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NMNAT suppresses Tau-induced neurodegeneration by promoting clearance of hyperphosphorylated Tau oligomers in a Drosophila model of tauopathy

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

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Association of GSK3B With Alzheimer Disease and Frontotemporal Dementia

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Alz-50 and MC-1, a new monoclonal antibody raised to paired helical filaments, recognize conformational epitopes on recombinant tau

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Tau and tau reporters disrupt central projections of sensory neurons inDrosophila

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Hyperphosphorylation of tau is mediated by ERK activation during anticancer drug-induced apoptosis in neuroblastoma cells

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Molecular chaperones in cellular protein folding

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Acetylcholinesterase mutants in drosophila and their effects on the structure and function of the cental nervous system

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Inhibition of proteasome and Shaggy/Glycogen synthase kinase‐3β kinase prevents clearance of phosphorylated tau in Drosophila

inferredcites →https://doi.org/10.1002/jnr.21232openalex-snapshot

S/P and T/P phosphorylation is critical for tau neurotoxicity in Drosophila

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The new indirubin derivative inhibitors of glycogen synthase kinase‐3, 6‐BIDECO and 6‐BIMYEO, prevent tau phosphorylation and apoptosis induced by the inhibition of protein phosphatase‐2A by okadaic acid in cultured neurons

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The in vitro formation of recombinant τ polymers

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Nicotinamide/nicotinic acid mononucleotide adenylyltransferase, new insights into an ancient enzyme

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Microtubule-associated protein tau is a substrate of ATP/Mg2+-dependent proteasome protease system

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Phosphorylated mitogen-activated protein kinase (MAPK/ERK-P), protein kinase of 38 kDa (p38-P), stress-activated protein kinase (SAPK/JNK-P), and calcium/calmodulin-dependent kinase II (CaM kinase II) are differentially expressed in tau deposits in neurons and glial cells in tauopathies

inferredcites →https://doi.org/10.1016/0896-6273(93)90200-bopenalex-snapshot

Defective Glia in the Drosophila Brain Degeneration Mutant drop-dead

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Tau phosphorylation: physiological and pathological consequences

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Tau protein as a differential biomarker of tauopathies

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Tau pathology in Alzheimer disease and other tauopathies

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TOR-Mediated Cell-Cycle Activation Causes Neurodegeneration in a Drosophila Tauopathy Model

inferredcites →https://doi.org/10.1016/j.neuint.2011.05.010openalex-snapshot

Tau phosphorylation and neuronal apoptosis induced by the blockade of PP2A preferentially involve GSK3β

inferredcites →https://doi.org/10.1016/j.neuron.2006.04.028openalex-snapshot

The Drosophila Cell Corpse Engulfment Receptor Draper Mediates Glial Clearance of Severed Axons

inferredcites →https://doi.org/10.1016/j.neuropharm.2009.07.021openalex-snapshot

The JNK pathway amplifies and drives subcellular changes in tau phosphorylation

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Proteasome-mediated degradation of tau proteins occurs independently of the chymotrypsin-like activity by a nonprocessive pathway

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Lithium reduces tau phosphorylation: effects in living cells and in neurons at therapeutic concentrations

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MARK, a Novel Family of Protein Kinases That Phosphorylate Microtubule-Associated Proteins and Trigger Microtubule Disruption

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PAR-1 Kinase Plays an Initiator Role in a Temporally Ordered Phosphorylation Process that Confers Tau Toxicity in Drosophila

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Unfolding the role of chaperones and chaperonins in human disease

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Regulation of the Phosphorylation State and Microtubule-Binding Activity of Tau by Protein Phosphatase 2A

inferredcites →https://doi.org/10.1016/s0896-6273(02)00706-7openalex-snapshot

Human Wild-Type Tau Interacts with wingless Pathway Components and Produces Neurofibrillary Pathology in Drosophila

inferredcites →https://doi.org/10.1016/s0896-6273(03)00259-9openalex-snapshot

Cdk5 Is a Key Factor in Tau Aggregation and Tangle Formation In Vivo

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Aberrant Cdk5 Activation by p25 Triggers Pathological Events Leading to Neurodegeneration and Neurofibrillary Tangles

inferredcites →https://doi.org/10.1016/s1471-4914(01)02123-2openalex-snapshot

Analysis of tauopathies with transgenic mice

inferredcites →https://doi.org/10.1038/381571a0openalex-snapshot

Molecular chaperones in cellular protein folding

inferredcites →https://doi.org/10.1038/70532openalex-snapshot

Suppression of polyglutamine-mediated neurodegeneration in Drosophila by the molecular chaperone HSP70

inferredcites →https://doi.org/10.1038/78078openalex-snapshot

Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein

inferredcites →https://doi.org/10.1038/cdd.2009.185openalex-snapshot

The cleaved-Caspase-3 antibody is a marker of Caspase-9-like DRONC activity in Drosophila

inferredcites →https://doi.org/10.1038/nature06721openalex-snapshot

NAD synthase NMNAT acts as a chaperone to protect against neurodegeneration

inferredcites →https://doi.org/10.1038/nm0796-783openalex-snapshot

Alzheimer's disease hyperphosphorylated tau sequesters normal tau into tangles of filaments and disassembles microtubules

inferredcites →https://doi.org/10.1046/j.1471-4159.1997.69052087.xopenalex-snapshot

A Conformation‐ and Phosphorylation‐Dependent Antibody Recognizing the Paired Helical Filaments of Alzheimer's Disease

inferredcites →https://doi.org/10.1046/j.1471-4159.2002.01137.xopenalex-snapshot

Proteasomal degradation of tau protein

inferredcites →https://doi.org/10.1073/pnas.040577797openalex-snapshot

Hyperphosphorylated tau and neurofilament and cytoskeletal disruptions in mice overexpressing human p25, an activator of cdk5

inferredcites →https://doi.org/10.1073/pnas.0500466102openalex-snapshot

Inhibition of glycogen synthase kinase-3 by lithium correlates with reduced tauopathy and degeneration in vivo

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An inhibitor of tau hyperphosphorylation prevents severe motor impairments in tau transgenic mice

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Bacterial and yeast chaperones reduce both aggregate formation and cell death in mammalian cell models of Huntington's disease

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Chaperones increase association of tau protein with microtubules

inferredcites →https://doi.org/10.1073/pnas.58.3.1112openalex-snapshot

BEHAVIORAL MUTANTS OF Drosophila ISOLATED BY COUNTERCURRENT DISTRIBUTION

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Nicotinamide Mononucleotide Adenylyltransferase Is a Stress Response Protein Regulated by the Heat Shock Factor/Hypoxia-inducible Factor 1α Pathway

inferredcites →https://doi.org/10.1074/jbc.m305838200openalex-snapshot

CHIP-Hsc70 Complex Ubiquitinates Phosphorylated Tau and Enhances Cell Survival

inferredcites →https://doi.org/10.1080/07853890410031948openalex-snapshot

Mechanism of neurodegenerative disease: role of the ubiquitin proteasome system

inferredcites →https://doi.org/10.1091/mbc.e07-04-0327openalex-snapshot

Tau Phosphorylation Sites Work in Concert to Promote Neurotoxicity In Vivo

inferredcites →https://doi.org/10.1093/emboj/20.1.27openalex-snapshot

Decreased nuclear β‐catenin, tau hyperphosphorylation and neurodegeneration in GSK‐3β conditional transgenic mice

inferredcites →https://doi.org/10.1093/hmg/10.12.1307openalex-snapshot

Geldanamycin activates a heat shock response and inhibits huntingtin aggregation in a cell culture model of Huntington's disease

inferredcites →https://doi.org/10.1093/hmg/ddh083openalex-snapshot

CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation

inferredcites →https://doi.org/10.1093/hmg/ddn326openalex-snapshot

Dissociation of tau toxicity and phosphorylation: role of GSK-3β, MARK and Cdk5 in a Drosophila model

inferredcites →https://doi.org/10.1093/hmg/ddq200openalex-snapshot

Tau Ser262 phosphorylation is critical for A 42-induced tau toxicity in a transgenic Drosophila model of Alzheimer's disease

inferredcites →https://doi.org/10.1093/jnen/62.4.389openalex-snapshot

Colocalization of Tau and Alpha-Synuclein Epitopes in Lewy Bodies

inferredcites →https://doi.org/10.1096/fj.03-0106fjeopenalex-snapshot

C‐terminal fragments of amyloid precursor protein exert neurotoxicity by inducing glycogen synthase kinase‐3β expression

inferredcites →https://doi.org/10.1096/fj.05-5343fjeopenalex-snapshot

HSP induction mediates selective clearance of tau phosphorylated at proline‐directed Ser/Thr sites but not KXGS (MARK) sites

inferredcites →https://doi.org/10.1101/lm.70804openalex-snapshot

Learning and Memory Deficits Upon TAU Accumulation in Drosophila Mushroom Body Neurons

inferredcites →https://doi.org/10.1111/j.1471-4159.1992.tb09432.xopenalex-snapshot

Brain Levels of Microtubule‐Associated Protein τ Are Elevated in Alzheimer's Disease: A Radioimmuno‐Slot‐Blot Assay for Nanograms of the Protein

inferredcites →https://doi.org/10.1111/j.1471-4159.2004.02713.xopenalex-snapshot

U‐box protein carboxyl terminus of Hsc70‐interacting protein (CHIP) mediates poly‐ubiquitylation preferentially on four‐repeat Tau and is involved in neurodegeneration of tauopathy

inferredcites →https://doi.org/10.1111/j.1471-4159.2005.03181.xopenalex-snapshot

Sequestosome 1/p62 shuttles polyubiquitinated tau for proteasomal degradation

inferredcites →https://doi.org/10.1126/science.1062382openalex-snapshot

Tauopathy in Drosophila : Neurodegeneration Without Neurofibrillary Tangles

inferredcites →https://doi.org/10.1172/jci29715openalex-snapshot

The high-affinity HSP90-CHIP complex recognizes and selectively degrades phosphorylated tau client proteins

inferredcites →https://doi.org/10.1371/journal.pbio.0040416openalex-snapshot

Drosophila NMNAT Maintains Neural Integrity Independent of Its NAD Synthesis Activity

inferredcites →https://doi.org/10.1523/jneurosci.17-19-07425.1997openalex-snapshot

The Swiss Cheese Mutant Causes Glial Hyperwrapping and Brain Degeneration in Drosophila

inferredcites →https://doi.org/10.1523/jneurosci.19-14-05782.1999openalex-snapshot

α-Synuclein Shares Physical and Functional Homology with 14-3-3 Proteins

inferredcites →https://doi.org/10.1523/jneurosci.23-26-08872.2003openalex-snapshot

Proteasome Inhibition Stabilizes Tau Inclusions in Oligodendroglial Cells that Occur after Treatment with Okadaic Acid

inferredcites →https://doi.org/10.3109/01677068609106845openalex-snapshot

The Structural Brain MutantVacuolar medullaofDrosophila melanogasterwith Specific Behavioral Defects and Cell Degeneration in the Adult

inferredcites →https://doi.org/10.3233/jad-2008-14402openalex-snapshot

Cytosolic Abnormally Hyperphosphorylated Tau But Not Paired Helical Filaments Sequester Normal MAPs and Inhibit Microtubule Assembly

inferredcites →https://doi.org/10.3233/jad-2008-14403openalex-snapshot

Hyperphosphorylated Tau is a Cause of Neuronal Dysfunction in Tauopathy

inferredcites →https://doi.org/10.3233/jad-2008-14406openalex-snapshot

Evidence that Non-Fibrillar Tau Causes Pathology Linked to Neurodegeneration and Behavioral Impairments

inferredcites →https://doi.org/10.3390/molecules15106859openalex-snapshot

Dealing with Misfolded Proteins: Examining the Neuroprotective Role of Molecular Chaperones in Neurodegeneration

inferredcites →https://doi.org/10.3758/bf03195958openalex-snapshot

Learned suppression of photopositive tendencies inDrosophila melanogaster

inferredcites →https://doi.org/10.3791/2504openalex-snapshot

Assaying Locomotor, Learning, and Memory Deficits in Drosophila Models of Neurodegeneration

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

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inferred← citeshttps://doi.org/10.2139/ssrn.3806068openalex-extracted

Sarm1 Haploinsufficiency and Low Expression Levels after Antisense Oligonucleotides Delays Programmed Axon Degeneration

inferred← citeshttps://doi.org/10.1002/acn3.308openalex-snapshot

Nmnat1 protects neuronal function without altering phospho‐tau pathology in a mouse model of tauopathy

inferred← citeshttps://doi.org/10.1002/dvg.22902openalex-snapshot

D rosophila glob1 expresses dynamically and is required for development and oxidative stress response

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Protein Quality Control in Brain Aging: Lessons from Protein Misfolding Disorders in Drosophila

inferred← citeshttps://doi.org/10.1007/s00018-020-03643-3openalex-snapshot

Differential effects of putative N-glycosylation sites in human Tau on Alzheimer’s disease-related neurodegeneration

inferred← citeshttps://doi.org/10.1007/s10528-015-9701-1openalex-snapshot

Biochemical and Behavioral Evaluation of Human MAPT Mutations in Transgenic Drosophila melanogaster

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Signaling pathways leading to ischemic mitochondrial neuroprotection

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Targeted Downregulation of dMyc Suppresses Pathogenesis of Human Neuronal Tauopathies in Drosophila by Limiting Heterochromatin Relaxation and Tau Hyperphosphorylation

inferred← citeshttps://doi.org/10.1007/s12038-023-00362-2openalex-snapshot

Drosophila olfaction as a model system for studying human neurological disorders

inferred← citeshttps://doi.org/10.1016/b978-0-12-405195-9.00054-8openalex-snapshot

Drosophila Models of Tauopathy

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Simple In Vivo Models of Alzheimer’s Disease

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Behavioral Studies in Drosophila Models of Human Diseases

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Simple in vivo models of Alzheimer's disease

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The Drosophila model system to study tau action

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Tau phosphorylation homeostasis: Mechanisms, targets, and therapeutic implications in Alzheimer’s disease

inferred← citeshttps://doi.org/10.1016/j.bbadis.2017.05.017openalex-snapshot

Targeted downregulation of dMyc restricts neurofibrillary tangles mediated pathogenesis of human neuronal tauopathies in Drosophila

inferred← citeshttps://doi.org/10.1016/j.bbr.2017.11.030openalex-snapshot

NAD-biosynthetic enzyme NMNAT1 reduces early behavioral impairment in the htau mouse model of tauopathy

inferred← citeshttps://doi.org/10.1016/j.bbrc.2017.12.021openalex-snapshot

Short-term exposure to dim light at night disrupts rhythmic behaviors and causes neurodegeneration in fly models of tauopathy and Alzheimer's disease

inferred← citeshttps://doi.org/10.1016/j.celrep.2019.08.104openalex-snapshot

Tau-Mediated Disruption of the Spliceosome Triggers Cryptic RNA Splicing and Neurodegeneration in Alzheimer’s Disease

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Sarm1 haploinsufficiency or low expression levels after antisense oligonucleotides delay programmed axon degeneration

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Overexpression of Nmnat improves the adaption of health span in aging Drosophila

inferred← citeshttps://doi.org/10.1016/j.expneurol.2015.05.013openalex-snapshot

Modeling the complex pathology of Alzheimer's disease in Drosophila

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Severe biallelic loss-of-function mutations in nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) in two fetuses with fetal akinesia deformation sequence

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NMNAT: It’s an NAD+ synthase… It’s a chaperone… It’s a neuroprotector

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Dynamic structural determinants underlie the neurotoxicity of the N-terminal tau 26-44 peptide in Alzheimer's disease and other human tauopathies

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MicroRNA miR-1002 Enhances NMNAT-Mediated Stress Response by Modulating Alternative Splicing

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The mouse nicotinamide mononucleotide adenylyltransferase chaperones diverse pathological amyloid client proteins

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Convolvulus pluricaulis (Shankhapushpi) ameliorates human microtubule-associated protein tau (hMAPτ) induced neurotoxicity in Alzheimer’s disease Drosophila model

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An evaluation of Drosophila as a model system for studying tauopathies such as Alzheimer’s disease

inferred← citeshttps://doi.org/10.1016/j.mcn.2012.11.008openalex-snapshot

The role of autophagy in Nmnat-mediated protection against hypoxia-induced dendrite degeneration

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Adequate expression of Globin1 is required for development and maintenance of nervous system in Drosophila

inferred← citeshttps://doi.org/10.1016/j.neurobiolaging.2018.07.022openalex-snapshot

Beta-sheet assembly of Tau and neurodegeneration in Drosophila melanogaster

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Amyloid-beta induced retrograde axonal degeneration in a mouse tauopathy model

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Poly(ADP-ribose)polymerase-1 hyperactivation in neurodegenerative diseases: The death knell tolls for neurons

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NMNATs, evolutionarily conserved neuronal maintenance factors

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Neurodegeneration models in Drosophila

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Drosophila model of cognitive disorders: Focus on memory abnormality

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Advances in Therapeutics for Neurodegenerative Tauopathies: Moving toward the Specific Targeting of the Most Toxic Tau Species

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The Role of Tau Oligomers in the Onset of Alzheimer's Disease Neuropathology

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Alternative splicing of Drosophila Nmnat functions as a switch to enhance neuroprotection under stress

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Wallerian degeneration: an emerging axon death pathway linking injury and disease

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Anti-tau single domain antibodies clear pathological tau and attenuate its toxicity and related functional defects

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Developmental Expression of 4-Repeat-Tau Induces Neuronal Aneuploidy in Drosophila Tauopathy Models

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Screening with an NMNAT2-MSD platform identifies small molecules that modulate NMNAT2 levels in cortical neurons

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What is the pathological significance of tau oligomers?

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Nmnat restores neuronal integrity by neutralizing mutant Huntingtin aggregate-induced progressive toxicity

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Implications of NAD metabolism in pathophysiology and therapeutics for neurodegenerative diseases

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An assessment of the translational relevance of Drosophila in drug discovery

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Potentiating tangle formation reduces acute toxicity of soluble tau species in the rat

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Tau-mediated axonal degeneration is prevented by activation of the WldS pathway

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Salvage NAD+ biosynthetic pathway enzymes moonlight as molecular chaperones to protect against proteotoxicity

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Mislocalization of neuronal mitochondria reveals regulation of Wallerian degeneration and NMNAT/WLDS-mediated axon protection independent of axonal mitochondria

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NAD+ salvage pathway proteins suppress proteotoxicity in yeast models of neurodegeneration by promoting the clearance of misfolded/oligomerized proteins

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Mechanisms of Axonal Degeneration and Regeneration

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Synchronized genetic activities in Alzheimer’s brains revealed by heterogeneity-capturing network analysis

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Selective human tau protein expression in different clock circuits of the Drosophila brain disrupts different aspects of sleep and circadian rhythms

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Mechanistic insights into NAD synthase NMNAT chaperoning phosphorylated Tau from pathological aggregation

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Modeling neurodegenerative and neurodevelopmental disorders in theDrosophilamushroom body

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Brain energy metabolism: A roadmap for future research

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DLK, NMNAT2, and SARM1: Judge, Jury, and Executioner in Axon Degeneration

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Axon Degeneration and Regeneration: Insights from Drosophila Models of Nerve Injury

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Probing Mechanisms That Underlie Human Neurodegenerative Diseases in Drosophila

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Nicotinamide, NAD(P)(H), and Methyl-Group Homeostasis Evolved and Became a Determinant of Ageing Diseases: Hypotheses and Lessons from Pellagra

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Tau Protein: Function and Pathology

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Evaluation of Traditional Medicines for Neurodegenerative Diseases Using Drosophila Models

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Cl-NQTrp Alleviates Tauopathy Symptoms in a Model Organism through the Inhibition of Tau Aggregation-Engendered Toxicity

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An AMPK-dependent regulatory pathway in tau-mediated toxicity

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Molecular chaperones protect against JNK- and Nmnat-regulated axon degeneration in Drosophila

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The Highwire Ubiquitin Ligase Promotes Axonal Degeneration by Tuning Levels of Nmnat Protein

inferred← citeshttps://doi.org/10.1371/journal.pgen.1006503openalex-snapshot

Mitochondria and Caspases Tune Nmnat-Mediated Stabilization to Promote Axon Regeneration

inferred← citeshttps://doi.org/10.1371/journal.pone.0047869openalex-snapshot

Nicotinamide Mononucleotide Adenylyltransferase 2 (Nmnat2) Regulates Axon Integrity in the Mouse Embryo

inferred← citeshttps://doi.org/10.1371/journal.pone.0136528openalex-snapshot

Unraveling Comparative Anti-Amyloidogenic Behavior of Pyrazinamide and D-Cycloserine: A Mechanistic Biophysical Insight

inferred← citeshttps://doi.org/10.15252/embr.201846975openalex-snapshot

The E3 ligase Highwire promotes synaptic transmission by targeting the NAD‐synthesizing enzyme dNmnat

inferred← citeshttps://doi.org/10.18632/aging.203634openalex-snapshot

Nmnat2 attenuates amyloidogenesis and up-regulates ADAM10 in AMPK activity-dependent manner

inferred← citeshttps://doi.org/10.21926/obm.genet.2001106openalex-snapshot

Knight in Splicing Armor: Alternative Splicing as a Neuroprotective Mechanism

inferred← citeshttps://doi.org/10.25959/23238449openalex-snapshot

A tauopathy model of Alzheimer's disease in Drosophila melanogaster

inferred← citeshttps://doi.org/10.26508/lsa.202402681openalex-snapshot

Regulation of proteostasis by sleep through autophagy in Drosophila models of Alzheimer’s disease

inferred← citeshttps://doi.org/10.3233/jad-122173openalex-snapshot

Nmnat2 Attenuates Tau Phosphorylation Through Activation of PP2A

inferred← citeshttps://doi.org/10.3233/jad-150927openalex-snapshot

Naphthoquinone-Tryptophan Hybrid Inhibits Aggregation of the Tau-Derived Peptide PHF6 and Reduces Neurotoxicity

inferred← citeshttps://doi.org/10.3389/fnagi.2022.852972openalex-snapshot

Human Nmnat1 Promotes Autophagic Clearance of Amyloid Plaques in a Drosophila Model of Alzheimer’s Disease

inferred← citeshttps://doi.org/10.3389/fneur.2013.00083openalex-snapshot

The Importance of Tau Phosphorylation for Neurodegenerative Diseases

inferred← citeshttps://doi.org/10.3389/fneur.2013.00093openalex-snapshot

Formation and Propagation of Tau Oligomeric Seeds

inferred← citeshttps://doi.org/10.3389/fneur.2013.00114openalex-snapshot

Are Tau Aggregates Toxic or Protective in Tauopathies?

inferred← citeshttps://doi.org/10.3389/fnins.2018.00080openalex-snapshot

Mechanisms of α-Synuclein Induced Synaptopathy in Parkinson's Disease

inferred← citeshttps://doi.org/10.3389/fphys.2021.702276openalex-snapshot

Dynamic Aging: Channeled Through Microenvironment

inferred← citeshttps://doi.org/10.3390/biom14121556openalex-snapshot

Pathobiochemistry of Aging and Neurodegeneration: Deregulation of NAD+ Metabolism in Brain Cells

inferred← citeshttps://doi.org/10.3390/cells12091329openalex-snapshot

Cellular and Mitochondrial NAD Homeostasis in Health and Disease

inferred← citeshttps://doi.org/10.3390/cells8030267openalex-snapshot

Why is NMNAT Protective against Neuronal Cell Death and Axon Degeneration, but Inhibitory of Axon Regeneration?

inferred← citeshttps://doi.org/10.3390/ijms22168465openalex-snapshot

Non-Rodent Genetic Animal Models for Studying Tauopathy: Review of Drosophila, Zebrafish, and C. elegans Models

inferred← citeshttps://doi.org/10.3390/ijms232112985openalex-snapshot

Differential Effects of Human Tau Isoforms to Neuronal Dysfunction and Toxicity in the Drosophila CNS

inferred← citeshttps://doi.org/10.3390/ijms25042092openalex-snapshot

Inhibitors of NAD+ Production in Cancer Treatment: State of the Art and Perspectives

inferred← citeshttps://doi.org/10.3390/ijms26157191openalex-snapshot

From Acute Injury to Chronic Neurodegeneration: Molecular Mechanisms Linking Secondary Brain Injury to Long-Term Pathology

inferred← citeshttps://doi.org/10.3390/ijms26189098openalex-snapshot

The Roles of Moonlighting Nicotinamide Mononucleotide Adenylyl Transferases in Cell Physiology

inferred← citeshttps://doi.org/10.3390/metabo16080597openalex-snapshot

Nicotinamide Mononucleotide Adenylyltransferase 1 and NAD+ Homeostasis in Neuroprotection and Aging

inferred← citeshttps://doi.org/10.4103/1673-5374.139475openalex-snapshot

The biochemical pathways of central nervous system neural degeneration in niacin deficiency

inferred← citeshttps://doi.org/10.4161/cc.28128openalex-snapshot

The NAD+synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target

inferred← citeshttps://doi.org/10.70675/b42db6dez88a0z4a14z93eez8f51d19d46f5openalex-snapshot

Altered neuronal activity in the hippocampal CA3 region in an in vitro model of tauopathy

inferred← citeshttps://doi.org/10.7554/elife.51859openalex-snapshot

Nicotinamide mononucleotide adenylyltransferase uses its NAD+ substrate-binding site to chaperone phosphorylated Tau

inferred← citeshttps://doi.org/10.7554/elife.79898openalex-snapshot

Specific binding of Hsp27 and phosphorylated Tau mitigates abnormal Tau aggregation-induced pathology

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