday, January 11, 2023
Hour: 10:00 - 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Gil Levkowitz
|
Departments of Molecular Cell Biology and Molecular Neuroscience

Capturing Neuronal Activity with more Precision and Fidelity in Time and Space

Lecture
Date:
Tuesday, January 10, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Peter Bandettini
|
Laboratory of Brain and Cognition NIMH Bethesda MD

My lab’s focus in recent years has been split between development of ultra-high resolution fMRI at high field and the exploration of more sensitive yet robust methods to find all the salient transients and trends in the signal. High field, high resolution fMRI relies heavily on the acquisition technology and the functional contrast used as well as unique processing approaches that segment, as well as possible, cortical layers for analysis. Our fMRI time series analysis research relies on creative paradigm design in conjunction with tailored processing methods that strike a balance between casting a wide net for potentially informative signals and applying just enough modeling to make sense of the data. Our goal is to use fMRI to see neuronal activity and capture neural correlates of behavior that have previously been elusive to more standard approaches.  Specifically, for our high resolution fMRI work, I will describe experiments demonstrating layer-specific activity in motor, somatosensory, and visual cortex that changes with tasks that modulate the hypothesized input and output cortical communication. In our lab, we perform layer fMRI using a functional contrast called VASO (vascular space occupancy) that is sensitive to blood volume changes in micro vessels - having more specificity than BOLD with only a small tradeoff in sensitivity. Layer fMRI has the potential to provide cortical hierarchy information and communication directionality based on the understanding that feedforward connections terminate predominantly in middle layers and feedback connections terminate in predominantly upper and lower layers. Hence by determining activation location across cortical depth, one can infer whether the activation is feedforward or feedback. I will also demonstrate how the use of resting state connectivity in conjunction with layer fMRI is able to discern such cortical hierarchy in visual areas. Lastly, I will also show examples of applications of layer fMRI in frontal cortex during a working memory task. In addition, I will show our high resolution fMRI work that has allowed us to discern a new digit organizational pattern in motor cortex.  For our time series work, I will show our recent results in using connectivity-based decoding for identifying, in an unsupervised manner, tasks being performed. In addition, I will show an application of naturalistic stimuli and inter subject correlation to characterize personality trait and language skills of individuals. Lastly, changes arousal state during scanning has been viewed as both a confound and opportunity. I demonstrate our effort to further characterize the temporal and spatial signatures of arousal state changes in fMRI time series.

Latent cause inference in learning and decision making

Lecture
Date:
Tuesday, January 3, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Yael Niv
|
Neuroscience Institute and Psychology Department Princeton University

No two events are alike. But still, we learn, which means that we implicitly decide what events are similar enough that experience with one can inform us about what to do in another. We have suggested that this relies on parsing of incoming information into “clusters” according to inferred hidden (latent) causes. In this talk, I will present a computational model of this latent-cause inference process, and show supporting data from a variety of behavioral experiments in humans and rodents spanning from simple conditioning to memory to social decision making. I will also briefly discuss the relevance of this theory to mental health treatments.

Renewal and plasticity in oral and gastrointestinal epithelia

Lecture
Date:
Monday, January 2, 2023
Hour: 11:15 - 12:15
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Ophir Klein
|
Executive Director of Cedars-Sinai Guerin Children's Vice Dean for Children’s Services David and Meredith Kaplan Distinguished Chair in Children’s Health Professor of Orofacial Sciences and Pediatrics, UC San Francisco

How movement regulates defensive behaviours in a social context

Lecture
Date:
Tuesday, December 13, 2022
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Marta Moita
|
Behavioural Neuroscience Champalimaud Center, Lisbon

Our work concerns the general problem of adaptive behavior in response to predatory threats, and of the neural mechanisms underlying a choice between strategies. Interacting predators and prey tightly regulate their motion, timing with precision when to hold, attack or escape. Motion cues are thus paramount in these interactions. Speed and (un)predictability have shaped the evolution of sensory and motor systems, the elucidation of which a great deal of research has been devoted. Much less attention has been paid to the role of motion as a social cue of threat or safety. We and others have found that prey animals use the movement of their neighbors to regulate their defensive responses. We have studied social regulation of freezing in rodents and found that rats use cessation of movement evoked sound, resulting from freezing, as a cue of danger. In addition, auto-conditioning, whereby rats learn the association between shock and their own freezing, during prior experience with shock, facilitates the use of freezing by others as an alarm cue. To further explore the social regulation of defensive responses we resorted to the use fruit flies as it easily allows testing of groups of varying sizes, the collection of large data sets and genetic access to individual neuronal types. We established that fruit flies in response to visual looming stimuli, simulating a large object on collision course, make rapid freeze/flee choices accompanied by lasting changes in the fly’s internal state, reflected in altered cardiac activity. Freezing in flies is also strongly modulated by the movement of surrounding neighbours. In contrast with rodents that use auditory cues, female flies use visual motion processed by visual projection neurons. Finally, I will discuss more preliminary findings suggesting that there are multiple states of freezing as measured by muscle activity in the fly legs. Having established the fly as a model to study freezing/fleeing decisions, we are in a great position to perform large scale integrative studies on the organization of defensive behaviours. Short Bio Marta Moita received her BSc degree in Biology at the University of Lisbon, in 1995. As part of Gulbenkian’s PhD programme in Biology and Medicine she developed her thesis work, on the encoding by place cells of threat conditioning under the supervision of Prof. Joseph Ledoux, at the New York University (1997-2002). In 2002, Marta Moita worked as a postdoctoral fellow in Dr. Tony Zador’s laboratory, at the Cold Spring Harbor Laboratory, to study the role of auditory cortex in sound discrimination. In 2004, she became a principal investigator, leading the Behavioral Neuroscience lab, at the Instituto Gulbenkian de Ciência. In 2008 her group joined the starting Champalimaud Neuroscience program. In 2018 and 2019 Marta Moita served as Deputy Director of Champalimaud Research. Her lab is primarily interested in understanding the mechanisms of behavior. To this end, the lab has focused on behaviors that are crucial for survival and present in a wide range of species, namely defensive behaviors triggered by external threats. Using a combination of state-of-the-art tools in Neuroscience (initially using rats and currently using fruit flies) and detailed quantitative descriptions of behavior, her lab aims to understand how contextual cues guide the selection between different defensive strategies and how the chosen defensive behavior and accompanying physiological responses are instantiated.    

Deciphering non-neuronal cells contribution to Alzheimer’s disease pathology using high throughput transcriptomic and proteomic methods

Lecture
Date:
Wednesday, November 30, 2022
Hour: 14:00 - 15:00
Location:
Sedi Medina (PhD Thesis Defense Seminar) on Zoom

Alzheimer's disease (AD) is a devastating pathology of the central nervous system (CNS) of unknown etiology which represents the most common neurodegenerative disorder. For decades, AD was perceived as a disease of the neuron alone. However, research advances in recent years have challenged this concept and shed light on the critical roles of non-neuronal cells on the development and progression of AD. In my PhD, I focused on understanding how two non-neuronal cell types - the Astrocytes and Microglia - respond to AD and how they possibly affect pathological processes. Our research identified a unique population of Astrocytes that significantly increased in association with brain pathology, which we termed disease-associated astrocytes (DAAs). This novel population of DAAs appeared at an early disease stage, increased in abundance with disease progression, and was not observed in young or in healthy adult animals. In addition, similar astrocytes appeared in aged wild-type (WT) mice and in aging human brains, suggesting their linkage to genetic and age-related factors. Aging is considered the greatest risk factor for AD, although the mechanism underlying the aging-related susceptibility to AD is unknown. One emerging factor that is involved in biological aging is the accumulation of senescent cells. Cellular senescence is a process in which aging cells change their characteristic phenotype. Under physiological conditions senescent cells can be removed by the immune system, however with aging, senescent cells accumulate in tissues, either due to a failure of effective removal or due to the accelerated formation of senescent cells. Our data highlight the contribution of non neuronal cells to AD pathogenesis by demonstrating  that 1. Overexpression of a specific gene by astrocytes affected the microglia cells' state, leading to a more homeostatic and less reactive microglial phenotype in comparison to the control group. 2. Accumulation of senescent microglia cells was observed in the brain of aged WT mice and AD mouse model (5xFAD), and by applying different therapeutic strategies we managed to observe significant quantitative differences in these cells, followed by a cognitive amelioration.

Pages

All events, All years

The development and molecular mechanisms of crystal-forming cells

Lecture
Date:
Wednesday, February 1, 2023
Hour: 10:00 - 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Dvir Gur
|
Departments of Molecular Genetics

My adventures in the rat interactive foraging facility (RIFF)

Lecture
Date:
Tuesday, January 31, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eli Nelken
|
ELSC-The Hebrew University of Jerusalem

We developed an arena (called colloquially the RIFF) for jointly studying behavior and neural activity in freely-behaving rats. The RIFF operates as a state machine, allowing us to implement a large number of different behaviors as Markov Decision Processes and therefore to analyze much of the data within the theoretical framework of reinforcement learning. In the studies I will show here, we recorded neural activity from auditory cortex while rats performed auditory-guided behavior. We observed an intricate interplay between behavior and neural activity that was much richer than we expected.

Naturalistic approaches for studying social interactions, communication and language at cellular scale

Lecture
Date:
Tuesday, January 24, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Ziv Williams
|
Center for Nervous System Repair Harvard Medical School, Boston MA

Social interactions are remarkably dynamic, requiring individuals to understand not only how their behavior may affect others but also how others may respond in return. In humans, social interactions are also often dominated by processes such as language and theory of mind which allow us to communicate complex thoughts and beliefs. Understanding the basic cellular processes that underlie social behavior or by which individuals communicate, however, has remained a challenge. Here, I describe naturalistic approaches developed in animals and humans that aim of investigating these questions. First, by developing an ethologically based group task in three-interacting rhesus macaques, I describe representations of other’s behavior by neurons in the prefrontal cortex, reflecting the other’s identities, their interactions, actions, and outcomes. I also show how these cells collectively represent the interaction between specific group members and how they enable mutually beneficial social behavior. Second, by recording from neurons in the human prefrontal cortex during language-based tasks, I describe neurons that reliably encode information about others’ beliefs across richly varying scenarios and that distinguish self- from other-belief-related representations. By further following their encoding dynamics, I also describe how these cells represent the contents of the others’ beliefs and predict whether they are true or false. Finally, I describe how these cell ensembles track linguistic information during natural speech processing and how language can be used to ask specific questions about the single-cellular constructs that underlie social reasoning. Together, these studies reveal cellular mechanisms for interactive social behavior in animals and humans and highlight the prospective use of naturalistic approaches in social neuroscience.

Rapid learning (and unlearning) in the human brain

Lecture
Date:
Thursday, January 19, 2023
Hour: 14:00 - 15:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Nitzan Censor
|
School of Psychological Sciences & Sagol School of Neuroscience Tel Aviv University

A plethora of studies have pointed to sensory plasticity in the adult visual system, documenting long-term improvements in perception. Such perceptual learning is enabled by repeated practice, inducing use-dependent plasticity in early visual areas and their readouts. I will discuss results from our lab challenging the fundamental assumption in low-level perceptual learning that only 'practice makes perfect', indicating that brief reactivations of visual memories induce efficient rapid perceptual learning. Utilizing behavioral psychophysics, brain stimulation and neuroimaging, we aim to reveal the neurobehavioral mechanisms by which brief exposure to learned information modulates brain plasticity and supports rapid learning processes. In parallel, we investigate how these learning mechanisms operate across domains, for example by testing the hypothesis that similar inherent mechanisms may also result in maladaptive consequences, when brief reactivations occur spontaneously as intrusive enhanced memories following negative events. Unraveling the mechanisms of this new form of rapid learning could set the foundations to enhance learning in daily life when beneficial, and to downregulate maladaptive consequences of negative memories.

Is behaviour a developmental trait?

Lecture
Date:
Wednesday, January 11, 2023
Hour: 10:00 - 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Gil Levkowitz
|
Departments of Molecular Cell Biology and Molecular Neuroscience

Capturing Neuronal Activity with more Precision and Fidelity in Time and Space

Lecture
Date:
Tuesday, January 10, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Peter Bandettini
|
Laboratory of Brain and Cognition NIMH Bethesda MD

My lab’s focus in recent years has been split between development of ultra-high resolution fMRI at high field and the exploration of more sensitive yet robust methods to find all the salient transients and trends in the signal. High field, high resolution fMRI relies heavily on the acquisition technology and the functional contrast used as well as unique processing approaches that segment, as well as possible, cortical layers for analysis. Our fMRI time series analysis research relies on creative paradigm design in conjunction with tailored processing methods that strike a balance between casting a wide net for potentially informative signals and applying just enough modeling to make sense of the data. Our goal is to use fMRI to see neuronal activity and capture neural correlates of behavior that have previously been elusive to more standard approaches.  Specifically, for our high resolution fMRI work, I will describe experiments demonstrating layer-specific activity in motor, somatosensory, and visual cortex that changes with tasks that modulate the hypothesized input and output cortical communication. In our lab, we perform layer fMRI using a functional contrast called VASO (vascular space occupancy) that is sensitive to blood volume changes in micro vessels - having more specificity than BOLD with only a small tradeoff in sensitivity. Layer fMRI has the potential to provide cortical hierarchy information and communication directionality based on the understanding that feedforward connections terminate predominantly in middle layers and feedback connections terminate in predominantly upper and lower layers. Hence by determining activation location across cortical depth, one can infer whether the activation is feedforward or feedback. I will also demonstrate how the use of resting state connectivity in conjunction with layer fMRI is able to discern such cortical hierarchy in visual areas. Lastly, I will also show examples of applications of layer fMRI in frontal cortex during a working memory task. In addition, I will show our high resolution fMRI work that has allowed us to discern a new digit organizational pattern in motor cortex.  For our time series work, I will show our recent results in using connectivity-based decoding for identifying, in an unsupervised manner, tasks being performed. In addition, I will show an application of naturalistic stimuli and inter subject correlation to characterize personality trait and language skills of individuals. Lastly, changes arousal state during scanning has been viewed as both a confound and opportunity. I demonstrate our effort to further characterize the temporal and spatial signatures of arousal state changes in fMRI time series.

Latent cause inference in learning and decision making

Lecture
Date:
Tuesday, January 3, 2023
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Yael Niv
|
Neuroscience Institute and Psychology Department Princeton University

No two events are alike. But still, we learn, which means that we implicitly decide what events are similar enough that experience with one can inform us about what to do in another. We have suggested that this relies on parsing of incoming information into “clusters” according to inferred hidden (latent) causes. In this talk, I will present a computational model of this latent-cause inference process, and show supporting data from a variety of behavioral experiments in humans and rodents spanning from simple conditioning to memory to social decision making. I will also briefly discuss the relevance of this theory to mental health treatments.

Renewal and plasticity in oral and gastrointestinal epithelia

Lecture
Date:
Monday, January 2, 2023
Hour: 11:15 - 12:15
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Ophir Klein
|
Executive Director of Cedars-Sinai Guerin Children's Vice Dean for Children’s Services David and Meredith Kaplan Distinguished Chair in Children’s Health Professor of Orofacial Sciences and Pediatrics, UC San Francisco

How movement regulates defensive behaviours in a social context

Lecture
Date:
Tuesday, December 13, 2022
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Marta Moita
|
Behavioural Neuroscience Champalimaud Center, Lisbon

Our work concerns the general problem of adaptive behavior in response to predatory threats, and of the neural mechanisms underlying a choice between strategies. Interacting predators and prey tightly regulate their motion, timing with precision when to hold, attack or escape. Motion cues are thus paramount in these interactions. Speed and (un)predictability have shaped the evolution of sensory and motor systems, the elucidation of which a great deal of research has been devoted. Much less attention has been paid to the role of motion as a social cue of threat or safety. We and others have found that prey animals use the movement of their neighbors to regulate their defensive responses. We have studied social regulation of freezing in rodents and found that rats use cessation of movement evoked sound, resulting from freezing, as a cue of danger. In addition, auto-conditioning, whereby rats learn the association between shock and their own freezing, during prior experience with shock, facilitates the use of freezing by others as an alarm cue. To further explore the social regulation of defensive responses we resorted to the use fruit flies as it easily allows testing of groups of varying sizes, the collection of large data sets and genetic access to individual neuronal types. We established that fruit flies in response to visual looming stimuli, simulating a large object on collision course, make rapid freeze/flee choices accompanied by lasting changes in the fly’s internal state, reflected in altered cardiac activity. Freezing in flies is also strongly modulated by the movement of surrounding neighbours. In contrast with rodents that use auditory cues, female flies use visual motion processed by visual projection neurons. Finally, I will discuss more preliminary findings suggesting that there are multiple states of freezing as measured by muscle activity in the fly legs. Having established the fly as a model to study freezing/fleeing decisions, we are in a great position to perform large scale integrative studies on the organization of defensive behaviours. Short Bio Marta Moita received her BSc degree in Biology at the University of Lisbon, in 1995. As part of Gulbenkian’s PhD programme in Biology and Medicine she developed her thesis work, on the encoding by place cells of threat conditioning under the supervision of Prof. Joseph Ledoux, at the New York University (1997-2002). In 2002, Marta Moita worked as a postdoctoral fellow in Dr. Tony Zador’s laboratory, at the Cold Spring Harbor Laboratory, to study the role of auditory cortex in sound discrimination. In 2004, she became a principal investigator, leading the Behavioral Neuroscience lab, at the Instituto Gulbenkian de Ciência. In 2008 her group joined the starting Champalimaud Neuroscience program. In 2018 and 2019 Marta Moita served as Deputy Director of Champalimaud Research. Her lab is primarily interested in understanding the mechanisms of behavior. To this end, the lab has focused on behaviors that are crucial for survival and present in a wide range of species, namely defensive behaviors triggered by external threats. Using a combination of state-of-the-art tools in Neuroscience (initially using rats and currently using fruit flies) and detailed quantitative descriptions of behavior, her lab aims to understand how contextual cues guide the selection between different defensive strategies and how the chosen defensive behavior and accompanying physiological responses are instantiated.    

Deciphering non-neuronal cells contribution to Alzheimer’s disease pathology using high throughput transcriptomic and proteomic methods

Lecture
Date:
Wednesday, November 30, 2022
Hour: 14:00 - 15:00
Location:
Sedi Medina (PhD Thesis Defense Seminar) on Zoom

Alzheimer's disease (AD) is a devastating pathology of the central nervous system (CNS) of unknown etiology which represents the most common neurodegenerative disorder. For decades, AD was perceived as a disease of the neuron alone. However, research advances in recent years have challenged this concept and shed light on the critical roles of non-neuronal cells on the development and progression of AD. In my PhD, I focused on understanding how two non-neuronal cell types - the Astrocytes and Microglia - respond to AD and how they possibly affect pathological processes. Our research identified a unique population of Astrocytes that significantly increased in association with brain pathology, which we termed disease-associated astrocytes (DAAs). This novel population of DAAs appeared at an early disease stage, increased in abundance with disease progression, and was not observed in young or in healthy adult animals. In addition, similar astrocytes appeared in aged wild-type (WT) mice and in aging human brains, suggesting their linkage to genetic and age-related factors. Aging is considered the greatest risk factor for AD, although the mechanism underlying the aging-related susceptibility to AD is unknown. One emerging factor that is involved in biological aging is the accumulation of senescent cells. Cellular senescence is a process in which aging cells change their characteristic phenotype. Under physiological conditions senescent cells can be removed by the immune system, however with aging, senescent cells accumulate in tissues, either due to a failure of effective removal or due to the accelerated formation of senescent cells. Our data highlight the contribution of non neuronal cells to AD pathogenesis by demonstrating  that 1. Overexpression of a specific gene by astrocytes affected the microglia cells' state, leading to a more homeostatic and less reactive microglial phenotype in comparison to the control group. 2. Accumulation of senescent microglia cells was observed in the brain of aged WT mice and AD mouse model (5xFAD), and by applying different therapeutic strategies we managed to observe significant quantitative differences in these cells, followed by a cognitive amelioration.

Pages

All events, All years

There are no events to display

All events, All years

There are no events to display

Pages