Prof Wei Cao

Our laboratory studies the biology of neuroinflammation and related pathogenic events associated with neurodegenerative diseases. A leading health and economic burden to an aging society, Alzheimer’s Disease (AD) is a condition with complex etiology and manifests in dysregulated neuronal functions and intercellular communications in the brain. Increasingly, neuroinflammatory signals and microglial responses are critically implicated in AD and other neurodegenerative diseases. We are keen to illuminate the fundamental principles that govern the neuroinflammatory phenomena in driving AD and brain aging (check our recent publications J. Clin. Invest. 130:1912 (2020); Front Neurosci 14:577744 (2020); BioRiv 2021.11.01.466525(2021)). Establishing a brand new presence in Univ of Texas Health Science Center at Houston, we are looking for an enthusiastic candidate to join a spirited group. The focus of the immediate project is to elucidate the mechanisms of neuroinflammation and to identify the key pathways and factors involved in AD by examining various CNS cells and analyzing mouse disease models. Additional projects will investigate cellular elements that modify glial functions in the aging brain and/or under the context of AD pathogenesis. Other areas of our research interest include devising strategies to target AD-relevant inflammatory and pathogenic mediators.

Nathan Skene

This project will involve the use single cell epigenetics to address key questions about the mechanisms of neurodegenerative disease. In a series of recent publications in Nature Genetics, the lab has demonstrated that single cell RNA-seq data from mice can be used to identify the cell types associated with genetic risk factors for neurodegenerative disease. To perform this mapping, we use GWAS summary statistics generated by our collaborators at a variety of international consortia and personal genomics companies. Identification of cell types genetically implicated in disease, enables better drug targeting efforts as it is free from the confounds associated with neuropathology and mouse modelling. Critical questions remain open about the etiologically relevant cell types and the regulatory effects of disease loci within those cells. We are looking to establish the use of single cell epigenetic techniques, such as ATAC-seq and CUT&TAG, as this will enhance our ability to map intergenic loci to cell type specific features. This project will involve working with human tissue brain banks, to apply these methods to targeted populations of cells. If you are interested in this position, then please email Dr Nathan Skene directly to discuss

Dr Nathan Skene

Using machine learning to predict cell-type specific effects of genetic variants which influence genome regulation. This PhD project is focused on using machine learning techniques to develop novel classifiers for predicting how changes in DNA sequences alter genomic regulatory features. Many regulatory proteins recognise particular DNA sequences known as motifs, for instance, EcoRI only binds to GAATTC. DNA sequences can be converted into a machine interpretable format, using one-hot encoding. The candidate will use publicly available and inhouse datasets of genomic regulatory features to train models. Machine learning techniques will be used to predict the cell-type specific regulatory effects of genetic variants. We will provide several true-positive datasets, wherein the effect of genetic mutations on particular regulatory features has been measured. These will form validation datasets to evaluate how well the trained classifier works. We are interested in how improvements in the machine learning approach (e.g. use of transfer learning, recurrent attentional networks or graph convolution networks) can be used to improve upon existing methods. The candidate will use these techniques to identify causal pathways and candidate drug targets for neurodegenerative diseases.

Biomolecular condensates as drivers of neuroinflammation

Expanding mechanisms and therapeutic targets for neurodegenerative disease

A hallmark pathological feature of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the depletion of RNA-binding protein TDP-43 from the nucleus of neurons in the brain and spinal cord. A major function of TDP-43 is as a repressor of cryptic exon inclusion during RNA splicing. By re-analyzing RNA-sequencing datasets from human FTD/ALS brains, we discovered dozens of novel cryptic splicing events in important neuronal genes. Single nucleotide polymorphisms in UNC13A are among the strongest hits associated with FTD and ALS in human genome-wide association studies, but how those variants increase risk for disease is unknown. We discovered that TDP-43 represses a cryptic exon-splicing event in UNC13A. Loss of TDP-43 from the nucleus in human brain, neuronal cell lines and motor neurons derived from induced pluripotent stem cells resulted in the inclusion of a cryptic exon in UNC13A mRNA and reduced UNC13A protein expression. The top variants associated with FTD or ALS risk in humans are located in the intron harboring the cryptic exon, and we show that they increase UNC13A cryptic exon splicing in the face of TDP-43 dysfunction. Together, our data provide a direct functional link between one of the strongest genetic risk factors for FTD and ALS (UNC13A genetic variants), and loss of TDP-43 function. Recent analyses have revealed even further changes in TDP-43 target genes, including widespread changes in alternative polyadenylation, impacting expression of disease-relevant genes (e.g., ELP1, NEFL, and TMEM106B) and providing evidence that alternative polyadenylation is a new facet of TDP-43 pathology.

LRRK2 – a master regulator of neurodegeneration: acting on multiple systems including neuroinflammatory signaling, vesicular trafficking, and cell death pathways

The synaptic functions of Alpha Synuclein and Lrrk2

Alpha synuclein and Lrrk2 are key players in Parkinson's disease and related disorders, but their normal role has been confusing and controversial. Data from acute gene-editing based knockdown, followed by functional assays, will be presented.

The many roles of microglia in the pathogenesis of neurodegeneration

‘Going South!’ Comparative mitochondrial biology in ageing and neurodegeneration

Effects of Presenilin1 FAD mutants on brain angiogenic functions and neuroprotection in Alzheimer’s Disease

Apathy and impulsivity in neurological disease – cause, effect and treatment

The Brain Conference (the Guarantors of Brain)

Join the Brain Conference on 24-25 February 2022 for the opportunity to hear from neurology’s leading scientists and clinicians. The two-day virtual programme features clinical teaching talks and research presentations from expert speakers including neuroscientist Professor Gina Poe, and the winner of the 2021 Brain Prize, neurologist Professor Peter Goadsby." "Tickets for The Brain Conference 2022 cost just £30, but register with promotional code BRAINCONEM20 for a discounted rate of £25.

The Brain Conference (the Guarantors of Brain)

Join the Brain Conference on 24-25 February 2022 for the opportunity to hear from neurology’s leading scientists and clinicians. The two-day virtual programme features clinical teaching talks and research presentations from expert speakers including neuroscientist Professor Gina Poe, and the winner of the 2021 Brain Prize, neurologist Professor Peter Goadsby." "Tickets for The Brain Conference 2022 cost just £30, but register with promotional code BRAINCONEM20 for a discounted rate of £25.

Mechanisms to medicines in neurodegeneration

Dysregulation of protein synthesis both globally and locally in neurons and astrocytes is a key feature of neurodegenerative diseases. Aberrant signalling through the Unfolded Protein Response (UPR) and related Integrated Stress Response (ISR) have become major targets for neuroprotection in these disorders. In addition, other homeostatic mechanisms and stress responses, including the cold shock response, appear to regulate local translation and RNA splicing to control synapse maintenance and regeneration and can also be targeted therapeutically for neuroprotection. We have defined the role of UPR/ISR and the cold-shock response in neurodegenerative disorders and have developed translational strategies targeting them for new treatments for dementia.

Dysfunction of neurons and circuits in Alzheimer’s disease

Evidence for the role of glymphatic dysfunction in the development of Alzheimer’s disease

Glymphatic perivascular exchange is supported by the astroglial water channel aquaporin-4 (AQP4), which localizes to perivascular astrocytic endfeet surrounding the cerebral vasculature. In aging mice, impairment of glymphatic function is associated with reduced perivascular AQP4 localization, yet whether these changes contribute to the development of neurodegenerative disease, such as Alzheimer’s disease (AD), remains unknown. Using post mortem human tissue, we evaluated perivascular AQP4 localization in the frontal cortical gray matter, white matter, and hippocampus of cognitively normal subjects and those with AD. Loss of perivascular and increasing cellular localization of AQP4 in the frontal gray matter was specifically associated with AD status, amyloid β (Aβ) and tau pathology, and cognitive decline in the early stages of disease. Using AAV-PHP.B to drive expression on non-perivascular AQP4 in wild type and Tg2576 (APPSwe, mouse model of Aβ deposition) mice, increased cellular AQP4 localization did not slow glymphatic function or change Aβ deposition. Using the Snta1 knockout line (which lacks perivascular AQP4 localization), we observed that loss AQP4 from perivascular endfeet slowed glymphatic function in wild type mice and accelerated Aβ plaque deposition in Tg2576 mice. These findings demonstrate that loss of perivascular AQP4 localization, and not increased cellular AQP4 localization, slows glymphatic function and promotes the development of AD pathology. To evaluate whether naturally occurring variation in the human AQP4 gene, or the alpha syntrophin (SNTA1), dystrobrevin (DTNA) or dystroglycan (DAG1) genes (whose products maintain perivascular AQP4 localization) confer risk for or protection from AD pathology or clinical progression, we evaluated 56 tag single nucleotide polymorphisms (SNPs) across these genes for association with CSF AD biomarkers, MRI measures of cortical and hippocampal atrophy, and longitudinal cognitive decline in the Alzheimer’s Disease Neuroimaging Initiative I (ADNI I) cohort. We identify 25 different significant associations between AQP4, SNTA1, DTNA, and DAG1 tag SNPs and phenotypic measures of AD pathology and progression. These findings provide complimentary human genetic evidence for the contribution of perivascular glymphatic dysfunction to the development of AD in human populations.

NAD+ metabolism in axon and neurodegeneration (from a fly’s perspective)

Microbiota in the health of the nervous system and the response to stress

Microbes have shaped the evolution of eukaryotes and contribute significantly to the physiology and behavior of animals. Some of these traits are inherited by the progenies. Despite the vast importance of microbe-host communication, we still do not know how bacteria change short term traits or long-term decisions in individuals or communities. In this seminar I will present our work on how commensal and pathogenic bacteria impact specific neuronal phenotypes and decision making. The traits we specifically study are the degeneration and regeneration of neurons and survival behaviors in animals. We use the nematode Caenorhabditis elegans and its dietary bacteria as model organisms. Both nematode and bacteria are genetically tractable, simplifying the detection of specific molecules and their effect on measurable characteristics. To identify these molecules we analyze their genomes, transcriptomes and metabolomes, followed by functional in vivo validation. We found that specific bacterial RNAs and bacterially produced neurotransmitters are key to trigger a survival behavioral and neuronal protection respectively. While RNAs cause responses that lasts for many generations we are still investigating whether bacterial metabolites are capable of inducing long lasting phenotypic changes.

Understanding the Mechanisms of Epilepsy in mTORopathies

Human stem cell models of neurodegeneration: complex, relevant and robust

Parp mutations protect from mitochondrial toxicity in Alzheimer’s disease

Alzheimer’s disease is the most common age-related neurodegenerative disorder. Familial forms of Alzheimer’s disease associated with the accumulation of a toxic form of amyloid-β (Aβ) peptides are linked to mitochondrial impairment. The coenzyme nicotinamide adenine dinucleotide (NAD+) is essential for both mitochondrial bioenergetics and nuclear DNA repair through NAD+-consuming poly (ADP-ribose) polymerases (PARPs). Here, we analysed the metabolomic changes in flies over-expressing Aβ and showed a decrease of metabolites associated with nicotinate and nicotinamide metabolism, which is critical for mitochondrial function in neurons. We show that increasing the bioavailability of NAD+ protects against Aβ toxicity. Pharmacological supplementation using NAM, a form of vitamin B that acts as a precursor for NAD+ or a genetic mutation of PARP rescues mitochondrial defects, protects neurons against degeneration and reduces behavioural impairments in a fly model of Alzheimer’s disease. Next, we looked at links between PARP polymorphisms and vitamin B intake in patients with Alzheimer’s disease. We show that polymorphisms in the human PARP1 gene or the intake of vitamin B, are associated with a decrease in the risk and severity of Alzheimer’s disease. We suggest that enhancing the availability of NAD+ by either vitamin B supplements or the inhibition of NAD+-dependent enzymes, such as PARPs are potential therapies for Alzheimer’s disease.

Can we repair the Parkinsonian brain?

Untitled Seminar

Understanding how photoreceptor degeneration alters retinal signaling, and how to intervene to rescue vision

Age-related Macular Degeneration (AMD) and Retinitis Pigmentosa (RP) are vision disorders caused by loss of rod and cone photoreceptors, but downstream retinal neurons also show physiological and morphological changes, resulting in the emergence of hyperactivity and rhythmic firing in many retinal ganglion cells (RGC). We recently discovered that retinoic acid (RA) is a key signal that triggers hyperactivity and that blockers of RA unmask light responses in RGCs that would otherwise be obscured. Recent work is revealing where in the retina circuit RA initiates functional changes. Moreover, interfering with the RA signaling pathway with drug or gene therapy can improve spatial vision in a mouse model of RP, providing a new strategy for enhancing low vision in human RP and AMD.

Blood phosphorylated tau as biomarkers for Alzheimer’s disease

Alzheimer's disease (AD) is the most common cause of dementia, and its health and socioeconomic burdens are of major concern. Presently, a definite diagnosis of AD is established by examining brain tissue after death. These examinations focus on two major pathological hallmarks of AD in the brain: (i) amyloid plaques consisting of aggregated amyloid beta (Aβ) peptides and (ii) neurofibrillary tangles made of abnormally phosphorylated tau protein. In living individuals, AD diagnosis relies on two main approaches: (i) brain imaging of tau tangles and Aβ plaques using a technique called positron emission tomography (PET) and (ii) measuring biochemical changes in tau (including phosphorylated tau at threonine-181 [p-tau181]) and the Aβ42 peptide metabolized into CSF. Unlike Aβ42, CSF p-tau181 is highly specific for AD but its usability is restricted by the need of a lumbar puncture. Moreover, PET imaging is expensive and only available in specialised medical centres. Due to these shortcomings, a simple blood test that can detect disease-related changes in the brain is a high priority for AD research, clinical care and therapy testing. In this webinar, I will discuss the discovery of p-tau biomarkers in blood and the biochemistry of how these markers differ from those found in CSF. Furthermore, I will critically review the performance of blood p-tau biomarkers across the AD pathological process and how they associate with and predict Aβ and tau pathophysiological and neuropathological changes. Furthermore, I will evaluate the potential advantages, challenges and context of use of blood p-tau in clinical practice, therapeutic trials and population screening.

Development and Application of PET Imaging for Dementia Research

Molecular imaging using Positron Emission Tomography (PET) has become a major biomedical imaging technology. Its application towards characterisation of biochemical processes in disease could enable early detection and diagnosis, development of novel therapies and treatment evaluation. The technology is underpinned by the use of imaging probes radiolabelled with short-lived radioisotopes which can be specific and selective for biological targets in vivo e.g. markers for receptors, protein deposits, enzymes and metabolism. My talk will focus on the increasing development and application of PET imaging to clinical research in neurodegenerative diseases, for which it can be applied to delineate and understand the various pathological components of these disorders.

Emergent scientists discuss Alzheimer's disease

This seminar is part of our “Emergent Scientists” series, an initiative that provides a platform for scientists at the critical PhD/postdoc transition period to share their work with a broad audience and network. Summary: These talks cover Alzheimer’s disease (AD) research in both mice and humans. Christiana will discuss in particular the translational aspects of applying mouse work to humans and the importance of timing in disease pathology and intervention (e.g. timing between AD biomarkers vs. symptom onset, timing of therapy, etc.). Siddharth will discuss a rare variant of Alzheimer’s disease called “Logopenic Progressive Aphasia”, which presents with temporo-parietal atrophy yet relative sparing of hippocampal circuitry. Siddharth will discuss how, despite the unusual anatomical basis underlying this AD variant, degeneration of the angular gyrus in the left inferior parietal lobule contributes to memory deficits similar to those of typical amnesic Alzheimer’s disease. Christiana’s abstract: Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder that causes severe deterioration of memory, cognition, behavior, and the ability to perform daily activities. The disease is characterized by the accumulation of two proteins in fibrillar form; Amyloid-β forms fibrils that accumulate as extracellular plaques while tau fibrils form intracellular tangles. Here we aim to translate findings from a commonly used AD mouse model to AD patients. Here we initiate and chronically inhibit neuropathology in lateral entorhinal cortex (LEC) layer two neurons in an AD mouse model. This is achieved by over-expressing P301L tau virally and chronically activating hM4Di DREADDs intracranially using the ligand dechloroclozapine. Biomarkers in cerebrospinal fluid (CSF) is measured longitudinally in the model using microdialysis, and we use this same system to intracranially administer drugs aimed at halting AD-related neuropathology. The models are additionally tested in a novel contextual memory task. Preliminary findings indicate that viral injections of P301L tau into LEC layer two reveal direct projections between this region and the outer molecular layer of dentate gyrus and the rest of hippocampus. Additionally, phosphorylated tau co-localize with ‘starter cells’ and appear to spread from the injection site. Preliminary microdialysis results suggest that the concentrations of CSF amyloid-β and tau proteins mirror changes observed along the disease cascade in patients. The disease-modifying drugs appear to halt neuropathological development in this preclincial model. These findings will lead to a novel platform for translational AD research, linking the extensive research done in rodents to clinical applications. Siddharth’s abstract: A distributed brain network supports our ability to remember past events. The parietal cortex is a critical member of this network, yet, its exact contributions to episodic remembering remain unclear. Neurodegenerative syndromes affecting the posterior neocortex offer a unique opportunity to understand the importance and role of parietal regions to episodic memory. In this talk, I introduce and explore the rare neurodegenerative syndrome of Logopenic Progressive Aphasia (LPA), an aphasic variant of Alzheimer’s disease presenting with early, left-lateralized temporo-parietal atrophy, amidst relatively spared hippocampal integrity. I then discuss two key studies from my recent Ph.D. work showcasing pervasive episodic and autobiographical memory dysfunction in LPA, to a level comparable to typical, amnesic Alzheimer’s disease. Using multimodal neuroimaging, I demonstrate how degeneration of the angular gyrus in the left inferior parietal lobule, and its structural connections to the hippocampus, contribute to amnesic profiles in this syndrome. I finally evaluate these findings in the context of memory profiles in other posterior cortical neurodegenerative syndromes as well as recent theoretical models underscoring the importance of the parietal cortex in the integration and representation of episodic contextual information.

Microglia function and dysfunction in Alzheimer’s disease

Emerging genetic studies of late-onset Alzheimer’s Disease implicate the brain’s resident macrophages in the pathogenesis of AD. More than half the risk genes associated with late-onset AD are selectively expressed in microglia and peripheral myeloid cells; yet we know little about the underlying biology or how myeloid cells contribute to AD pathogenesis. Using single-cell RNA sequencing and spatial transcriptomics we identified molecular signatures that can be used to localize and monitor distinct microglia functional states in the human and mouse brain. Our results show that microglia assume diverse functional states in development, aging and injury, including populations corresponding to known microglial functions including proliferation, migration, inflammation, and synaptic phagocytosis. We identified several innate immune pathways by which microglia recognize and prune synapses during development and in models of Alzheimer’s disease, including the classical complement cascade. Illuminating the mechanisms by which developing synaptic circuits are sculpted is providing important insight on understanding how to protect synapses in Alzheimer’s and other neurodegenerative diseases of synaptic dysfunction.

More than Bystanders in Dementia, Learning What Microglia Do

Genome-wide association studies implicate microglia in Alzheimer’s disease (AD) pathogenesis, but how microglia contribute to cognitive decline in AD is unclear. Emerging research suggests microglia, the resident macrophages of the central nervous system, to be active participants in brain wiring. One mechanism by which microglia help eliminate synapses is through the classical complement pathway (C1q, CR3/C3). Data from multiple laboratories collectively suggest that there may be an aberrant reactivation of the complement-dependent pruning pathway in multiple models of neurologic diseases including AD. These data altogether suggest that microglia participate in synaptic pathology. However, how and which synapses are targeted are unknown. Furthermore, whether microglia directly impair synaptic function is unknown. Primary goals of my laboratory are to understand how higher cognitive functions such as learning and memory involve microglial biology in the healthy adult brain and dissect immune mechanisms behind the region-specific vulnerability of synapse loss and neuronal dysfunction during disease. Mechanistic insight into local signals that regulate neuroglia interactions will be key to developing potential therapeutic avenues to target in disease.

CRISPR-based functional genomics in iPSC-based models of brain disease

Human genes associated with brain-related diseases are being discovered at an accelerating pace. A major challenge is an identification of the mechanisms through which these genes act, and of potential therapeutic strategies. To elucidate such mechanisms in human cells, we established a CRISPR-based platform for genetic screening in human iPSC-derived neurons, astrocytes and microglia. Our approach relies on CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa), in which a catalytically dead version of the bacterial Cas9 protein recruits transcriptional repressors or activators, respectively, to endogenous genes to control their expression, as directed by a small guide RNA (sgRNA). Complex libraries of sgRNAs enable us to conduct genome-wide or focused loss-of-function and gain-of-function screens. Such screens uncover molecular players for phenotypes based on survival, stress resistance, fluorescent phenotypes, high-content imaging and single-cell RNA-Seq. To uncover disease mechanisms and therapeutic targets, we are conducting genetic modifier screens for disease-relevant cellular phenotypes in patient-derived neurons and glia with familial mutations and isogenic controls. In a genome-wide screen, we have uncovered genes that modulate the formation of disease-associated aggregates of tau in neurons with a tauopathy-linked mutation (MAPT V337M). CRISPRi/a can also be used to model and functionally evaluate disease-associated changes in gene expression, such as those caused by eQTLs, haploinsufficiency, or disease states of brain cells. We will discuss an application to Alzheimer’s Disease-associated genes in microglia.

Mechanisms of pathogenesis in the tauopathies

The distribution of pathological tau in the brain of patients with AD is highly predicable, and as disease worsens, it spreads transynaptically from initial regions of vulnerability. The reason why only some neurons are vulnerable to the accumulation and propagation of pathological forms of tau, and the mechanisms by which tauopathy spreads through the brain are not well understood. Using a combination of immunohistochemistry and computational analysis we have examined pathway differences between vulnerable and resistant neurons. How tau spreads across a synapse has been examined in vitro using different model systems. Our data show that dysregulation of tau homeostasis determines the cellular and regional vulnerability of specific neurons to tau pathology (H. Fu et al. 2019. Nat. Neuro. 22 (1):47-56) and that deficits in tau homeostasis can exacerbate tau accumulation and propagation. Aging appears to impact similar neuronal populations. Mechanisms and consequences of abnormal tau accumulation within neurons, its transfer between cells, pathology propagation and therapeutic opportunities will be discussed.

Novel immunotherapy to treat Alzheimer’s disease and Dementia: from curiosity-driven research to prospect of therapy

Untitled Seminar

Neuroscience Investigations in the Virgin Lands of African Biodiversity

Africa is blessed with a rich diversity and abundance in rodent and avian populations. This natural endowment on the continent portends research opportunities to study unique anatomical profiles and investigate animal models that may confer better neural architecture to study neurodegenerative diseases, adult neurogenesis, stroke and stem cell therapies. To this end, African researchers are beginning to pay closer attention to some of her indigenous rodents and birds in an attempt to develop spontaneous laboratory models for homegrown neuroscience-based research. For this presentation, I will be showing studies in our lab, involving cellular neuroanatomy of two rodents, the African giant rat (AGR) and Greater cane rat (GCR), Eidolon Bats (EB) and also the Striped Owl (SO). Using histological stains (Cresyl violet and Rapid Golgi) and immunohistochemical biomarkers (GFAP, NeuN, CNPase, Iba-1, Collagen 2, Doublecortin, Ki67, Calbindin, etc), and Electron Microscopy, morphology and functional organizations of neuronal and glial populations of the AGR , GCR, EB and SO brains have been described, with our work ongoing. In addition, the developmental profiles of the prenatal GCR brains have been chronicled across its entire gestational period. Brains of embryos/foetuses were harvested for gross morphological descriptions and then processed using immunofluorescence biomarkers to determine the pattern, onset, duration and peak of neurogenesis (Pax6, Tbr1, Tbr2, NF, HuCD, MAP2) and the onset and peak of glial cell expressions and myelination in the prenatal GCR. The outcome of these research efforts has shown unique neuroanatomical expressions and networks amongst Africa’s rich biodiversity. It is hopeful that continuous effort in this regard will provide sufficient basic research data on neural developments and cellular neuroanatomy with subsequent translational consequences.

Calcium released by dying neurons mediates Iba-1 dependent polarization of microglial cells in Parkinsonian neurodegeneration

FENS Forum 2024

Cell-specific regulation of neuronal and glial glucose metabolism by neurodegeneration-associated protein TDP-43

FENS Forum 2024

Cerebellar neurodegeneration in phospholipid flippases ATP8A1/ATP8A2 double knock-out mice can be ameliorated by inactivating a microglial PS receptor

FENS Forum 2024

Is dysfunctional neuronal differentiation the link between diet and neurodegeneration?

FENS Forum 2024

Effect of DREAM inhibition on aging and neurodegeneration

FENS Forum 2024

Epigenetic modulation of astrocyte reactivity to prevent neurodegeneration

FENS Forum 2024

Exacerbation of Alzheimer’s neurodegeneration due to Aβ–NETosis cross-talk is rescued by G6PD pharmacological inhibition in neutrophils

FENS Forum 2024

GPR37 processing in neurodegeneration: A potential marker for Parkinson’s disease progression rate

FENS Forum 2024

An IgLON5 knockout mouse model results in mild behavioral alterations, without neurodegeneration

FENS Forum 2024

The impact of neurodegeneration on the electrical activity of brain tissue: Multielectrode array analysis

FENS Forum 2024

The interplay between mTORC2 and oxidative stress in neurotoxic models of neurodegeneration

FENS Forum 2024

PML is involved in microglia functions in neuroinflammation and neurodegeneration

FENS Forum 2024

The Janus faces of nanoparticles at the neurovascular unit: A double-edged sword in neurodegeneration

FENS Forum 2024

Longitudinal assessment of neurodegeneration in a mouse model of tauopathy using multiparametric magnetic resonance imaging

FENS Forum 2024

Microglial senescence: Unraveling the link to aging-related neurodegeneration in Alzheimer's disease

FENS Forum 2024

Neurodegeneration risk factors’ interplay: Characterization of APOE3 and APOE4 genotype upon chronic inflammation

FENS Forum 2024

Neuronal network dysfunction and neurodegeneration mediated by TLR7/8-activated microglia depend on the immunological context

FENS Forum 2024

NF-κB-mediated tolerant phenotype in microglia: Implications for Parkinson’s disease dopaminergic neurodegeneration

FENS Forum 2024

Novel pathways translating astrocyte-derived signalling into cell fate specification of neural progenitor cells: Relevance in neurodevelopment and neurodegeneration

FENS Forum 2024

3D organization of microglia in physiology and neurodegeneration

FENS Forum 2024

P2Y1 receptor participates in dopaminergic neurodegeneration in a rat model of Parkinson’s disease

FENS Forum 2024

The protective role of Alchornea laxiflora (Benth.) Pax & K. Hoffman extract against lead-induced neurodegeneration in cockerel chickens

FENS Forum 2024

Rate of neuromelanin accumulation in the locus coeruleus is a critical factor for neurodegeneration

FENS Forum 2024

Regulation of TMEM106b, a gene implicated in neurodegeneration, by neuronal Src kinase

FENS Forum 2024

Role of late endosomal autophagy-dependent secretion in neurodegeneration

FENS Forum 2024

Study of lipid droplets in brain aging and neurodegeneration

FENS Forum 2024

Unveiling cortical microvascular dysfunction and neurodegeneration mechanisms in experimental autoimmune encephalomyelitis

FENS Forum 2024