Engraftment of mouse embryonic stem cells differentiated by default leads to neuroprotection, behaviour revival and astrogliosis in parkinsonian rats.
Tripathy D, Haobam R, Nair R, Mohanakumar KP
Transplanting mouse stem cells that were grown into dopamine-producing neurons protected rats with Parkinson's-like symptoms, improved movement, and boosted brain recovery, likely due to support from astrocytes and growth factors. The cells survived better when pre-differentiated for 7 days before transplant.
- Pre-differentiated stem cells improved Parkinson's symptoms in rats
- Grafted cells survived and boosted dopamine levels
- Astrocytes and growth factors helped repair brain function
- 7-day differentiated cells worked better than undifferentiated ones
- Microglia may limit long-term graft survival
Activation of developmental nuclear fibroblast growth factor receptor 1 signaling and neurogenesis in adult brain by α7 nicotinic receptor agonist.
Narla ST, Klejbor I, Birkaya B, Lee YW, Morys J, Stachowiak EK, Prokop D, Bencherif M, Stachowiak MK
Activating a specific brain receptor with a drug called TC-7020 boosts the movement of a key protein into the nucleus of brain stem cells, turning them into new neurons in adult mice. This process involves a pathway linked to NR4A2 (Nurr1), a gene critical in brain development and function, and may help treat brain injuries and neurodevelopmental conditions like NR4A2-related syndrome.
- TC-7020 activates brain stem cell conversion into neurons
- It triggers nuclear FGFR1 and NR4A2/Nurr1 signaling
- New neurons form in key brain areas including substantia nigra
- The effect is linked to a known neurodevelopmental gene pathway
- Potential for treating NR4A2-related disorders
MicroRNA profiling and the role of microRNA-132 in neurodegeneration using a rat model.
Lungu G, Stoica G, Ambrus A
MicroRNA-132 is increased in a rat model of neurodegeneration, leading to reduced levels of Nurr1, a protein critical for dopamine neuron development and function. This suggests miR-132 may disrupt brain health by suppressing Nurr1 and its downstream target BDNF.
- miR-132 is elevated in neurodegenerative rats
- Nurr1 protein levels are reduced in brain neurons
- BDNF, a key brain growth factor, is also decreased
- miR-132 may disrupt dopamine neuron development
- Findings link miR-132 to Nurr1 regulation in neurodegeneration
Nurr1 represses tyrosine hydroxylase expression via SIRT1 in human neural stem cells.
Kim TE, Seo JS, Yang JW, Kim MW, Kausar R, Joe E, Kim BY, Lee MA
Nurr1 can either activate or repress the gene for tyrosine hydroxylase (TH) in human neural stem cells, depending on the presence of SIRT1, a protein that helps turn off gene activity. In cells where SIRT1 is in the nucleus, Nurr1 represses TH, which may affect dopamine production during brain development. This switch may help fine-tune dopamine neuron formation in humans.
- Nurr1 represses TH gene in human neural stem cells
- SIRT1 in the nucleus enables Nurr1 to repress TH
- SIRT1 inhibition reverses Nurr1's repression
- Nurr1's role depends on cell type and SIRT1 location
- This mechanism may control dopamine neuron development
α7 nicotinic receptor agonist reactivates neurogenesis in adult brain.
Narla S, Klejbor I, Birkaya B, Lee YW, Morys J, Stachowiak EK, Terranova C, Bencherif M, Stachowiak MK
Activating the α7 nicotinic receptor with a drug called TC-7020 boosts the creation of new neurons in the adult brain, including in areas linked to movement and memory, by turning on a key developmental pathway involving FGFR1 and Nurr1. This process may help repair brain damage or treat conditions like Parkinson’s and neurodevelopmental disorders.
- TC-7020 reactivates neuron production in adult brains
- New neurons form in brain regions critical for movement and memory
- The drug works by activating FGFR1 and Nurr1 signaling
- This pathway is normally active during development but dormant in adults
- Potential for treating brain injuries and neurodegenerative diseases
Improved cell therapy protocols for Parkinson's disease based on differentiation efficiency and safety of hESC-, hiPSC-, and non-human primate iPSC-derived dopaminergic neurons.
Sundberg M, Bogetofte H, Lawson T, Jansson J, Smith G, Astradsson A, Moore M, Osborn T, Cooper O, Spealman R, Hallett P, Isacson O
This study developed a safer and more efficient way to grow dopamine-producing brain cells from stem cells, showing that sorting specific cells improves their ability to restore movement in animal models of Parkinson's disease and survive long-term without immune drugs. The method enriches cells with key genes linked to healthy brain development, including NURR1, which is relevant to NR4A2-related syndrome.
- Sorting NCAM+/CD29low cells boosts dopamine neuron quality
- These cells express NURR1 and other critical brain genes
- They restore movement in Parkinson's rats after transplant
- Cells survived a year in primates without immune drugs
- Method improves safety and effectiveness for cell therapy
Nuclear receptor-mediated regulation of lipid droplet-associated protein gene expression in adipose tissue.
Christian M
This study shows that nuclear receptors, including NURR1, help control genes that manage fat storage in fat cells by regulating the proteins on lipid droplets. These receptors influence how much fat cells store and how droplets grow, which is relevant to conditions like obesity and lipodystrophy.
- NURR1 and other nuclear receptors regulate fat-storing proteins in fat cells
- These receptors control lipid droplet size and fat storage capacity
- PPARγ and NURR1 bind to genes that shape fat cell function
- Findings may help treat disorders of fat metabolism
- Lipid droplet regulation is key in obesity and lipodystrophy
Specification of dopaminergic subsets involves interplay of En1 and Pitx3.
Veenvliet JV, Dos Santos MT, Kouwenhoven WM, von Oerthel L, Lim JL, van der Linden AJ, Koerkamp MJ, Holstege FC, Smidt MP
En1 and Pitx3 work together to guide the development of specific dopamine neurons in the brain, with their interaction critical for forming the part of the brain affected in Parkinson's disease. Disruptions in this process lead to neuron loss similar to what happens in Parkinson's, highlighting a key mechanism behind the disease's specific vulnerability.
- En1 and Pitx3 jointly shape dopamine neurons in the brain
- Their interaction determines which neurons survive and function
- Disruption mimics Parkinson's disease neuron loss
- This process may explain why Parkinson's targets specific brain areas
- The findings could inform future treatments for Parkinson's
Correlation of Nr4a2 expression with the neuron progenitors in adult zebrafish brain.
Chen S, Luo GR, Li T, Liu TX, Le W
Nr4a2 is active in neural stem cells in adult zebrafish and helps guide the development of dopamine-producing neurons, especially in areas linked to brain function. Its levels drop with age, which may relate to neurodegeneration.
- Nr4a2 marks dopamine neuron progenitors in zebrafish brain
- It helps control the formation of dopamine neurons from stem cells
- Nr4a2 declines with aging in key brain regions
- This decline may connect to neurodegenerative processes
- Zebrafish findings may inform human NR4A2-related conditions
NGF-induced cell differentiation and gene activation is mediated by integrative nuclear FGFR1 signaling (INFS).
Lee YW, Stachowiak EK, Birkaya B, Terranova C, Capacchietti M, Claus P, Aletta JM, Stachowiak MK
This study shows that nerve growth factor (NGF) triggers neuronal development by activating a nuclear signaling pathway involving FGFR1 and the NR4A2-related proteins Nurr1 and Nur77. The findings reveal that FGFR1 moves into the nucleus, where it works with Nurr1/Nur77 to turn on genes critical for neuron formation and function.
- NGF activates nuclear FGFR1 signaling to drive neuron development
- FGFR1 works with Nurr1 and Nur77 to turn on key neuronal genes
- Blocking nuclear FGFR1 stops NGF from promoting neuron growth
- This pathway links NGF to NR4A2-related gene regulation
- Suggests a potential target for therapies in NR4A2-related disorders
A New Experimental Model for Neuronal and Glial Differentiation Using Stem Cells Derived from Human Exfoliated Deciduous Teeth.
Jarmalavičiūtė A, Tunaitis V, Strainienė E, Aldonytė R, Ramanavičius A, Venalis A, Magnusson KE, Pivoriūnas A
Stem cells from baby teeth can be turned into both neurons and glial cells in the lab, offering a new tool to study brain development and test treatments for neurological conditions, including those involving dopamine-producing neurons.
- Baby tooth stem cells become neurons and glial cells in lab tests
- Cells express markers for sensory, sympathetic, and dopamine neurons
- Key genes for nerve development and myelination are activated
- Protocol creates mixed neural cultures useful for research
- Potential for modeling brain disorders and testing therapies
Neuronal development genes are key elements mediating the reinforcing effects of methamphetamine, amphetamine, and methylphenidate.
Dela Peña I, Jeon SJ, Lee E, Ryu JH, Shin CY, Noh M, Cheong JH
Genes involved in brain development, including NR4A2, are activated in response to methamphetamine, amphetamine, and methylphenidate, suggesting they play a key role in how these drugs affect the brain and may influence addiction risk.
- NR4A2 is among brain development genes linked to stimulant effects
- These genes are upregulated in the striatum after stimulant exposure
- The same genes are also seen in response to morphine in mice
- This suggests a shared molecular pathway for addiction vulnerability
- Findings may inform future treatments targeting brain development genes
A novel strategy to increase the proliferative potential of adult human β-cells while maintaining their differentiated phenotype.
Aly H, Rohatgi N, Marshall CA, Grossenheider TC, Miyoshi H, Stappenbeck TS, Matkovich SJ, McDaniel ML
This study found a way to make adult human insulin-producing cells multiply much more while keeping their ability to make and release insulin. The method uses a special growth medium and drugs that activate key cell signals and block others, leading to a 20-fold increase in cell division without harming cell function.
- A combination of growth factors and inhibitors boosts human beta-cell division 20-fold
- Cells maintain insulin production and glucose response after treatment
- The approach activates multiple key cell signaling pathways together
- No loss of beta-cell identity or function was observed
- Results suggest potential for regenerating insulin-making cells
Late maternal hypothyroidism alters the expression of Camk4 in neocortical subplate neurons: a comparison with Nurr1 labeling.
Navarro D, Alvarado M, Morte B, Berbel D, Sesma J, Pacheco P, Morreale de Escobar G, Bernal J, Berbel P
Low thyroid levels in mothers during late pregnancy delay the normal shutdown of a key brain protein (Camk4) in developing brain cells, which may disrupt brain wiring and contribute to learning and attention problems in children, especially preterm infants.
- Low maternal thyroid levels delay brain protein changes in newborns
- This delay may affect brain connectivity and function
- Preterm babies are especially at risk due to lack of maternal thyroid support
- Camk4 and Nurr1 proteins are disrupted in brain development
- These changes may underlie attention and learning issues
Three-dimensional neural differentiation of embryonic stem cells with ACM induction in microfibrous matrices in bioreactors.
Liu N, Ouyang A, Li Y, Yang ST
This study developed a scalable method to grow neural cells from mouse stem cells using 3D microfibrous matrices in bioreactors, producing high-quality neural cells with key markers like Nurr1 and tyrosine hydroxylase, which are relevant to NR4A2-related disorders.
- 3D stem cell cultures produce more neural cells than traditional 2D methods
- The process uses bioreactors for scalable, high-purity neural cell production
- Key genes like Nurr1 and tyrosine hydroxylase are upregulated
- No embryoid bodies needed, simplifying the process
- Results support future development of cell-based therapies
Rapid generation of functional dopaminergic neurons from human induced pluripotent stem cells through a single-step procedure using cell lineage transcription factors.
Theka I, Caiazzo M, Dvoretskova E, Leo D, Ungaro F, Curreli S, Managò F, Dell'Anno MT, Pezzoli G, Gainetdinov RR, Dityatev A, Broccoli V
This study developed a fast method to turn human stem cells into dopamine-producing brain cells in just 21 days using three key genes, including NURR1, which is directly linked to NR4A2-related syndrome. The resulting neurons are mature, electrically active, and release dopamine, making them useful for studying the condition and testing treatments.
- Creates dopamine neurons in 21 days using NURR1 and two other genes
- Over 93% efficiency in turning stem cells into dopamine neurons
- Neurons show real brain cell functions like firing and dopamine release
- Ideal for modeling NR4A2-related disorders and drug testing
- Bypasses slow, complex steps used in older methods
Rotenone could activate microglia through NFκB associated pathway.
Yuan YH, Sun JD, Wu MM, Hu JF, Peng SY, Chen NH
Rotenone, a pesticide linked to Parkinson's disease, activates brain immune cells called microglia through a specific inflammatory pathway. This activation increases harmful brain inflammation and reduces levels of a protective protein called Nurr1, which is important for brain cell health.
- Rotenone triggers brain inflammation via microglia activation
- It boosts inflammatory signals linked to Parkinson's disease
- Rotenone reduces Nurr1, a key protective protein
- The NFκB pathway is central to this harmful process
- This suggests environmental toxins may worsen neurodegeneration
Foxa1 and foxa2 are required for the maintenance of dopaminergic properties in ventral midbrain neurons at late embryonic stages.
Stott SR, Metzakopian E, Lin W, Kaestner KH, Hen R, Ang SL
Foxa1 and Foxa2 genes are essential for maintaining the dopamine-producing identity of midbrain neurons in late embryonic development, not just their initial formation. Without these genes, neurons lose their ability to produce dopamine, even though they survive and remain in the brain for years.
- Foxa1 and Foxa2 maintain dopamine traits in midbrain neurons
- Loss leads to reduced dopamine-producing neurons in the substantia nigra
- Neurons survive but lose dopamine function, not due to cell death
- Nurr1 fails to bind to the dopamine gene promoter without Foxa1/2
- Findings suggest a lifelong role for Foxa genes in dopamine neuron stability
Conditioned medium from human amniotic epithelial cells may induce the differentiation of human umbilical cord blood mesenchymal stem cells into dopaminergic neuron-like cells.
Yang S, Sun HM, Yan JH, Xue H, Wu B, Dong F, Li WS, Ji FQ, Zhou DS
Conditioned medium from human amniotic cells can turn umbilical cord stem cells into dopamine-producing cells, which may help treat Parkinson's disease. This process involves key growth factors like BDNF and NGF, and the resulting cells improved symptoms in Parkinson's rats.
- Amniotic cell medium turns stem cells into dopamine cells
- BDNF and NGF help drive this transformation
- Treated cells improved movement in Parkinson's rats
- Uses ethical, easily available stem cells
- Potential for future Parkinson's cell therapy
Intracranial self-stimulation facilitates active-avoidance retention and induces expression of c-Fos and Nurr1 in rat brain memory systems.
Aldavert-Vera L, Huguet G, Costa-Miserachs D, Ortiz SP, Kádár E, Morgado-Bernal I, Segura-Torres P
In rats, giving brain stimulation right after learning improves memory retention and increases activity in brain regions linked to memory and plasticity. This stimulation boosts levels of two key proteins, c-Fos and Nurr1, especially in the hippocampus, which may help strengthen memory formation.
- Brain stimulation after learning improves memory in rats
- Stimulation increases c-Fos and Nurr1 in memory brain areas
- Nurr1 rise in hippocampus may support memory consolidation
- Combined learning and stimulation boosts brain activity more
- Findings suggest a pathway for enhancing memory through brain activity
Early life permethrin exposure induces long-term brain changes in Nurr1, NF-kB and Nrf-2.
Carloni M, Nasuti C, Fedeli D, Montani M, Vadhana MS, Amici A, Gabbianelli R
Early exposure to permethrin in rats causes lasting changes in brain genes linked to dopamine function and aging, including reduced Nurr1 in the striatum and altered NF-kB and Nrf-2 activity, which may increase risk for neurodegenerative issues later in life.
- Permethrin exposure in early life alters Nurr1, NF-kB, and Nrf-2 genes
- Changes persist into old age, affecting brain regions tied to movement and cognition
- Nurr1 disruption may increase risk for dopamine-related brain disorders
- Altered inflammation and antioxidant pathways suggest accelerated brain aging
- Findings highlight environmental risks for neurodevelopmental and neurodegenerative conditions
Chronic co-administration of nicotine and methamphetamine causes differential expression of immediate early genes in the dorsal striatum and nucleus accumbens of rats.
Saint-Preux F, Bores LR, Tulloch I, Ladenheim B, Kim R, Thanos PK, Volkow ND, Cadet JL
Chronic use of nicotine and methamphetamine together alters the expression of immediate early genes in brain regions linked to reward and addiction, with changes in NR4A2 (NURR1) and related genes that may influence long-term brain adaptations. These findings suggest the combination of drugs has unique effects on gene activity compared to either drug alone.
- Nicotine and methamphetamine together change gene activity in reward brain areas
- NR4A2 (NURR1) levels increase in the striatum with both drugs
- Combination use alters multiple genes differently than single drugs
- These changes may contribute to the strong co-use of nicotine and methamphetamine
- Findings highlight potential molecular targets for treating co-addiction
Morphine administration modulates expression of Argonaute 2 and dopamine-related transcription factors involved in midbrain dopaminergic neurons function.
García-Pérez D, Sáez-Belmonte F, Laorden ML, Núñez C, Milanés MV
Morphine use and withdrawal affect key brain proteins involved in dopamine regulation, with changes in Nurr1 and Pitx3 potentially helping protect dopamine function during withdrawal. These findings suggest that the brain's response to opioid exposure involves complex adjustments in gene regulation and dopamine control.
- Morphine increases dopamine activity and Nurr1/Pitx3 in the brain's reward center
- Withdrawal reduces dopamine activity and lowers Ago2, a key gene regulator
- Increased Nurr1 and Pitx3 may help stabilize dopamine function during withdrawal
- These changes could influence behavior and addiction-related processes
Intellectual disability and hemizygous GPD2 mutation.
Barge-Schaapveld DQ, Ofman R, Knegt AC, Alders M, Höhne W, Kemp S, Hennekam RC
A woman with intellectual disability and developmental delays has a rare mutation in the GPD2 gene, which appears to reduce enzyme activity, but the link to her condition is not fully proven. The mutation is inherited from her unaffected mother and sister, suggesting it may not be the sole cause. Functional testing confirmed reduced GPD2 activity in the patient, but more evidence is needed to confirm causation.
- GPD2 mutation linked to reduced enzyme activity in patient
- Mutation inherited from unaffected mother and sister
- Functional testing shows 50% activity in carriers
- Causal link to intellectual disability remains uncertain
- Need for international databases to confirm gene variants
Altered gene expression in the dorsolateral prefrontal cortex of individuals with schizophrenia.
Guillozet-Bongaarts AL, Hyde TM, Dalley RA, Hawrylycz MJ, Henry A, Hof PR, Hohmann J, Jones AR, Kuan CL, Royall J, Shen E, Swanson B, Zeng H, Kleinman JE
People with schizophrenia show specific changes in gene activity in a key brain region involved in thinking and behavior, especially in one part of the prefrontal cortex. The gene NR4A2 is among those altered, suggesting it may play a role in the disorder’s brain changes.
- NR4A2 gene expression is altered in schizophrenia brains
- Changes are mainly in brain area 9, not area 46
- GABA-related genes are also affected
- These findings point to specific brain circuit disruptions
- High-throughput imaging helps identify affected genes
Nuclear receptor NR4A2 orchestrates Th17 cell-mediated autoimmune inflammation via IL-21 signalling.
Raveney BJ, Oki S, Yamamura T
NR4A2 is a key regulator of Th17 cells, which drive autoimmune diseases like multiple sclerosis and uveitis. Blocking NR4A2 stops these cells from producing harmful cytokines, reduces inflammation, and protects against disease in animal models, suggesting NR4A2 could be a target for treating autoimmune conditions.
- NR4A2 controls Th17 cell development and function
- Blocking NR4A2 reduces IL-17 and IL-21 production
- NR4A2 inhibition protects mice from autoimmune disease
- IL-21 can restore Th17 cells if NR4A2 is blocked
- NR4A2 is elevated in human autoimmune diseases
Systemic administration of valproic acid and zonisamide promotes differentiation of induced pluripotent stem cell-derived dopaminergic neurons.
Yoshikawa T, Samata B, Ogura A, Miyamoto S, Takahashi J
Giving valproic acid and zonisamide to rats after transplanting stem cell-derived dopamine neurons improved the survival and maturation of those neurons in the brain, suggesting these approved drugs could help make stem cell therapies more effective for Parkinson's disease.
- Valproic acid and zonisamide boosted dopamine neuron survival
- Both drugs increased mature midbrain dopamine neurons
- Effects seen in both lab and live animal studies
- Drugs are already approved for human use
- Findings may improve stem cell treatments for Parkinson's
The N-terminal region of Nurr1 (a.a 1-31) is essential for its efficient degradation by the ubiquitin proteasome pathway.
Alvarez-Castelao B, Losada F, Ahicart P, Castaño JG
The Nurr1 protein is broken down by the cell's waste system, and its first 31 amino acids are crucial for this process. Removing this region makes Nurr1 more stable and longer-lasting in cells, without reducing its function, making it a promising candidate for therapies targeting Parkinson's disease.
- The first 31 amino acids of Nurr1 trigger its breakdown
- Deleting these amino acids makes Nurr1 last longer in cells
- The modified Nurr1 works just as well in gene regulation
- This stable version could improve gene or cell-based Parkinson's treatments
- Nurr1 stability may be key to effective therapies
An intra-articular salmon calcitonin-based nanocomplex reduces experimental inflammatory arthritis.
Ryan SM, McMorrow J, Umerska A, Patel HB, Kornerup KN, Tajber L, Murphy EP, Perretti M, Corrigan OI, Brayden DJ
A nanocomplex combining salmon calcitonin and hyaluronic acid reduces joint inflammation and NR4A2 expression in a mouse model of arthritis when injected directly into the joint. The treatment preserved bone structure and showed strong anti-inflammatory effects by targeting a key gene involved in inflammation.
- NR4A2 is a key gene driving inflammation in arthritis.
- Salmon calcitonin and hyaluronic acid together reduce NR4A2 levels.
- Nanoparticles deliver the treatment effectively into joints.
- Treatment reduced inflammation and protected bone in mice.
- This approach may lead to new arthritis therapies targeting NR4A2.
Dopaminergic cells, derived from a high efficiency differentiation protocol from umbilical cord derived mesenchymal stem cells, alleviate symptoms in a Parkinson's disease rodent model.
Shetty P, Thakur AM, Viswanathan C
Dopamine-producing cells made from umbilical cord stem cells improved Parkinson's symptoms in rats for up to a year, suggesting a promising cell therapy approach that may be safer and more effective than using undifferentiated stem cells.
- Umbilical cord stem cells can become dopamine-producing cells
- These cells reduced Parkinson's symptoms in rats for a full year
- Differentiated cells worked better than undifferentiated ones
- The cells are less likely to cause immune reactions
- This could lead to new treatments using donor stem cells
Human Stem Cell Derivatives Retain More Open Epigenomic Landscape When Derived from Pluripotent Cells than from Tissues.
Parsons XH
Stem cells made from human embryonic stem cells have a more open and flexible epigenome compared to those taken directly from brain tissue, meaning they retain greater potential to become different types of cells, which may improve their ability to regenerate damaged tissue.
- Stem cells from embryonic sources have a more open epigenome
- This openness supports greater developmental flexibility
- Cells from brain tissue are more epigenetically restricted
- Open chromatin may enhance regenerative potential
- In vitro-derived cells may be better for cell therapy
PIASγ enhanced SUMO-2 modification of Nurr1 activation-function-1 domain limits Nurr1 transcriptional synergy.
Arredondo C, Orellana M, Vecchiola A, Pereira LA, Galdames L, Andrés ME
Nurr1, a key protein for brain dopamine neurons, is turned down by a process called SUMOylation at a specific site (lysine 91) when modified by SUMO-2, which is controlled by a protein called PIASγ. This modification reduces Nurr1's ability to activate genes, especially on complex gene promoters, and may explain why Nurr1 function is limited in some conditions. The study identifies two ways PIASγ suppresses Nurr1, one through SUMOylation and another through direct binding without needing its enzyme activity.
- SUMO-2 modifies Nurr1 at lysine 91, reducing its activity
- PIASγ boosts this modification and represses Nurr1
- Blocking SUMOylation increases Nurr1 activity on complex gene promoters
- PIASγ represses Nurr1 in two separate ways
- This regulation may affect dopamine neuron development and function
Transcription factor Nurr1 maintains fiber integrity and nuclear-encoded mitochondrial gene expression in dopamine neurons.
Kadkhodaei B, Alvarsson A, Schintu N, Ramsköld D, Volakakis N, Joodmardi E, Yoshitake T, Kehr J, Decressac M, Björklund A, Sandberg R, Svenningsson P, Perlmann T
Nurr1 is essential for maintaining the health and function of dopamine neurons, particularly by supporting mitochondrial energy production and preventing axon and dendrite damage. Loss of Nurr1 leads to symptoms similar to early Parkinson's disease, including motor problems and reduced dopamine levels.
- Nurr1 keeps dopamine neurons healthy and functioning
- It supports mitochondrial energy production in these neurons
- Without Nurr1, neurons develop damage and lose function
- This mirrors early Parkinson's disease changes
- Nurr1 loss leads to motor and dopamine deficits
Wnt5a cooperates with canonical Wnts to generate midbrain dopaminergic neurons in vivo and in stem cells.
Andersson ER, Saltó C, Villaescusa JC, Cajanek L, Yang S, Bryjova L, Nagy II, Vainio SJ, Ramirez C, Bryja V, Arenas E
Wnt1 and Wnt5a work together to generate midbrain dopamine neurons in living animals and in stem cells, and combining both signals improves the production of these neurons from stem cells, which could help develop better stem cell therapies for Parkinson's disease.
- Wnt1 and Wnt5a cooperate to build dopamine neurons
- Loss of both genes causes greater neuron loss than either alone
- Combining Wnt signals boosts dopamine neuron production from stem cells
- This approach may improve stem cell treatments for Parkinson’s disease