TY  - JOUR
AB  - NMDA receptors (NMDARs) are ionotropic receptors crucial for brain information processing. Yet, evidence also supports an ion-flux-independent signaling mode mediating synaptic long-term depression (LTD) and spine shrinkage. Here, we identify AETA (Aη), an amyloid-β precursor protein (APP) cleavage product, as an NMDAR modulator with the unique dual regulatory capacity to impact both signaling modes. AETA inhibits ionotropic NMDAR activity by competing with the co-agonist and induces an intracellular conformational modification of GluN1 subunits. This favors non-ionotropic NMDAR signaling leading to enhanced LTD and favors spine shrinkage. Endogenously, AETA production is increased by in vivo chemogenetically induced neuronal activity. Genetic deletion of AETA production alters NMDAR transmission and prevents LTD, phenotypes rescued by acute exogenous AETA application. This genetic deletion also impairs contextual fear memory. Our findings demonstrate AETA-dependent NMDAR activation (ADNA), characterizing AETA as a unique type of endogenous NMDAR modulator that exerts bidirectional control over NMDAR signaling and associated information processing.
AU  - Dunot, J.*
AU  - Moreno, S.G.*
AU  - Gandin, C.*
AU  - Pousinha, P.A.*
AU  - Amici, M.*
AU  - Dupuis, J.*
AU  - Anisimova, M.*
AU  - Winschel, A.*
AU  - Uriot, M.*
AU  - Petshow, S.J.*
AU  - Mensch, M.*
AU  - Bethus, I.*
AU  - Giudici, C.*
AU  - Hampel, H.*
AU  - Wefers, B.
AU  - Wurst, W.
AU  - Naumann, R.*
AU  - Ashby, M.C.*
AU  - Laube, B.*
AU  - Zito, K.*
AU  - Mellor, J.R.*
AU  - Groc, L.*
AU  - Willem, M.*
AU  - Marie, H.*
C1  - 70845
C2  - 55763
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 2708-2720.e9
TI  - APP fragment controls both ionotropic and non-ionotropic signaling of NMDA receptors.
JO  - Neuron
VL  - 112
IS  - 16
PB  - Cell Press
PY  - 2024
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Glucocorticoids are important for proper organ maturation, and their levels are tightly regulated during development. Here, we use human cerebral organoids and mice to study the cell-type-specific effects of glucocorticoids on neurogenesis. We show that glucocorticoids increase a specific type of basal progenitors (co-expressing PAX6 and EOMES) that has been shown to contribute to cortical expansion in gyrified species. This effect is mediated via the transcription factor ZBTB16 and leads to increased production of neurons. A phenome-wide Mendelian randomization analysis of an enhancer variant that moderates glucocorticoid-induced ZBTB16 levels reveals causal relationships with higher educational attainment and altered brain structure. The relationship with postnatal cognition is also supported by data from a prospective pregnancy cohort study. This work provides a cellular and molecular pathway for the effects of glucocorticoids on human neurogenesis that relates to lasting postnatal phenotypes.
AU  - Krontira, A.C.*
AU  - Cruceanu, C.*
AU  - Dony, L.
AU  - Kyrousi, C.*
AU  - Link, M.H.*
AU  - Rek, N.*
AU  - Pöhlchen, D.*
AU  - Raimundo, C.*
AU  - Penner-Goeke, S.*
AU  - Schowe, A.*
AU  - Czamara, D.*
AU  - Lahti-Pulkkinen, M.*
AU  - Sammallahti, S.*
AU  - Wolford, E.*
AU  - Heinonen, K.*
AU  - Roeh, S.*
AU  - Sportelli, V.*
AU  - Wölfel, B.*
AU  - Ködel, M.*
AU  - Sauer, S.*
AU  - Rex-Haffner, M.*
AU  - Räikkönen, K.*
AU  - Labeur, M.*
AU  - Cappello, S.*
AU  - Binder, E.B.*
C1  - 70187
C2  - 55448
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 1426-1443.e11
TI  - Human cortical neurogenesis is altered via glucocorticoid-mediated regulation of ZBTB16 expression.
JO  - Neuron
VL  - 112
IS  - 9
PB  - Cell Press
PY  - 2024
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Mitochondria account for essential cellular pathways, from ATP production to nucleotide metabolism, and their deficits lead to neurological disorders and contribute to the onset of age-related diseases. Direct neuronal reprogramming aims at replacing neurons lost in such conditions, but very little is known about the impact of mitochondrial dysfunction on the direct reprogramming of human cells. Here, we explore the effects of mitochondrial dysfunction on the neuronal reprogramming of induced pluripotent stem cell (iPSC)-derived astrocytes carrying mutations in the NDUFS4 gene, important for Complex I and associated with Leigh syndrome. This led to the identification of the unfolded protein response as a major hurdle in the direct neuronal conversion of not only astrocytes and fibroblasts from patients but also control human astrocytes and fibroblasts. Its transient inhibition potently improves reprogramming by influencing the mitochondria-endoplasmic-reticulum-stress-mediated pathways. Taken together, disease modeling using patient cells unraveled novel general hurdles and ways to overcome these in human astrocyte-to-neuron reprogramming.
AU  - Sonsalla, G.
AU  - Malpartida, A.B.
AU  - Riedemann, T.*
AU  - Gusic, M.
AU  - Rusha, E.
AU  - Bulli, G.
AU  - Najas, S.
AU  - Janjic, A.*
AU  - Hersbach, B.A.
AU  - Smialowski, P.
AU  - Drukker, M.
AU  - Enard, W.*
AU  - Prehn, J.H.M.*
AU  - Prokisch, H.
AU  - Götz, M.
AU  - Masserdotti, G.
C1  - 69869
C2  - 55295
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 1117-1132.e9
TI  - Direct neuronal reprogramming of NDUFS4 patient cells identifies the unfolded protein response as a novel general reprogramming hurdle.
JO  - Neuron
VL  - 112
IS  - 7
PB  - Cell Press
PY  - 2024
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Cortical projection neurons polarize and form an axon while migrating radially. Even though these dynamic processes are closely interwoven, they are regulated separately-the neurons terminate their migration when reaching their destination, the cortical plate, but continue to grow their axons. Here, we show that in rodents, the centrosome distinguishes these processes. Newly developed molecular tools modulating centrosomal microtubule nucleation combined with in vivo imaging uncovered that dysregulation of centrosomal microtubule nucleation abrogated radial migration without affecting axon formation. Tightly regulated centrosomal microtubule nucleation was required for periodic formation of the cytoplasmic dilation at the leading process, which is essential for radial migration. The microtubule nucleating factor γ-tubulin decreased at neuronal centrosomes during the migratory phase. As distinct microtubule networks drive neuronal polarization and radial migration, this provides insight into how neuronal migratory defects occur without largely affecting axonal tracts in human developmental cortical dysgeneses, caused by mutations in γ-tubulin.
AU  - Vinopal, S.*
AU  - Dupraz, S.*
AU  - Alfadil, E.*
AU  - Pietralla, T.*
AU  - Bendre, S.*
AU  - Stiess, M.*
AU  - Falk, S.
AU  - Camargo Ortega, G.
AU  - Maghelli, N.*
AU  - Tolić, I.M.*
AU  - Smejkal, J.*
AU  - Götz, M.
AU  - Bradke, F.*
C1  - 67467
C2  - 54122
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 1241-1263.e16
TI  - Centrosomal microtubule nucleation regulates radial migration of projection neurons independently of polarization in the developing brain.
JO  - Neuron
VL  - 111
IS  - 8
PB  - Cell Press
PY  - 2023
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Differentiated cells have long been considered fixed in their identity. However, about 20 years ago, the first direct conversion of glial cells into neurons in vitro opened the field of “direct neuronal reprogramming.” Since then, neuronal reprogramming has achieved the generation of fully functional, mature neurons with remarkable efficiency, even in diseased brain environments. Beyond their clinical implications, these discoveries provided basic insights into crucial mechanisms underlying conversion of specific cell types into neurons and maintenance of neuronal identity. Here we discuss such principles, including the importance of the starter cell for shaping the outcome of neuronal reprogramming. We further highlight technical concerns for in vivo reprogramming and propose a code of conduct to avoid artifacts and pitfalls. We end by pointing out next challenges for development of less invasive cell replacement therapies for humans.
AU  - Bocchi, R.
AU  - Masserdotti, G.
AU  - Götz, M.
C1  - 63862
C2  - 51727
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 366-393
TI  - Direct neuronal reprogramming: Fast forward from new concepts toward therapeutic approaches.
JO  - Neuron
VL  - 110
IS  - 3
PB  - Cell Press
PY  - 2022
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - PTEN-induced kinase 1 (PINK1) is a short-lived protein required for the removal of damaged mitochondria through Parkin translocation and mitophagy. Because the short half-life of PINK1 limits its ability to be trafficked into neurites, local translation is required for this mitophagy pathway to be active far from the soma. The Pink1 transcript is associated and cotransported with neuronal mitochondria. In concert with translation, the mitochondrial outer membrane proteins synaptojanin 2 binding protein (SYNJ2BP) and synaptojanin 2 (SYNJ2) are required for tethering Pink1 mRNA to mitochondria via an RNA-binding domain in SYNJ2. This neuron-specific adaptation for the local translation of PINK1 provides distal mitochondria with a continuous supply of PINK1 for the activation of mitophagy.
AU  - Harbauer, A.B.*
AU  - Hees, J.T.*
AU  - Wanderoy, S.*
AU  - Segura, I.*
AU  - Gibbs, W.*
AU  - Cheng, Y.
AU  - Ordonez, M.*
AU  - Cai, Z.*
AU  - Cartoni, R.*
AU  - Ashrafi, G.*
AU  - Wang, C.*
AU  - Perocchi, F.
AU  - He, Z.*
AU  - Schwarz, T.L.*
C1  - 64542
C2  - 51935
SP  - 1516-1531.e9
TI  - Neuronal mitochondria transport Pink1 mRNA via synaptojanin 2 to support local mitophagy.
JO  - Neuron
VL  - 110
IS  - 9
PY  - 2022
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - A single sub-anesthetic dose of ketamine produces a rapid and sustained antidepressant response, yet the molecular mechanisms responsible for this remain unclear. Here, we identified cell-type-specific transcriptional signatures associated with a sustained ketamine response in mice. Most interestingly, we identified the Kcnq2 gene as an important downstream regulator of ketamine action in glutamatergic neurons of the ventral hippocampus. We validated these findings through a series of complementary molecular, electrophysiological, cellular, pharmacological, behavioral, and functional experiments. We demonstrated that adjunctive treatment with retigabine, a KCNQ activator, augments ketamine's antidepressant-like effects in mice. Intriguingly, these effects are ketamine specific, as they do not modulate a response to classical antidepressants, such as escitalopram. These findings significantly advance our understanding of the mechanisms underlying the sustained antidepressant effects of ketamine, with important clinical implications.
AU  - Lopez, J.P.*
AU  - Luecken, M.
AU  - Brivio, E.*
AU  - Karamihalev, S.*
AU  - Kos, A.*
AU  - De Donno, C.
AU  - Benjamin, A.*
AU  - Yang, H.*
AU  - Dick, A.L.W.*
AU  - Stoffel, R.*
AU  - Flachskamm, C.*
AU  - Ressle, A.*
AU  - Roeh, S.*
AU  - Huettl, R.E.*
AU  - Parl, A.*
AU  - Eggert, C.*
AU  - Novak, B.*
AU  - Yan, Y.*
AU  - Yeoh, K.*
AU  - Holzapfel, M.*
AU  - Hauger, B.*
AU  - Harbich, D.*
AU  - Schmid, B.*
AU  - Di Giaimo, R.*
AU  - Turck, C.W.*
AU  - Schmidt, M.V.*
AU  - Deussing, J.M.*
AU  - Eder, M.*
AU  - Dine, J.*
AU  - Theis, F.J.
AU  - Chen, A.*
C1  - 65472
C2  - 52313
SP  - 2283-2298.e9
TI  - Ketamine exerts its sustained antidepressant effects via cell-type-specific regulation of Kcnq2.
JO  - Neuron
VL  - 110
IS  - 14
PY  - 2022
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Evidence suggests interplay among the three major risk factors for Alzheimer's disease (AD): age, APOE genotype, and sex. Here, we present comprehensive datasets and analyses of brain transcriptomes and blood metabolomes from human apoE2-, apoE3-, and apoE4-targeted replacement mice across young, middle, and old ages with both sexes. We found that age had the greatest impact on brain transcriptomes highlighted by an immune module led by Trem2 and Tyrobp, whereas APOE4 was associated with upregulation of multiple Serpina3 genes. Importantly, these networks and gene expression changes were mostly conserved in human brains. Finally, we observed a significant interaction between age, APOE genotype, and sex on unfolded protein response pathway. In the periphery, APOE2 drove distinct blood metabolome profile highlighted by the upregulation of lipid metabolites. Our work identifies unique and interactive molecular pathways underlying AD risk factors providing valuable resources for discovery and validation research in model systems and humans.
AU  - Zhao, N.*
AU  - Ren, Y.*
AU  - Yamazaki, Y.*
AU  - Qiao, W.*
AU  - Li, F.*
AU  - Felton, L.M.*
AU  - MahmoudianDehkordi, S.*
AU  - Kueider-Paisley, A.*
AU  - Sonoustoun, B.*
AU  - Arnold, M.
AU  - Shue, F.*
AU  - Zheng, J.*
AU  - Attrebi, O.N.*
AU  - Martens, Y.A.*
AU  - Li, Z.*
AU  - Bastea, L.*
AU  - Meneses, A.D.*
AU  - Chen, K.*
AU  - Thompson, K.*
AU  - St John-Williams, L.*
AU  - Tachibana, M.*
AU  - Aikawa, T.*
AU  - Oue, H.*
AU  - Job, L.*
AU  - Yamazaki, A.*
AU  - Liu, C.C.*
AU  - Storz, P.*
AU  - Asmann, Y.W.*
AU  - Ertekin-Taner, N.*
AU  - Kanekiyo, T.*
AU  - Kaddurah-Daouk, R.*
AU  - Bu, G.*
C1  - 58838
C2  - 48627
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 727-742
TI  - Alzheimer's risk factors age, APOE genotype, and sex drive distinct. 3 molecular pathways.
JO  - Neuron
VL  - 106
IS  - 5
PB  - Cell Press
PY  - 2020
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Astrocytes are particularly promising candidates for reprogramming into neurons, as they maintain some of the original patterning information from their radial glial ancestors. However, to which extent the position of astrocytes influences the fate of reprogrammed neurons remains unknown. To elucidate this, we performed stab wound injury covering an entire neocortical column, including the gray matter (GM) and white matter (WM), and targeted local reactive astrocytes via injecting FLEx switch (Cre-On) adeno-associated viral (AAV) vectors into mGFAP-Cre mice. Single proneural factors were not sufficient for adequate reprogramming, although their combination with the nuclear receptor-related 1 protein (Nurr1) improved reprogramming efficiency. Nurr1 and Neurogenin 2 (Ngn2) resulted in high-efficiency reprogramming of targeted astrocytes into neurons that develop lamina-specific hallmarks, including the appropriate long-distance axonal projections. Surprisingly, in the WM, we did not observe any reprogrammed neurons, thereby unveiling a crucial role of region- and layer-specific differences in astrocyte reprogramming.
AU  - Mattugini, N.
AU  - Bocchi, R.
AU  - Scheuss, V.
AU  - Russo, G.L.
AU  - Torper, O.
AU  - Lao, C.L.
AU  - Götz, M.
C1  - 56958
C2  - 47462
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 1086-1095.e5
TI  - Inducing different neuronal subtypes from astrocytes in the injured mouse cerebral cortex.
JO  - Neuron
VL  - 103
IS  - 6
PB  - Cell Press
PY  - 2019
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - In an interview with Neuron, Magdalena Gotz highlights the responsibility of scientists to educate the public about the process of scientific discovery and how ideas evolve. She also describes how her current research on neuronal reprogramming is influenced by her earlier findings that radial glial cells give rise to neurons.
AU  - Götz, M.
C1  - 53945
C2  - 45109
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 1069-1071
TI  -   Q&A Magdalena Götz
JO  - Neuron
VL  - 98
IS  - 6
PB  - Cell Press
PY  - 2018
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.
AU  - Nicolas, A.*
AU  - Kenna, K.P.*
AU  - Renton, A.E.*
AU  - Ticozzi, N.*
AU  - Faghri, F.*
AU  - Chia, R.*
AU  - Dominov, J.A.*
AU  - Kenna, B.J.*
AU  - Nalls, M.A.*
AU  - Keagle, P.*
AU  - Rivera, A.M.*
AU  - van Rheenen, W.*
AU  - Murphy, N.A.*
AU  - van Vugt, J.J.F.A.*
AU  - Geiger, J.T.*
AU  - van der Spek, R.A.*
AU  - Pliner, H.A.*
AU  - Shankaracharya, B.N.S.*
AU  - Smith, B.N.*
AU  - Marangi, G.*
AU  - Topp, S.D.*
AU  - Abramzon, Y.*
AU  - Gkazi, A.S.*
AU  - Eicher, J.D.*
AU  - Kenna, A.*
AU  - Mora, G.*
AU  - Calvo, A.*
AU  - Mazzini, L.*
AU  - Riva, N.*
AU  - Mandrioli, J.*
AU  - Caponnetto, C.*
AU  - Battistini, S.*
AU  - Volanti, P.*
AU  - La Bella, V.*
AU  - Conforti, F.L.*
AU  - Borghero, G.*
AU  - Messina, S.*
AU  - Simone, I.L.*
AU  - Trojsi, F.*
AU  - Salvi, F.*
AU  - Logullo, F.O.*
AU  - D'Alfonso, S.*
AU  - Corrado, L.*
AU  - Capasso, M.*
AU  - Ferrucci, L.*
AU  - Moreno, C.A.M.*
AU  - Kamalakaran, S.*
AU  - Goldstein, D.B.*
AU  - Gitler, A.D.*
AU  - Harris, T.*
AU  - Myers, R.M.*
AU  - Phatnani, H.*
AU  - Musunuri, R.L.*
AU  - Evani, U.S.*
AU  - Abhyankar, A.*
AU  - Zody, M.C.*
AU  - Kaye, J.*
AU  - Finkbeiner, S.*
AU  - Wyman, S.K.*
AU  - LeNail, A.*
AU  - Lima, L.*
AU  - Fraenkel, E.*
AU  - Svendsen, C.N.*
AU  - Thompson, L.M.*
AU  - Van Eyk, J.E.*
AU  - Berry, J.D.*
AU  - Miller, T.M.*
AU  - Kolb, S.J.*
AU  - Cudkowicz, M.*
AU  - Baxi, E.*
AU  - Benatar, M.*
AU  - Taylor, J.P.*
AU  - Rampersaud, E.*
AU  - Wu, G.M.*
AU  - Wuu, J.*
AU  - Lauria, G.*
AU  - Verde, F.*
AU  - Fogh, I.*
AU  - Tiloca, C.*
AU  - Comi, G.P.*
AU  - Sorarù, G.*
AU  - Cereda, C.*
AU  - Corcia, P.*
AU  - Laaksovirta, H.*
AU  - Myllykangas, L.*
AU  - Jansson, L.*
AU  - Valori, M.*
AU  - Ealing, J.*
AU  - Hamdalla, H.*
AU  - Rollinson, S.*
AU  - Pickering-Brown, S.*
AU  - Orrell, R.W.*
AU  - Sidle, K.C.*
AU  - Malaspina, A.*
AU  - Hardy, J.*
AU  - Singleton, A.B.*
AU  - Johnson, J.O.*
AU  - Arepalli, S.*
AU  - Sapp, P.C.*
AU  - McKenna-Yasek, D.*
AU  - Polak, M.*
AU  - Asress, S.*
AU  - Al-Sarraj, S.*
AU  - King, A.*
AU  - Troakes, C.*
AU  - Vance, C.*
AU  - de Belleroche, J.*
AU  - Baas, F.*
AU  - Ten Asbroek, A.L.M.A.*
AU  - Muñoz-Blanco, J.L.*
AU  - Hernandez, D.G.*
AU  - Ding, J.*
AU  - Gibbs, J.R.*
AU  - Scholz, S.W.*
AU  - Floeter, M.K.*
AU  - Campbell, R.H.*
AU  - Landi, F.*
AU  - Bowser, R.*
AU  - Pulst, S.M.*
AU  - Ravits, J.M.*
AU  - MacGowan, D.J.L.*
AU  - Kirby, J.*
AU  - Pioro, E.P.*
AU  - Pamphlett, R.*
AU  - Broach, J.*
AU  - Gerhard, G.*
AU  - Dunckley, T.L.*
AU  - Brady, C.B.*
AU  - Kowall, N.W.*
AU  - Troncoso, J.C.*
AU  - Le Ber, I.*
AU  - Mouzat, K.*
AU  - Lumbroso, S.*
AU  - Heiman-Patterson, T.D.*
AU  - Kamel, F.*
AU  - Van Den Bosch, L.*
AU  - Baloh, R.H.*
AU  - Strom, T.M.
AU  - Meitinger, T.
AU  - Shatunov, A.*
AU  - van Eijk, K.R.*
AU  - de Carvalho, M.*
AU  - Kooyman, M.*
AU  - Middelkoop, B.*
AU  - Moisse, M.*
AU  - McLaughlin, R.L.*
AU  - van Es, M.A.*
AU  - Weber, M.*
AU  - Boylan, K.B.*
AU  - van Blitterswijk, M.*
AU  - Rademakers, R.*
AU  - Morrison, K.E.*
AU  - Basak, A.N.*
AU  - Mora, J.S.*
AU  - Drory, V.E.*
AU  - Shaw, P.J.*
AU  - Turner, M.R.*
AU  - Talbot, K.*
AU  - Hardiman, O.*
AU  - Williams, K.L.*
AU  - Fifita, J.A.*
AU  - Nicholson, G.A.*
AU  - Blair, I.P.*
AU  - Rouleau, G.A.*
AU  - Esteban-Pérez, J.*
AU  - García-Redondo, A.*
AU  - Al-Chalabi, A.*
AU  - Rogaeva, E.*
AU  - Zinman, L.*
AU  - Ostrow, L.W.*
AU  - Maragakis, N.J.*
AU  - Rothstein, J.D.*
AU  - Simmons, Z.*
AU  - Cooper-Knock, J.*
AU  - Brice, A.*
AU  - Goutman, S.A.*
AU  - Feldman, E.L.*
AU  - Gibson, S.B.*
AU  - Taroni, F.*
AU  - Ratti, A.*
AU  - Gellera, C.*
AU  - van Damme, P.*
AU  - Robberecht, W.*
AU  - Fratta, P.*
AU  - Sabatelli, M.*
AU  - Lunetta, C.*
AU  - Ludolph, A.C.*
AU  - Andersen, P.M.*
AU  - Weishaupt, J.H.*
AU  - Camu, W.*
AU  - Trojanowski, J.Q.*
AU  - van Deerlin, V.M.*
AU  - Brown, R.H.*
AU  - van den Berg, L.H.*
AU  - Veldink, J.H.*
AU  - Harms, M.B.*
AU  - Glass, J.D.*
AU  - Stone, D.J.*
AU  - Tienari, P.*
AU  - Silani, V.*
AU  - Chio, A.*
AU  - Shaw, C.E.*
AU  - Traynor, B.J.*
AU  - Landers, J.E.*
C1  - 53299
C2  - 44573
CY  - Cambridge
SP  - 1268-1283.e6
TI  - Genome-wide analyses identify KIF5A as a novel ALS gene.
JO  - Neuron
VL  - 97
IS  - 6
PB  - Cell Press
PY  - 2018
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Flatworms of the species Schmidtea mediterranea are immortal-adult animals contain a large pool of pluripotent stem cells that continuously differentiate into all adult cell types. Therefore, single-cell transcriptome profiling of adult animals should reveal mature and progenitor cells. By combining perturbation experiments, gene expression analysis, a computational method that predicts future cell states from transcriptional changes, and a lineage reconstruction method, we placed all major cell types onto a single lineage tree that connects all cells to a single stem cell compartment. We characterized gene expression changes during differentiation and discovered cell types important for regeneration. Our results demonstrate the importance of single-cell transcriptome analysis for mapping and reconstructing fundamental processes of developmental and regenerative biology at high resolution.
AU  - Oexle, K.
AU  - Winkelmann, J.
C1  - 53547
C2  - 44901
CY  - 1200 New York Ave, Nw, Washington, Dc 20005 Usa
SP  - 671-672
TI  - Common grounds for family maladies.
JO  - Neuron
VL  - 98
IS  - 4
PB  - Amer Assoc Advancement Science
PY  - 2018
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Autophagy is a conserved catabolic pathway with emerging functions in mammalian neurodevelopment and human neurodevelopmental diseases. The mechanisms controlling autophagy in neuronal development are not fully understood. Here, we found that conditional deletion of the Forkhead Box O transcription factors FoxO1, FoxO3, and FoxO4 strongly impaired autophagic flux in developing neurons of the adult mouse hippocampus. Moreover, FoxO deficiency led to altered dendritic morphology, increased spine density, and aberrant spine positioning in adult-generated neurons. Strikingly, pharmacological induction of autophagy was sufficient to correct abnormal dendrite and spine development of FoxO-deficient neurons. Collectively, these findings reveal a novel link between FoxO transcription factors, autophagic flux, and maturation of developing neurons.
AU  - Schäffner, I.*
AU  - Minakaki, G.*
AU  - Khan, M.A.
AU  - Balta, E.A.*
AU  - Schlötzer-Schrehardt, U.*
AU  - Schwarz, T.J.
AU  - Beckervordersandforth, R.*
AU  - Winner, B.*
AU  - Webb, A.E.*
AU  - DePinho, R.A.*
AU  - Paik, J.*
AU  - Wurst, W.
AU  - Klucken, J.*
AU  - Lie, D.C.C.*
C1  - 54257
C2  - 45456
CY  - 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
SP  - 1188-1203.e6
TI  - FoxO function is essential for maintenance of autophagic flux and neuronal morphogenesis in adult neurogenesis.
JO  - Neuron
VL  - 99
IS  - 6
PB  - Cell Press
PY  - 2018
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Precise regulation of cellular metabolism is hypothesized to constitute a vital component of the developmental sequence underlying the life-long generation of hippocampal neurons from quiescent neural stem cells (NSCs). The identity of stage-specific metabolic programs and their impact on adult neurogenesis are largely unknown. We show that the adult hippocampal neurogenic lineage is critically dependent on the mitochondrial electron transport chain and oxidative phosphorylation machinery at the stage of the fast proliferating intermediate progenitor cell. Perturbation of mitochondrial complex function by ablation of the mitochondrial transcription factor A (Tfam) reproduces multiple hallmarks of aging in hippocampal neurogenesis, whereas pharmacological enhancement of mitochondrial function ameliorates age-associated neurogenesis defects. Together with the finding of age-associated alterations in mitochondrial function and morphology in NSCs, these data link mitochondrial complex function to efficient lineage progression of adult NSCs and identify mitochondrial function as a potential target to ameliorate neurogenesis-defects in the aging hippocampus. Beckervordersandforth, Ebert et al. demonstrate that mitochondrial complex function functionally demarcates an early developmental step in adult hippocampal neurogenesis and identify mitochondrial dysfunction as a candidate target to counter age-associated neurogenesis deficits.
AU  - Beckervordersandforth, R.*
AU  - Ebert, B.
AU  - Schäffner, I.*
AU  - Moss, J.*
AU  - Fiebig, C.*
AU  - Shin, J.*
AU  - Moore, D.L.*
AU  - Ghosh, L.*
AU  - Trinchero, M.F.*
AU  - Stockburger, C.*
AU  - Friedland, K.*
AU  - Steib, K.
AU  - von Wittgenstein, J.*
AU  - Keiner, S.*
AU  - Redecker, C.*
AU  - Hölter, S.M.
AU  - Xiang, W.*
AU  - Wurst, W.
AU  - Jagasia, R.
AU  - Schinder, A.F.*
AU  - Ming, G.l.*
AU  - Toni, N.*
AU  - Jessberger, S.*
AU  - Song, H.*
AU  - Lie, D.C.C.*
C1  - 50416
C2  - 41819
CY  - Cambridge
SP  - 560-573.e6
TI  - Role of mitochondrial metabolism in the control of early lineage progression and aging phenotypes in adult hippocampal neurogenesis.
JO  - Neuron
VL  - 93
IS  - 3
PB  - Cell Press
PY  - 2017
SN  - 0896-6273
ER  - 

TY  - JOUR
AU  - Beckervordersandforth, R.*
AU  - Ebert, B.
AU  - Schäffner, I.*
AU  - Moss, J.*
AU  - Fiebig, C.*
AU  - Shin, J.*
AU  - Moore, D.L.*
AU  - Ghosh, L.*
AU  - Trinchero, M.F.*
AU  - Stockburger, C.*
AU  - Friedland, K.*
AU  - Steib, K.
AU  - von Wittgenstein, J.*
AU  - Keiner, S.*
AU  - Redecker, C.*
AU  - Hölter, S.M.
AU  - Xiang, W.*
AU  - Wurst, W.
AU  - Jagasia, R.
AU  - Schinder, A.F.*
AU  - Ming, G.l.*
AU  - Toni, N.*
AU  - Jessberger, S.*
AU  - Song, H.*
AU  - Lie, D.C.C.*
C1  - 52827
C2  - 44189
SP  - 1518
TI  - Role of mitochondrial metabolism in the control of early lineage progression and aging phenotypes in adult hippocampal neurogenesis.
JO  - Neuron
VL  - 93
IS  - 6
PY  - 2017
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - The developmental mechanisms regulating the number of adult neural stem cells (aNSCs) are largely unknown. Here we show that the cleavage plane orientation in murine embryonic radial glia cells (RGCs) regulates the number of aNSCs in the lateral ganglionic eminence (LGE). Randomizing spindle orientation in RGCs by overexpression of Insc or a dominant-negative form of Lgn (dnLgn) reduces the frequency of self-renewing asymmetric divisions while favoring symmetric divisions generating two SNPs. Importantly, these changes during embryonic development result in reduced seeding of aNSCs. Interestingly, no effects on aNSC numbers were observed when Insc was overexpressed in postnatal RGCs or aNSCs. These data suggest a new mechanism for controlling aNSC numbers and show that the role of spindle orientation during brain development is highly time and region dependent.
AU  - Falk, S.
AU  - Ninkovic, J.
AU  - Pilz, G.A.
AU  - Götz, M.
C1  - 50639
C2  - 42543
CY  - Cambridge
SP  - 777-791.e3
TI  - Time-specific effects of spindle positioning on embryonic progenitor pool composition and adult neural stem cell seeding.
JO  - Neuron
VL  - 93
IS  - 4
PB  - Cell Press
PY  - 2017
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Unraveling the brain control of metabolism may generate opportunities to discover novel precision medicines for obesity and diabetes. In this issue of Neuron, Liu et al. (2017) identify a novel glucagon-like peptide (GLP)-1 receptor-dependent signaling process that exerts anorexigenic action via the regulation of AMPA receptor subunit composition in the hypothalamus.
AU  - Lefort, S.
AU  - Tschöp, M.H.
AU  - García-Cáceres, C.
C1  - 52367
C2  - 43911
CY  - Cambridge
SP  - 713-715
TI  - A synaptic basis for GLP-1 action in the brain.
JO  - Neuron
VL  - 96
IS  - 4
PB  - Cell Press
PY  - 2017
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - With the central ability to visualize a variety of endogenous chromophores and biomarkers or exogenous contrast agents, optoacoustic (photoacoustic) imaging empowers new experimental capabilities for investigating brain mechanisms and functions. Here, the operational principles of optoacoustic neuroimaging are reviewed in conjunction with recent advances enabling high-resolution and real-time observation, which extend beyond the reach of optical imaging methods. Multiple implementations of optoacoustics for monitoring hemodynamics and neuro-vascular responses in the brain are showcased. The unique capabilities of optoacoustic imaging for multi-spectral cellular and molecular sensing are discussed with reference to recent application for visualizing healthy and diseased brains. Outstanding challenges in the field are considered in the context of current and future applications of optoacoustic neuroimaging for basic and translational neuroscience research. In pushing the boundaries of brain imaging, optoacoustic methods afford major insights into the neuronal mechanisms of brain functions and organization of behavior.
AU  - Ovsepian, S.V.
AU  - Olefir, I.
AU  - Westmeyer, G.G.
AU  - Razansky, D.
AU  - Ntziachristos, V.
C1  - 52504
C2  - 43995
CY  - Cambridge
SP  - 966-988
TI  - Pushing the boundaries of neuroimaging with optoacoustics.
JO  - Neuron
VL  - 96
IS  - 5
PB  - Cell Press
PY  - 2017
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Subcellular target recognition in the CNS is the culmination of a multiple-step program including axon guidance, target recognition, and synaptogenesis. In cerebellum, basket cells (BCs) innervate the soma and axon initial segment (AIS) of Purkinje cells (PCs) to form the pinceau synapse, but the underlying mechanisms remain incompletely understood. Here, we demonstrate that neuropilin-1 (NRP1), a Semaphorin receptor expressed in BCs, controls both axonal guidance and subcellular target recognition. We show that loss of Semaphorin 3A function or specific deletion of NRP1 in BCs alters the stereotyped organization of BC axon and impairs pinceau synapse formation. Further, we identified NRP1 as a trans-synaptic binding partner of the cell adhesion molecule neurofascin-186 (NF186) expressed in the PC AIS during pinceau synapse formation. These findings identify a dual function of NRP1 in both axon guidance and subcellular target recognition in the construction of GABAergic circuitry.
AU  - Telley, L.*
AU  - Cadilhac, C.*
AU  - Cioni, J.M.*
AU  - Saywell, V.*
AU  - Jahannault-Talignani, C.*
AU  - Huettl, R.E.
AU  - Sarrailh-Faivre, C.*
AU  - Dayer, A.*
AU  - Huber, A.B.
AU  - Ango, F.*
C1  - 49463
C2  - 30403
CY  - Cambridge
SP  - 1276-1291
TI  - Dual function of NRP1 in axon guidance and subcellular target recognition in cerebellum.
JO  - Neuron
VL  - 91
IS  - 6
PB  - Cell Press
PY  - 2016
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Neurogenesis in the dentate gyrus (DG) of the adult hippocampus is a process regulated by experience. To understand whether experience also modifies the connectivity of new neurons, we systematically investigated changes in their innervation following environmental enrichment (EE). We found that EE exposure between 2-6 weeks following neuron birth, rather than merely increasing the number of new neurons, profoundly affected their pattern of monosynaptic inputs. Both local innervation by interneurons and to even greater degree long-distance innervation by cortical neurons were markedly enhanced. Furthermore, following EE, new neurons received inputs from CA3 and CA1 inhibitory neurons that were rarely observed under control conditions. While EE-induced changes in inhibitory innervation were largely transient, cortical innervation remained increased after returning animals to control conditions. Our findings demonstrate an unprecedented experience-dependent reorganization of connections impinging onto adult-born neurons, which is likely to have important impact on their contribution to hippocampal information processing.
AU  - Bergami, M.*
AU  - Masserdotti, G.
AU  - Temprana, S.G.*
AU  - Motori, E.*
AU  - Eriksson, T.M.*
AU  - Göbel, J.*
AU  - Yang, S.M.*
AU  - Conzelmann, K.K.*
AU  - Schinder, A.F.*
AU  - Götz, M.
AU  - Berninger, B.*
C1  - 43268
C2  - 36376
CY  - Cambridge
SP  - 710-717
TI  - A critical period for experience-dependent remodeling of adult-born neuron connectivity.
JO  - Neuron
VL  - 85
IS  - 4
PB  - Cell Press
PY  - 2015
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Depression risk is exacerbated by genetic factors and stress exposure; however, the biological mechanisms through which these factors interact to confer depression risk are poorly understood. One putative biological mechanism implicates variability in the ability of cortisol, released in response to stress, to trigger a cascade of adaptive genomic and non-genomic processes through glucocorticoid receptor (GR) activation. Here, we demonstrate that common genetic variants in long-range enhancer elements modulate the immediate transcriptional response to GR activation in human blood cells. These functional genetic variants increase risk for depression and co-heritable psychiatric disorders. Moreover, these risk variants are associated with inappropriate amygdala reactivity, a transdiagnostic psychiatric endophenotype and an important stress hormone response trigger. Network modeling and animal experiments suggest that these genetic differences in GR-induced transcriptional activation may mediate the risk for depression and other psychiatric disorders by altering a network of functionally related stress-sensitive genes in blood and brain.
AU  - Knauer-Arloth, J.*
AU  - Bogdan, R.*
AU  - Weber, P.*
AU  - Frishman, G.
AU  - Menke, A.*
AU  - Wagner, K.V.*
AU  - Balsevich, G.*
AU  - Schmidt, M.V.*
AU  - Karbalai, N.*
AU  - Czamara, D.*
AU  - Altmann, A.*
AU  - Trümbach, D.
AU  - Wurst, W.
AU  - Mehta, D.*
AU  - Uhr, M.*
AU  - Klengel, T.*
AU  - Erhardt, A.*
AU  - Carey, C.E.*
AU  - Conley, E.D.*
AU  - Ruepp, A.
AU  - Müller-Myhsok, B.*
AU  - Hariri, A.R.*
AU  - Binder, E.B.*
C1  - 45120
C2  - 37226
CY  - Cambridge
SP  - 1189-1202
TI  - Genetic differences in the immediate transcriptome response to stress predict risk-related brain function and psychiatric disorders.
JO  - Neuron
VL  - 86
IS  - 5
PB  - Cell Press
PY  - 2015
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - The positioning of neurons in the cerebral cortex is of crucial importance for its function as highlighted by the severe consequences of migrational disorders in patients. Here we show that genetic deletion of the small GTPase RhoA in the developing cerebral cortex results in two migrational disorders: subcortical band heterotopia (SBH), a heterotopic cortex underlying the normotopic cortex, and cobblestone lissencephaly, in which neurons protrude beyond layer I at the pial surface of the brain. Surprisingly, RhoA(-/-) neurons migrated normally when transplanted into wild-type cerebral cortex, whereas the converse was not the case. Alterations in the radial glia scaffold are demonstrated to cause these migrational defects through destabilization of both the actin and the microtubules cytoskeleton. These data not only demonstrate that RhoA is largely dispensable for migration in neurons but also showed that defects in radial glial cells, rather than neurons, can be sufficient to produce SBH.
AU  - Cappello, S.
AU  - Böhringer, C.R.
AU  - Bergami, M.*
AU  - Conzelmann, K.K.*
AU  - Ghanem, A.*
AU  - Tomassy, G.S.*
AU  - Arlotta, P.*
AU  - Mainardi, M.*
AU  - Allegra, M.*
AU  - Caleo, M.*
AU  - van Hengel, J.*
AU  - Brakebusch, C.*
AU  - Götz, M.
C1  - 7295
C2  - 29656
SP  - 911-924
TI  - A radial glia-specific role of RhoA in double cortex formation.
JO  - Neuron
VL  - 73
IS  - 5
PB  - Elsevier
PY  - 2012
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Intrinsically photosensitive retinal ganglion cells (ipRGCs) and their nuclear targets in the subcortical visual shell (SVS) are components of the non-image-forming visual system, which regulates important physiological processes, including photoentrainment of the circadian rhythm. While ipRGCs have been the subject of much recent research, less is known about their central targets and how they develop to support specific behavioral functions. We describe Sox14 as a marker to follow the ontogeny of the SVS and find that the complex forms from two narrow stripes of Dlx2-negative GABAergic progenitors in the early diencephalon through sequential waves of tangential migration. We characterize the requirement for Sox14 to orchestrate the correct distribution of neurons among the different nuclei of the network and describe how Sox14 expression is required both to ensure robustness in circadian entrainment and for masking of motor activity.
AU  - Delogu, A.*
AU  - Sellers, K.*
AU  - Zagoraiou, L.*
AU  - Bocianowska-Zbrog, A.*
AU  - Mandal, S.*
AU  - Guimera, J.
AU  - Rubenstein, J.L.R.*
AU  - Sugden, D.*
AU  - Jessell, T.*
AU  - Lumsden, A.*
C1  - 10717
C2  - 30373
SP  - 648-662
TI  - Subcortical visual shell nuclei targeted by ipRGCs develop from a Sox14+-GABAergic progenitor and require Sox14 to regulate daily activity rhythms.
JO  - Neuron
VL  - 75
IS  - 4
PB  - Cell Press
PY  - 2012
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Most neurons in the adult mammalian brain survive for the entire life of an individual. However, it is not known which transcriptional pathways regulate this survival in a healthy brain. Here, we identify a pathway regulating neuronal survival in a highly subtype-specific manner. We show that the transcription factor Pax6 expressed in dopaminergic neurons of the olfactory bulb regulates the survival of these neurons by directly controlling the expression of crystallin αA (CryαA), which blocks apoptosis by inhibition of procaspase-3 activation. Re-expression of CryαA fully rescues survival of Pax6-deficient dopaminergic interneurons in vivo and knockdown of CryαA by shRNA in wild-type mice reduces the number of dopaminergic OB interneurons. Strikingly, Pax6 utilizes different DNA-binding domains for its well-known role in fate specification and this role of regulating the survival of specific neuronal subtypes in the mature, healthy brain.
AU  - Ninkovic, J.
AU  - Pinto, L.
AU  - Petricca, S.
AU  - Lepier, A.*
AU  - Sun, J.*
AU  - Rieger, M.
AU  - Schroeder, T.
AU  - Cvekl, A.*
AU  - Favor, J.
AU  - Götz, M.
C1  - 5768
C2  - 27729
SP  - 682-694
TI  - The transcription factor Pax6 regulates survival of dopaminergic olfactory bulb neurons via crystallin αA.
JO  - Neuron
VL  - 68
IS  - 4
PB  - Elsevier
PY  - 2010
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Engrailed transcription factors regulate the expression of guidance cues that pattern retinal axon terminals in the dorsal midbrain. They also act directly to guide axon growth in vitro. We show here that an extracellular En gradient exists in the tectum along the anterior-posterior axis. Neutralizing extracellular Engrailed in vivo with antibodies expressed in the tectum causes temporal axons to map aberrantly to the posterior tectum in chick and Xenopus. Furthermore, posterior membranes from wild-type tecta incubated with anti-Engrailed antibodies or posterior membranes from Engrailed-1 knockout mice exhibit diminished repulsive activity for temporal axons. Since EphrinAs play a major role in anterior-posterior mapping, we tested whether Engrailed cooperates with EphrinA5 in vitro. We find that Engrailed restores full repulsion to axons given subthreshold doses of EphrinA5. Collectively, our results indicate that extracellular Engrailed contributes to retinotectal mapping in vivo by modulating the sensitivity of growth cones to EphrinA.
AU  - Wizenmann, A.
AU  - Brunet, I.*
AU  - Lam, J.S.Y.*
AU  - Sonnier, L.*
AU  - Beurdeley, M.*
AU  - Zarbalis, K.
AU  - Vogt Weisenhorn, D.M.
AU  - Weinl, C.*
AU  - Dwivedy, A.*
AU  - Joliot, A.*
AU  - Wurst, W.
AU  - Holt, C.*
AU  - Prochiantz, A.*
C1  - 2966
C2  - 26838
SP  - 355-366
TI  - Extracellular engrailed participates in the topographic guidance of retinal axons in vivo.
JO  - Neuron
VL  - 64
IS  - 3
PB  - Cell Press
PY  - 2009
SN  - 0896-6273
ER  - 

TY  - JOUR
AB  - Arc/Arg3.1 is robustly induced by plasticity-producing stimulation and specifically targeted to stimulated synaptic areas. To investigate the role of Arc/Arg3.1 in synaptic plasticity and learning and memory, we generated Arc/Arg3.1 knockout mice. These animals fail to form long-lasting memories for implicit and explicit learning tasks, despite intact short-term memory. Moreover, they exhibit a biphasic alteration of hippocampal long-term potentiation in the dentate gyrus and area CA1 with an enhanced early and absent late phase. In addition, long-term depression is significantly impaired. Together, these results demonstrate a critical role for Arc/Arg3.1 in the consolidation of enduring synaptic plasticity and memory storage. © 2006 Elsevier Inc. All rights reserved.
AU  - Plath, N.*
AU  - Ohana, O.*
AU  - Dammermann, B.*
AU  - Errington, M.L.*
AU  - Schmitz, D.*
AU  - Gross, C.*
AU  - Mao, X.*
AU  - Engelsberg, A.*
AU  - Mahlke, C.*
AU  - Welzl, H.*
AU  - Kobalz, U.*
AU  - Stawrakakis, A.*
AU  - Fernandez, E.*
AU  - Waltereit, R.*
AU  - Bick-Sander, A.*
AU  - Therstappen, E.*
AU  - Cooke, S.F.*
AU  - Blanquet, V.
AU  - Wurst, W.
AU  - Salmen, B.*
AU  - Bösl, M.R.*
AU  - Lipp, H.P.*
AU  - Grant, S.G.*
AU  - Bliss, T.V.*
AU  - Wolfer, D.P.*
AU  - Kuhl, D.*
C1  - 5107
C2  - 24140
SP  - 437-444
TI  - Arc/Arg3.1 is essential for the consolidation of synaptic plasticity and memories.
JO  - Neuron
VL  - 52
IS  - 3
PY  - 2006
SN  - 0896-6273
ER  - 

TY  - JOUR
AU  - Götz, M.
AU  - Barde, Y.-A.
C1  - 2643
C2  - 23403
SP  - 369-372
TI  - Radial glial cells defined and major intermediates between embryonic stem cells and CNS neurons.
JO  - Neuron
VL  - 46
PY  - 2005
SN  - 0896-6273
ER  - 

TY  - JOUR
AU  - Huber, A.B.
AU  - Kania, A.*
AU  - Tran, T.S.*
AU  - Gu, C.*
AU  - de Marco Gacia, N.*
AU  - Lieberam, I.*
AU  - Johnson, D.*
AU  - Jessell, T.M.*
AU  - Ginty, D.D.*
AU  - Kolodkin, A.L.*
C1  - 4186
C2  - 23979
SP  - 949-964
TI  - Distinct roles for secreted semaphorin signaling in spinal motor axon guidance.
JO  - Neuron
VL  - 48
PY  - 2005
SN  - 0896-6273
ER  - 

TY  - JOUR
AU  - *
AU  - Biskup, S.
AU  - Leitner, P.*
AU  - Lichtner, P.
AU  - Farrer, M.*
AU  - Lincoln, S.*
AU  - Kachergus, J.*
AU  - Hulihan, M.*
AU  - Uitti, R.J.*
AU  - Calne, D.B.*
AU  - Stoessl, A.J.*
C1  - 2126
C2  - 22270
SP  - 601-607
TI  - Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology.
JO  - Neuron
VL  - 44
PY  - 2004
SN  - 0896-6273
ER  -