Farrukh Abbas Chaudhry

• Belhaj, Imen; Åmellem, Ingrid; Tartanoglu, Can H.; Weidemann, Hanne Margrete; Vallenari, Evan Michael & Yang, Mingyi [Vis alle 10 forfattere av denne artikkelen] (2026). Lactate treatment improves brain biochemistry and cognitive function in transgenic Alzheimer’s and wild-type mice. Scientific Reports. 16(1). doi: 10.1038/s41598-026-48154-6. Fulltekst i vitenarkiv Vis sammendrag

  Lactate, a well-known metabolite and signalling molecule, holds therapeutic potential for neurodegenerative diseases. Here, we investigated the effects of chronic lactate treatment on cognition and molecular biomarkers in the 5XFAD mouse model of Alzheimer’s disease (AD) and in wild-type (WT) controls using behavioural testing alongside proteomic and transcriptomic analyses. Mice received lactate or vehicle injections 4 days per week for 11 weeks, with behavioural testing before and after the treatment period. Lactate improved working memory in late-treated AD mice, without eliciting anxiety-like behaviour. At the molecular level, lactate reduced Il1b expression, and in a sex-dependent manner, normalised NEFL, and enhanced synaptic integrity proteins (OPCML, PPFIA2, STXBP3, SYT1, VGLUT2, VSNL1) in AD mice, while also augmenting mitochondrial regulators (ATP5G2, GRPEL1, SLC25A23) across genotypes. Notably, lactate upregulated low-abundance ionotropic glutamate receptor mRNAs (Grik3, Grin2c, Grid2ip) in female AD mice, indicating enhanced glutamatergic signalling. In WT mice, lactate increased expression of neurotrophic factors (Bdnf, Igf1, Vegfa), anti-inflammatory cytokines (Il4 and Il13), and the neuronal lactate transporter Mct2, suggesting promoted neuronal resilience. Together, these findings indicate that lactate treatment can mitigate cognitive decline and enhance molecular pathways of resilience in AD, warranting larger, age-stratified studies to validate its therapeutic potential and elucidate underlying mechanisms.

• Ai, Ruixue; Mao, Lipeng; Jin, Xurui; Campos-Marques, Carlos; Zhang, Shi-qi & Pan, Junping [Vis alle 33 forfattere av denne artikkelen] (2025). NAD+ reverses Alzheimer’s neurological deficits via regulating differential alternative RNA splicing of EVA1C. Science Advances. 11(45). doi: 10.1126/sciadv.ady9811. Fulltekst i vitenarkiv Vis sammendrag

  Dysfunctional alternative splicing events (ASEs) in RNA are markers of aging and Alzheimer’s disease (AD). As a key neuronal resilience metabolite, the oxidized nicotinamide adenine dinucleotide (NAD+) slows down AD progression in preclinical studies with several clinical trials ongoing. However, the underlying molecular mechanisms around how NAD+ enhances neuronal resilience, especially whether it has any effect on ASEs, have remained elusive. This study shows that NAD+ augmentation corrects the ASEs of many genes via a key protein, EVA1C (epithelial V-like antigen 1 homolog C), which is involved in neuronal development and activities. EVA1C is reduced in the hippocampus in patients with AD compared to cognitively normal ones. NAD+-induced memory retention is partially dependent on EVA1C, as adeno-associated virus–based Eva1c knockdown in the hippocampal CA1 region annuls NAD+-induced memory improvement in pathological Tau–bearing mice. We propose that NAD+ reduces AD pathologies, at least partially, via amplification of the NAD+-EVA1C splicing axis, pointing to a potential splice-switching therapy for AD.

• Aksnes, Mari; Schibstad, Mari Haavig; Chaudhry, Farrukh Abbas; Neerland, Bjørn Erik; Caplan, Gideon A. & Saltvedt, Ingvild Tina [Vis alle 17 forfattere av denne artikkelen] (2024). Differences in metalloproteinases and their tissue inhibitors in the cerebrospinal fluid are associated with delirium. Communications Medicine. 4(1). doi: 10.1038/s43856-024-00558-z. Fulltekst i vitenarkiv Vis sammendrag

  Background The aetiology of delirium is not known, but pre-existing cognitive impairment is a predisposing factor. Here we explore the associations between delirium and cerebrospinal fluid (CSF) levels of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), proteins with important roles in both acute injury and chronic neurodegeneration. Methods Using a 13-plex Discovery Assay®, we quantified CSF levels of 9 MMPs and 4 TIMPs in 280 hip fracture patients (140 with delirium), 107 cognitively unimpaired individuals, and 111 patients with Alzheimer’s disease dementia. The two delirium-free control groups without acute trauma were included to unravel the effects of acute trauma (hip fracture), dementia, and delirium. Results Here we show that delirium is associated with higher levels of MMP-2, MMP-3, MMP-10, TIMP-1, and TIMP-2; a trend suggests lower levels of TIMP-4 are also associated with delirium. Most delirium patients had pre-existing dementia and low TIMP-4 is the only marker associated with delirium in adjusted analyses. MMP-2, MMP-12, and TIMP-1 levels are clearly higher in the hip fracture patients than in both control groups and several other MMP/TIMPs are impacted by acute trauma or dementia status. Conclusions Several CSF MMP/TIMPs are significantly associated with delirium in hip fracture patients, but alterations in most of these MMP/TIMPs could likely be explained by acute trauma and/or pre-fracture dementia. Low levels of TIMP-4 appear to be directly associated with delirium, and the role of this marker in delirium pathophysiology should be further explored.

• Sapkota, Dipak; Wang, Daxin; Schreurs, Olaf Joseph Franciscus; Vallenari, Evan Michael; Pandey, Sushma & Küntziger, Thomas M. [Vis alle 9 forfattere av denne artikkelen] (2024). Investigation of Roles of SLC38A1 in Proliferation and Differentiation of Mouse Tongue Epithelium and Expression in Human Oral Tongue Squamous Cell Carcinoma. Cancers. 16(2). doi: 10.3390/cancers16020405. Fulltekst i vitenarkiv Vis sammendrag

  The aerobic glycolytic pathway, boosting lactate formation, and glutamine addiction are two hallmarks of cancer pathophysiology. Consistent with this, several cell membrane glutamine transporters, belonging to different solute carrier (SLC) families, have been shown to be upregulated in a cell-specific manner to furnish the cells with glutamine and glutamine-derived metabolic intermediates. Among them, the system A transporter Slc38a1 has a higher affinity for glutamine compared to other SLC transporters, and it undergoes highly multifaceted regulation at gene and protein levels. The current study aimed to investigate the functional role of Slc38a1 in the proliferation and maturation of the mouse tongue epithelium. Secondly, we aimed to examine the expression of SLC38A1 and its regulation in human tongue oral squamous cell carcinoma (OTSCC). Employing Slc38a1 wild-type and knockout mice, we showed that Slc38a1 was not directly linked to the regulation of the proliferation and differentiation of the mouse tongue epithelium. External transcriptomic datasets and Western blot analyses showed upregulation of SLC38A1 mRNA/protein in human OTSCC and oral cancer cell lines as compared to the corresponding controls. Further, an investigation of external datasets indicated that mechanisms other than the amplification of the SLC38A1 chromosomal locus or hypomethylation of the SLC38A1 promoter region might be important for the upregulation of SLC38A1 in OTSCC.

• Aksnes, Mari; Edwin, Trine Holt; Saltvedt, Ingvild Tina; Eldholm, Rannveig Sakshaug; Chaudhry, Farrukh Abbas & Halaas, Nathalie Bodd [Vis alle 9 forfattere av denne artikkelen] (2023). Sex-specific associations of matrix metalloproteinases in Alzheimer’s disease. Biology of Sex Differences. 14(1). doi: 10.1186/s13293-023-00514-x. Fulltekst i vitenarkiv Vis sammendrag

  Introduction Alzheimer’s disease (AD) can be characterised in vivo by biomarkers reflecting amyloid-β (Aβ) and tau pathology. However, there is a need for biomarkers reflecting additional pathological pathways. Matrix metalloproteinases (MMPs) have recently been highlighted as candidate biomarkers for sex-specific mechanisms and progression in AD. Methods In this cross-sectional study, we investigated nine MMPs and four tissue inhibitors of metalloproteinases (TIMPs) in the cerebrospinal fluid of 256 memory clinic patients with mild cognitive impairment or dementia due to AD and 100 cognitively unimpaired age-matched controls. We studied group differences in MMP/TIMP levels and examined the associations with established markers of Aβ and tau pathology as well as disease progression. Further, we studied sex-specific interactions. Results MMP-10 and TIMP-2 levels differed significantly between the memory clinic patients and the cognitively unimpaired controls. Furthermore, MMP- and TIMP-levels were generally strongly associated with tau biomarkers, whereas only MMP-3 and TIMP-4 were associated with Aβ biomarkers; these associations were sex-specific. In terms of progression, we found a trend towards higher MMP-10 at baseline predicting more cognitive and functional decline over time exclusively in women. Conclusion Our results support the use of MMPs/TIMPs as markers of sex differences and progression in AD. Our findings show sex-specific effects of MMP-3 and TIMP-4 on amyloid pathology. Further, this study highlights that the sex-specific effects of MMP-10 on cognitive and functional decline should be studied further if MMP-10 is to be used as a prognostic biomarker for AD.

• Aksnes, Mari; Capogna, Elettra; Vidal-Piñeiro, Didac; Chaudhry, Farrukh Abbas; Myrstad, Marius & Idland, Ane-Victoria [Vis alle 13 forfattere av denne artikkelen] (2023). Matrix metalloproteinases are associated with brain atrophy in cognitively unimpaired individuals. Neurobiology of Aging. ISSN 0197-4580. 131, s. 11–23. doi: 10.1016/j.neurobiolaging.2023.05.012. Fulltekst i vitenarkiv Vis sammendrag

  Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) have been linked to age-related neurodegeneration and Alzheimer’s disease (AD), but their role in normal aging is poorly understood. We used linear mixed models to determine if baseline or rate of yearly change in cerebrospinal fluid (CSF) levels of MMP-2; MMP-3; MMP-10; TIMP-123 (composite of TIMP-1, TIMP-2, and TIMP-3); or TIMP-4 predicted changes in bilateral entorhinal cortex thickness, hippocampal volume, or lateral ventricle volume in cognitively unimpaired individuals. We also assessed effects on the CSF AD biomarkers amyloid-β42 and phosphorylated tau181. Low baseline levels of MMP-3 predicted larger ventricle volumes and more entorhinal cortex thinning. Increased CSF MMP-2 levels over time predicted more entorhinal thinning, hippocampal atrophy, and ventricular expansion, while increased TIMP-123 over time predicted ventricular expansion. No MMP/TIMPs predicted changes in CSF AD biomarkers. Notably, we show for the first time that longitudinal increases in MMP-2 and TIMP-123 levels may predict age-associated brain atrophy. In conclusion, MMPs and TIMPs may play a role in brain atrophy in cognitively unimpaired aging.

• Hamdani, El Hassan; Popek, Mariusz; Frontczak-Baniewicz, Małgorzata; Utheim, Tor Paaske; Albrecht, Jan & Zielińska, Magdalena [Vis alle 7 forfattere av denne artikkelen] (2021). Perturbation of astroglial Slc38 glutamine transporters by NH4 + contributes to neurophysiologic manifestations in acute liver failure. The FASEB Journal. ISSN 0892-6638. 35(7). doi: 10.1096/fj.202001712RR. Fulltekst i vitenarkiv Vis sammendrag

  Ammonia is considered the main pathogenic toxin in hepatic encephalopathy (HE). However, the molecular mechanisms involved have been disputed. As altered glutamatergic and GABAergic neurotransmission has been reported in HE, we investigated whether four members of the solute carrier 38 (Slc38) family of amino acid transporters—involved in the replenishment of glutamate and GABA—contribute to ammonia neurotoxicity in HE. We show that ammonium ion exerts multiple actions on the Slc38 transporters: It competes with glutamine for the binding to the system N transporters Slc38a3 and Slc38a5, consequently inhibiting bidirectional astroglial glutamine transport. It also competes with H+, Na+, and K+ for uncoupled permeation through the same transporters, which may perturb astroglial intracellular pH, membrane potential, and K+-buffering. Knockdown of Slc38a3 in mice results in cerebral cortical edema and disrupted neurotransmitter synthesis mimicking events contributing to HE development. Finally, in a mouse model of acute liver failure (ALF), we demonstrate the downregulation of Slc38a3 protein, impeded astroglial glutamine release, and cytotoxic edema. Altogether, we demonstrate contribution of Slc38 transporters to the ammonia-induced impairment of glutamine recycling between astrocytes and neurons, a phenomenon underlying acute ammonia neurotoxicity in the setting of ALF.

• Raheel, Tayyaba Qureshi; Bjørkmo, Mona; Nordengen, Kaja; Gundersen, Vidar; Utheim, Tor Paaske & Watne, Leiv Otto [Vis alle 9 forfattere av denne artikkelen] (2020). Slc38a1 Conveys Astroglia-Derived Glutamine into GABAergic Interneurons for Neurotransmitter GABA Synthesis. Cells. 9(7), s. 1–12. doi: 10.3390/cells9071686. Fulltekst i vitenarkiv Vis sammendrag

  GABA signaling is involved in a wide range of neuronal functions, such as synchronization of action potential firing, synaptic plasticity and neuronal development. Sustained GABA signaling requires efficient mechanisms for the replenishment of the neurotransmitter pool of GABA. The prevailing theory is that exocytotically released GABA may be transported into perisynaptic astroglia and converted to glutamine, which is then shuttled back to the neurons for resynthesis of GABA—i.e., the glutamate/GABA-glutamine (GGG) cycle. However, an unequivocal demonstration of astroglia-to-nerve terminal transport of glutamine and the contribution of astroglia-derived glutamine to neurotransmitter GABA synthesis is lacking. By genetic inactivation of the amino acid transporter Solute carrier 38 member a1 (Slc38a1)—which is enriched on parvalbumin+ GABAergic neurons—and by intraperitoneal injection of radiolabeled acetate (which is metabolized to glutamine in astroglial cells), we show that Slc38a1 mediates import of astroglia-derived glutamine into GABAergic neurons for synthesis of GABA. In brain slices, we demonstrate the role of Slc38a1 for the uptake of glutamine specifically into GABAergic nerve terminals for the synthesis of GABA depending on demand and glutamine supply. Thus, while leaving room for other pathways, our study demonstrates a key role of Slc38a1 for newly formed GABA, in harmony with the existence of a GGG cycle.

• Sajjad, Muhammad Umar; Blennow, Kaj; Knapskog, Anne Brita; Idland, Ane-Victoria; Chaudhry, Farrukh Abbas & Wyller, Torgeir Bruun [Vis alle 8 forfattere av denne artikkelen] (2020). Cerebrospinal Fluid Levels of Interleukin-8 in Delirium, Dementia, and Cognitively Healthy Patients. Journal of Alzheimer's Disease. ISSN 1387-2877. 73(4), s. 1363–1372. doi: 10.3233/JAD-190941. Fulltekst i vitenarkiv Vis sammendrag

  Background: Delirium is a common and serious complication in geriatric patients. The pathophysiology of delirium is not known. Objective: The objective of the current study was to test the hypothesis that cerebrospinal fluid (CSF) levels of inflammatory markers at the time of spinal anesthesia for hip surgery are associated with delirium. Methods: In total 133 hip fracture patients and 125 cognitively healthy controls undergoing elective surgery, together with 73 Alzheimer’s disease (AD) dementia patients, were recruited at Oslo University Hospital and Diakonhjemmet Hospital, Oslo, Norway. Delirium was evaluated daily in hip fracture patients by the Confusion Assessment Method (CAM). Depression was evaluated by Cornell Scale for Depression in Dementia (CSDD). Tumor necrosis factor alpha (TNF-α), interleukin-1beta (IL-1β), and interleukin-8 (IL-8) levels were measured in CSF using a Mesoscale Discovery (MSD) immunoassay. Results: Hip fracture patients had significantly higher IL-8 levels (p < 0.001) compared to cognitively healthy controls or patients with stable AD dementia. Furthermore, preoperative IL-8 levels were significantly higher (p = 0.013) in hip fracture patients who developed delirium (incident delirium) after surgery as compared to patients with no delirium. However, subgroup analyses showed that IL-8 levels were only significantly higher in delirium patients without dementia (p = 0.006). In contrast, depression subgroup analysis showed that IL-8 concentration was significantly higher (p = 0.002) in delirium patients with depression. Both TNF-α and IL-1β were undetected in most patients. Conclusions: Our study suggests that IL-8 levels are associated with delirium onset and that underlying depression or dementia influences IL-8 levels.

• Chaudhry, Farrukh Abbas; loland, claus juul; Ortega, Arturo & Schousboe, Arne (2019). Special issue on neurotransmitter transporters. Neuropharmacology. ISSN 0028-3908. 161. doi: 10.1016/j.neuropharm.2019.107859. Fulltekst i vitenarkiv
• Raheel, Tayyaba Qureshi; Sørensen, Christina; Berghuis, Paul; Jensen, Vidar; Dobszay, Marton B. & Farkas, Tamás [Vis alle 15 forfattere av denne artikkelen] (2019). The glutamine transporter Slc38a1 regulates GABAergic neurotransmission and synaptic plasticity. Cerebral Cortex. ISSN 1047-3211. 29(12), s. 5166–5179. doi: 10.1093/cercor/bhz055. Fulltekst i vitenarkiv Vis sammendrag

  GABA signaling sustains fundamental brain functions, from nervous system development to the synchronization of population activity and synaptic plasticity. Despite these pivotal features, molecular determinants underscoring the rapid and cell-autonomous replenishment of the vesicular neurotransmitter GABA and its impact on synaptic plasticity remain elusive. Here, we show that genetic disruption of the glutamine transporter Slc38a1 in mice hampers GABA synthesis, modifies synaptic vesicle morphology in GABAergic presynapses and impairs critical period plasticity. We demonstrate that Slc38a1-mediated glutamine transport regulates vesicular GABA content, induces high-frequency membrane oscillations and shapes cortical processing and plasticity. Taken together, this work shows that Slc38a1 is not merely a transporter accumulating glutamine for metabolic purposes, but a key component regulating several neuronal functions.

• Vohra, Rupali; Dalgaard, Line Marie; Vibæk, Jeppe; Langbøl, Mia Aggergaard; Bergersen, Linda Hildegard & Olsen, Niels Vidiendal [Vis alle 9 forfattere av denne artikkelen] (2019). Potential metabolic markers in glaucoma and their regulation in response to hypoxia. Acta Ophthalmologica. ISSN 1755-375X. s. 1–10. doi: 10.1111/aos.14021. Fulltekst i vitenarkiv
• Menchini, Robin Johansen & Chaudhry, Farrukh Abbas (2019). Multifaceted regulation of the system A transporter Slc38a2 suggests nanoscale regulation of amino acid metabolism and cellular signaling. Neuropharmacology. ISSN 0028-3908. 161:107789, s. 1–12. doi: 10.1016/j.neuropharm.2019.107789. Fulltekst i vitenarkiv Vis sammendrag

  Amino acids are essential for cellular protein synthesis, growth, metabolism, signaling and in stress responses. Cell plasma membranes harbor specialized transporters accumulating amino acids to support a variety of cellular biochemical pathways. Several transporters for neutral amino acids have been characterized. However, Slc38a2 (also known as SA1, SAT2, ATA2, SNAT2) representing the classical transport system A activity stands in a unique position: Being a secondarily active transporter energized by the electrochemical gradient of Na+, it creates steep concentration gradients for amino acids such as glutamine: this may subsequently drive the accumulation of additional neutral amino acids through exchange via transport systems ASC and L. Slc38a2 is ubiquitously expressed, yet in a cell-specific manner. In this review, we show that Slc38a2 is regulated at the transcriptional and translational levels as well as by ions and proteins through direct interactions. We describe how Slc38a2 senses amino acid availability and passes this onto intracellular signaling pathways and how it regulates protein synthesis, cellular proliferation and apoptosis through the mechanistic (mammalian) target of rapamycin (mTOR) and general control nonderepressible 2 (GCN2) pathways. Furthermore, we review how this extensively regulated transporter contributes to cellular osmoadaptation and how it is regulated by endoplasmic reticulum stress and various hormonal stimuli to promote cellular metabolism, cellular signaling and cell survival.

• Hassel, Bjørnar; Mariussen, Espen; Idland, Ane-Victoria; Dahl, Gry Torsæter; Ræder, Johan & Frihagen, Frede Jon [Vis alle 10 forfattere av denne artikkelen] (2018). CSF sodium at toxic levels precedes delirium in hip fracture patients. Neurotoxicology. ISSN 0161-813X. 69(December), s. 11–16. doi: 10.1016/j.neuro.2018.08.010. Fulltekst i vitenarkiv
• Wefers, Annika K; Haberlandt, Christian; Tekin, Nuriye Basdag; Fedorov, D.; Timmermann, A. & Want, Johannes Van der [Vis alle 10 forfattere av denne artikkelen] (2017). Synaptic input as a directional cue for migrating interneuron precursors. Development. ISSN 0950-1991. 144(22), s. 4125–4136. doi: 10.1242/dev.154096. Fulltekst i vitenarkiv Vis sammendrag

  During CNS development, interneuron precursors have to migrate extensively before they integrate in specific microcircuits. Known regulators of neuronal motility include classical neurotransmitters, yet the mechanisms that assure interneuron dispersal and interneuron/projection neuron matching during histogenesis remain largely elusive. We combined time-lapse video microscopy and electrophysiological analysis of the nascent cerebellum of transgenic Pax2-EGFP mice to address this issue. We found that cerebellar interneuronal precursors regularly show spontaneous postsynaptic currents, indicative of synaptic innervation, well before settling in the molecular layer. In keeping with the sensitivity of these cells to neurotransmitters, ablation of synaptic communication by blocking vesicular release in acute slices of developing cerebella slows migration. Significantly, abrogation of exocytosis primarily impedes the directional persistence of migratory interneuronal precursors. These results establish an unprecedented function of the early synaptic innervation of migrating neuronal precursors and demonstrate a role for synapses in the regulation of migration and pathfinding.

• Hov, Karen Roksund; Bolstad, Nils; Idland, Ane-Victoria; Zetterberg, Henrik; Blennow, Kaj & Chaudhry, Farrukh Abbas [Vis alle 10 forfattere av denne artikkelen] (2017). Cerebrospinal Fluid S100B and Alzheimer's Disease Biomarkers in Hip Fracture Patients with Delirium. Dementia and Geriatric Cognitive Disorders Extra. 7(3), s. 374–385. doi: 10.1159/000481853. Fulltekst i vitenarkiv Vis sammendrag

  Objectives: This study aimed to investigate the relationship between cerebrospinal fluid (CSF) S100B astrocyte-derived protein and delirium and to perform stratified analyses according to clinical and CSF markers of dementia. Methods: We performed a prospective cohort study in a university hospital setting. The participants were patients admitted for hip fracture (n = 98) or for elective surgery (n = 50). Delirium was assessed daily perioperatively in hip fracture patients using the Confusion Assessment Method. A consensus-based diagnosis of prefracture dementia was made using all available information. CSF was drawn at the onset of spinal anesthesia. S100B and phosphorylated tau (P-tau) concentrations were measured using electrochemiluminescence immunoassay and enzyme-linked immunosorbent assays, respectively. Results: In the hip fracture population (n = 98) there was no significant difference in CSF S100B concentrations between patients with ongoing preoperative (i.e., prevalent) delirium (n = 36, median [interquartile range] 1.11 μg/L [0.91–1.29]) and patients who never developed delirium (n = 46, 1.08 μg/L [0.92–1.28], p = 0.92). In patients without preoperative delirium, those who developed delirium postoperatively (i.e., incident delirium) (n = 16, 1.38 μg/L [1.08–1.62]) had higher concentrations of S100B than the 46 who never did (p = 0.013). This difference was confined to patients with pathological concentrations of P-tau (≥60 ng/L, n = 38). We also found that P-tau and S100B were correlated in CSF in the elective surgery patients. Conclusions: CSF S100B was elevated in patients with incident delirium who also had pathological levels of the Alzheimer disease biomarker P-tau, suggesting vulnerability caused by a preexisting process of astrocytic activation and tau pathology.

• Lancellotti, Patrizio; Pellikka, Patricia A.; Budts, Werner; Chaudhry, Farrukh Abbas; Donal, Erwan & Dulgheru, Raluca [Vis alle 17 forfattere av denne artikkelen] (2017). The clinical use of stress echocardiography in non-ischaemic heart disease: recommendations from the European Association of Cardiovascular Imaging and the American Society of Echocardiography. Journal of the American Society of Echocardiography. ISSN 0894-7317. 30(2), s. 101–138. doi: 10.1016/j.echo.2016.10.016. Fulltekst i vitenarkiv
• Idland, Ane-Victoria; Wyller, Torgeir Bruun; Støen, Randi; Eri, Lars Magne; Frihagen, Frede Jon & Ræder, Johan [Vis alle 13 forfattere av denne artikkelen] (2016). Preclinical amyloid-β and axonal degeneration pathology in delirium. Journal of Alzheimer's Disease. ISSN 1387-2877. 55(1), s. 371–379. doi: 10.3233/JAD-160461. Fulltekst i vitenarkiv
• Lee, Hyun-Wook; Osis, Gunars; Handlogten, Mary E.; Lamers, Wouter H.; Chaudhry, Farrukh Abbas & Verlander, Jill W. [Vis alle 7 forfattere av denne artikkelen] (2016). Proximal tubule-specific glutamine synthetase deletion alters basal and acidosis-stimulated ammonia metabolism. American Journal of Physiology - Renal, fluid and electrolyte physiology. ISSN 0363-6127. 310(11), s. F1229–F1242. doi: 10.1152/ajprenal.00547.2015. Fulltekst i vitenarkiv
• Moen, Marivi Nabong; Fjær, Roar; Hamdani, El Hassan; Lærdahl, Jon Kristen; Menchini, Robin Johansen & Vigeland, Magnus Dehli [Vis alle 13 forfattere av denne artikkelen] (2016). Pathogenic variants in KCTD7 perturb neuronal K+ fluxes and glutamine transport. Brain. ISSN 0006-8950. 139, s. 3109–3120. doi: 10.1093/brain/aww244. Fulltekst i vitenarkiv
• Watne, Leiv Otto; Idland, Ane-Victoria; Fekkes, Durk; Ræder, Johan; Frihagen, Frede Jon & Ranhoff, Anette Hylen [Vis alle 10 forfattere av denne artikkelen] (2016). Increased CSF levels of aromatic amino acids in hip fracture patients with delirium suggests higher monoaminergic activity. BMC Geriatrics. doi: 10.1186/s12877-016-0324-0. Fulltekst i vitenarkiv Vis sammendrag

  Background To examine whether delirium in hip fracture patients was associated with changes in the levels of amino acids and/or monoamine metabolites in cerebrospinal fluid (CSF) and serum.Methods In this prospective cohort study, 77 patients admitted with an acute hip fracture to Oslo University Hospital, Norway, were studied. The concentrations of amino acids in CSF and serum were determined by high performance liquid chromatography. The patients were assessed daily for delirium by the Confusion Assessment Method (pre-operatively and post-operative day 1–5 (all) or until discharge (delirious patients)). Pre-fracture dementia status was decided by an expert panel. Serum was collected pre-operatively and CSF immediately before spinal anesthesia.Results Fifty-three (71 %) hip fracture patients developed delirium. In hip fracture patients without dementia (n = 39), those with delirium had significantly higher CSF levels of tryptophan (40 % higher), tyrosine (60 % higher), phenylalanine (59 % higher) and the monoamine metabolite 5-hydroxyindoleacetate (23 % higher) compared to those without delirium. The same amino acids were also higher in CSF in delirious patients with dementia (n = 38). The correlations between serum and CSF amino acid levels were poor.Conclusion Higher CSF levels of monoamine precursors in hip fracture patients with delirium suggest a higher monoaminergic activity in the central nervous system during delirium in this patient group.

• Hu, Liyan; Ibrahim, Khalid; Stucki, Martin; Frapolli, Michele; Shahbeck, Noora & Chaudhry, Farrukh Abbas [Vis alle 11 forfattere av denne artikkelen] (2015). Secondary NAD+ deficiency in the inherited defect of glutamine synthetase. The Journal of Inherited Metabolic Disease (JIMD). ISSN 0141-8955. 38(6), s. 1075–1083. doi: 10.1007/s10545-015-9846-4. Fulltekst i vitenarkiv
• Soussi, Rabia; Boulland, Jean-Luc; Emilie, Bassot; Bras, Hélène; Coulon, Patrice & Chaudhry, Farrukh Abbas [Vis alle 9 forfattere av denne artikkelen] (2014). Reorganization of supramammillary–hippocampal pathways in the rat pilocarpine model of temporal lobe epilepsy: evidence for axon terminal sprouting. Brain Structure and Function. ISSN 1863-2653. 220(4), s. 2449–2468. doi: 10.1007/s00429-014-0800-2. Fulltekst i vitenarkiv
• Jenstad, Monica & Chaudhry, Farrukh Abbas (2013). The Amino Acid Transporters of the Glutamate/GABA-Glutamine Cycle and Their Impact on Insulin and Glucagon Secretion. Frontiers in Endocrinology. 4. doi: 10.3389/fendo.2013.00199. Fulltekst i vitenarkiv Vis sammendrag

  Intercellular communication is pivotal in optimizing and synchronizing cellular responses to keep homeostasis and to respond adequately to external stimuli. In the central nervous system (CNS), glutamatergic and GABAergic signals are postulated to be dependent on the glutamate/GABA-glutamine cycle for vesicular loading of neurotransmitters, for inactivating the signal and for the replenishment of the neurotransmitters. Islets of Langerhans release the hormones insulin and glucagon, but share similarities with CNS cells in for example transcriptional control of development and differentiation, and chromatin methylation. Interestingly, CNS proteins involved in secretion of the neurotransmitters and emitting their responses as well as the regulation of these processes, are also found in islet cells. Moreover, high levels of glutamate, GABA, and glutamine and their respective vesicular and plasma membrane transporters have been shown in the islet cells and there is emerging support for these amino acids and their transporters playing important roles in the maturation and secretion of insulin and glucagon. In this review, we will discuss the feasibility of recent data in the field in relation to the biophysical properties of the transporters (Slc1, Slc17, Slc32, and Slc38) and physiology of hormone secretion in islets of Langerhans.

• Nissen-Meyer, Lise Sofie Haug & Chaudhry, Farrukh Abbas (2013). Protein kinase C phosphorylates the system N glutamine transporter SN1 (Slc38a3) and regulates its membrane trafficking and degradation. Frontiers in Endocrinology. 4, s. 1–7. doi: 10.3389/fendo.2013.00138. Fulltekst i vitenarkiv Vis sammendrag

  The system N transporter SN1 (also known as SNAT3) is enriched on perisynaptic astroglial cell membranes. SN1 mediates electroneutral and bidirectional glutamine transport, and regulates the intracellular as well as the extracellular concentrations of glutamine. We hypothesize that SN1 participates in the glutamate/?-aminobutyric acid (GABA)-glutamine cycle and regulates the amount of glutamine supplied to the neurons for replenishment of the neurotransmitter pools of glutamate and GABA. We also hypothesize that its activity on the plasma membrane is regulated by protein kinase C (PKC)-mediated phosphorylation and that SN1 activity has an impact on synaptic plasticity. This review discusses reports on the regulation of SN1 by PKC and presents a consolidated model for regulation and degradation of SN1 and the subsequent functional implications. As SN1 function is likely also regulated by PKC-mediated phosphorylation in peripheral organs, the same mechanisms may, thus, have impact on e.g., pH regulation in the kidney, urea formation in the liver, and insulin secretion in the pancreas.

• Stensrud, Mats Julius; Chaudhry, Farrukh Abbas; Leergaard, Trygve Brauns; Bjaalie, Jan G. & Gundersen, Vidar (2013). Vesicular glutamate transporter-3 in the rodent brain: Vesicular colocalization with vesicular -aminobutyric acid transporter. Journal of Comparative Neurology. ISSN 0021-9967. 521(13), s. 3042–3056. doi: 10.1002/cne.23331. Fulltekst i vitenarkiv
• Haberle, Johannes; Shahbeck, Noora; Khalid, Ibrahim; Schmitt, Bernhard; Scheer, Ianina & O’Gorman, Ruth [Vis alle 8 forfattere av denne artikkelen] (2012). Glutamine supplementation in a child with inherited GS deficiency improves the clinical status and partially corrects the peripheral and central amino acid imbalance. Orphanet Journal of Rare Diseases. 7(48). doi: 10.1186/1750-1172-7-48. Fulltekst i vitenarkiv
• Boulland, Jean-Luc & Chaudhry, Farrukh Abbas (2012). Ontogenetic changes in the distribution of the vesicular GABA transporter VGAT correlate with the excitation/inhibition shift of GABA action. Neurochemistry International. ISSN 0197-0186. 61(4), s. 506–516. doi: 10.1016/j.neuint.2012.03.018. Fulltekst i vitenarkiv
• Ormel, Lasse; Stensrud, Mats Julius; Chaudhry, Farrukh Abbas & Gundersen, Vidar (2012). A distinct set of synaptic-like microvesicles in atroglial cells contain VGLUT3. Glia. ISSN 0894-1491. 60(9), s. 1289–1300. doi: 10.1002/glia.22348. Fulltekst i vitenarkiv
• Antonucci, Flavia; Alpar, Alán; Kacza, Johannes; Caleo, Matteo; Verderio, Claudia & Giani, Alice [Vis alle 16 forfattere av denne artikkelen] (2012). Cracking Down on Inhibition: Selective Removal of GABAergic Interneurons from Hippocampal Networks. Journal of Neuroscience. ISSN 0270-6474. 32(6), s. 1989–2001. doi: 10.1523/JNEUROSCI.2720-11.2012. Fulltekst i vitenarkiv
• Oguchi, Tomohiro; Suzuki, Nobuyoshi; Hashimoto, Shigenari; Chaudhry, Gauhar Ayub; Chaudhry, Farrukh Abbas & Usami, Shin-ichi [Vis alle 7 forfattere av denne artikkelen] (2012). Inner hair cells of mice express the glutamine transporter SAT1. Hearing Research. ISSN 0378-5955. 292(1-2), s. 59–63. doi: 10.1016/j.heares.2012.07.005. Fulltekst i vitenarkiv
• Perez, Edgar L.; Lauritzen, Fredrik; Wang, Yue; Lee, Tih-Shih W.; Kang, Dewey & Zaveri, Hitten P. [Vis alle 10 forfattere av denne artikkelen] (2012). Evidence for astrocytes as a potential source of the glutamate excess in temporal lobe epilepsy. Neurobiology of Disease. ISSN 0969-9961. 47(3), s. 331–337. doi: 10.1016/j.nbd.2012.05.010. Fulltekst i vitenarkiv
• Hamdani, El Hassan; Gudbrandsen, Marius; Bjørkmo, Mona & Chaudhry, Farrukh Abbas (2012). The system N transporter SN2 doubles as a transmitter precursor furnisher and a potential regulator of NMDA receptors. Glia. ISSN 0894-1491. 60(11), s. 1671–1683. doi: 10.1002/glia.22386. Fulltekst i vitenarkiv
• Gammelsaeter, Runhild; Coppola, Thierry; Marcaggi, Païkan; Storm-Mathisen, Jon; Chaudhry, Farrukh Abbas & Attwell, David [Vis alle 8 forfattere av denne artikkelen] (2011). A Role for Glutamate Transporters in the Regulation of Insulin Secretion. PLOS ONE. 6(8). doi: 10.1371/journal.pone.0022960. Fulltekst i vitenarkiv
• Nissen-Meyer, Lise-Sofie; Popescu, Mark-Christian; Hamdani, El Hassan & Chaudhry, Farrukh Abbas (2011). Protein Kinase C-Mediated Phosphorylation of a Single Serine Residue on the Rat Glial Glutamine Transporter SN1 Governs Its Membrane Trafficking. Journal of Neuroscience. ISSN 0270-6474. 31(17), s. 6565–6575. doi: 10.1523/JNEUROSCI.3694-10.2011. Fulltekst i vitenarkiv
• Nemani, Venu; Lu, Weiping; Berge, Victoria; Nakamura, K; Onoa, Bibiana & Lee, Michael K [Vis alle 9 forfattere av denne artikkelen] (2010). Increased Expression of alpha-Synuclein Reduces Neurotransmitter Release by Inhibiting Synaptic Vesicle Reclustering after Endocytosis. Neuron. ISSN 0896-6273. 65(1), s. 66–79. doi: 10.1016/j.neuron.2009.12.023. Fulltekst i vitenarkiv
• Jenstad, Monica; Quazi, Abrar Zaheer; Zilberter, M; Haglerød, Camilla Margrete; Berghuis, P & Saddique, Navida [Vis alle 16 forfattere av denne artikkelen] (2009). System A transporter SAT2 mediates replenishment of dendritic glutamate pools controlling retrograde signalling by glutamate. Cerebral Cortex. ISSN 1047-3211. 19(5), s. 1092–1106. doi: 10.1093/cercor/bhn151. Fulltekst i vitenarkiv
• Blot, A; Billups, D; Bjørkmo, Mona; Quazi, Abrar Zaheer; Uwechue, NM & Chaudhry, Farrukh Abbas [Vis alle 7 forfattere av denne artikkelen] (2009). FUNCTIONAL EXPRESSION OF TWO SYSTEM A GLUTAMINE TRANSPORTER ISOFORMS IN RAT AUDITORY BRAINSTEM NEURONS. Neuroscience. ISSN 0306-4522. 164(3), s. 998–1008. doi: 10.1016/j.neuroscience.2009.09.015. Fulltekst i vitenarkiv
• Gammelsaeter, Runhild; Jenstad, Monica; Bredahl, May Kristin Lyamouri; Gundersen, Vidar & Chaudhry, Farrukh Abbas (2009). Complementary expression of SN1 and SAT2 in the islets of Langerhans suggests concerted action of glutamine transport in the regulation of insulin secretion. Biochemical and Biophysical Research Communications - BBRC. ISSN 0006-291X. 381(3), s. 378–382. doi: 10.1016/j.bbrc.2009.02.062. Fulltekst i vitenarkiv
• Boulland, Jean-Luc; Jenstad, Monica; Boekel, AJ; Wouterlood, FG; Edwards, RH & Storm-Mathisen, Jon [Vis alle 7 forfattere av denne artikkelen] (2009). Vesicular Glutamate and GABA Transporters Sort to Distinct Sets of Vesicles in a Population of Presynaptic Terminals. Cerebral Cortex. ISSN 1047-3211. 19(1), s. 241–248. doi: 10.1093/cercor/bhn077. Fulltekst i vitenarkiv
• Buntup, D; Skare, Øivind; Solbu, Tom Tallak; Chaudhry, Farrukh Abbas; Storm-Mathisen, Jon & Thangnipon, W (2008). beta-amyloid 25-35 peptide reduces the expression of glutamine transporter SAT1 in cultured cortical neurons. Neurochemical Research. ISSN 0364-3190. 33(2), s. 248–256. doi: 10.1007/s11064-007-9527-2. Fulltekst i vitenarkiv
• Boulland, Jean-Luc; Jenstad, Monica; Wouterlood, FG; Edwards, RH; Storm-Mathisen, Jon & Chaudhry, Farrukh Abbas (2008). Vesicular glutamate and GABA transporters are expressed on distinct subsets of synaptic vesicles at a synapse. Cerebral Cortex. ISSN 1047-3211. Fulltekst i vitenarkiv
• Martens, H; Weston, MC; Boulland, Jean-Luc; Harkany, T; Grosche, J. & Kacza, J [Vis alle 14 forfattere av denne artikkelen] (2008). Unique luminal localization of VGAT carboxy-terminus allows for selective labelling of active cortical GABAergic synapses. Journal of Neuroscience. ISSN 0270-6474. 3(28), s. 13125–13131. Fulltekst i vitenarkiv
• Jenstad, Monica; Quazi, AZ; Haglerød, C.; Saddique, Navida; Buntup, D & Ottersen, OP [Vis alle 12 forfattere av denne artikkelen] (2008). Replenishment of glutamate neurotransmitter pools in excitatory neurons requires glutamine uptake by system A transporter SAT2. Cerebral Cortex. ISSN 1047-3211. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Edwards, RH & Fonnum, Frode (2008). Vesicular neurotransmitter transporters as targets for endogenous and exogenous toxic substances. Annual Review of Pharmacology and Toxicology. ISSN 0362-1642. 48. doi: 10.1146/annurev.pharmtox.46.120604.141146. Fulltekst i vitenarkiv
• Leibovici, A; Rossignol, C; Montrowl, JA; Erickson, JD; Varoqui, H & Watanabe, M [Vis alle 10 forfattere av denne artikkelen] (2007). The effects of hypoxia-ischemia on neutral amino acid transporters in the developing rat brain. Developmental Neuroscience. ISSN 0378-5866. 29, s. 268–274. doi: 10.1159/000097410. Fulltekst i vitenarkiv
• Boulland, Jean-Luc; Ferhat, L; Solbu, TT; Ferrand, N; Chaudhry, Farrukh Abbas & Storm-Mathisen, Jon [Vis alle 7 forfattere av denne artikkelen] (2007). Changes in vesicular transporters for gamma-aminobutyric acid and glutamate reveal vulnerability and reorganization of hippocampal neurons following pilocarpine-induced seizures. Journal of Comparative Neurology. ISSN 0021-9967. 503, s. 466–485. doi: 10.1002/cne.21384. Fulltekst i vitenarkiv
• Martin-Ibanez, R; Jenstad, Monica; Berghuis, P; Edwards, RH; Hioki, H & Kaneko, T [Vis alle 11 forfattere av denne artikkelen] (2006). Vesicular glutamate transporter 3 (VGLUT3) identifies spatially segregated excitatory terminals in the rat substantia nigra. European Journal of Neuroscience. ISSN 0953-816X. 23. Fulltekst i vitenarkiv
• Larsen, Kristin E.; Schmitz, Yvonne; Troyer, Matthew D.; Mosharov, Eugene; Dietrich, Paula & Quazi, Abrar Zaheer [Vis alle 12 forfattere av denne artikkelen] (2006). alpha-synuclein overexpression in PC12 and chromaffin cells impairs catecholamine release by interfering with a late step in exocytosis. Journal of Neuroscience. ISSN 0270-6474. 26, s. 11915–11922. Fulltekst i vitenarkiv
• Persson, S; Boulland, Jean-Luc; Aspling, M; Larsson, M; Fremeau, RT & Edwards, RH [Vis alle 9 forfattere av denne artikkelen] (2006). Distribution of vesicular glutamate transporters 1 and 2 in the rat spinal cord, with a note on the spinocervical tract. Journal of Comparative Neurology. ISSN 0021-9967. 497. Fulltekst i vitenarkiv
• Solbu, Tom Tallak & Chaudhry, Farrukh Abbas (2005). Glutamin-transportrers funksjoner i fysiologiske prosesser og i patologi. NBS-nytt. ISSN 0801-3535. s. 6–8. Fulltekst i vitenarkiv
• Solbu, Tom Tallak; Boulland, Jean-Luc; Zahid, W; Bredahl, May Kristin Lyamouri; Amiry-Moghaddam, Mahmood Reza & Storm-Mathisen, Jon [Vis alle 8 forfattere av denne artikkelen] (2005). Induction and targeting of the glutamine transporter SN1 to the basolateral membranes of cortical kidney tubule cells during chronic metabolic acidosis suggest a role in pH regulation. Journal of the American Society of Nephrology. ISSN 1046-6673. 16. Fulltekst i vitenarkiv
• Maghazachi, Azzam; Knudsen, Eirunn; Jin, Yixin; Jenstad, Monica & Chaudhry, Farrukh Abbas (2004). D-galactosyl-b1-1' sphingosine and D-glucosyl-b1-1' sphingosine induce human natural killer cell apoptosis. Biochemical and Biophysical Research Communications - BBRC. ISSN 0006-291X. 320, s. 810–815. Fulltekst i vitenarkiv
• Boulland, Jean-Luc; Qureshi, T.; Seal, R; Rafiki, A; Gundersen, Vidar & Bergersen, Linda Hildegard [Vis alle 10 forfattere av denne artikkelen] (2004). Expression of the vesicular glutamate transporters during development indicates the widespread co-release of multiple neurotransmitters. Journal of Comparative Neurology. ISSN 0021-9967. 480(3), s. 264–280. Fulltekst i vitenarkiv
• Harkany, T; Holmgren, C; Hartig, W; Qureshi, T; Chaudhry, Farrukh Abbas & Storm-Mathisen, Jon [Vis alle 15 forfattere av denne artikkelen] (2004). Endocannabinoid-independent retrograde signaling at inhibitory synapses in layer 2/3 of neocortex: Involvement of vesicular glutamate transporter 3. Journal of Neuroscience. ISSN 0270-6474. 24(21), s. 4978–4988. Fulltekst i vitenarkiv
• Fremeau, RT; Kam, K; Qureshi, T; Johnson, J; Copenhagen, DR & Storm-Mathisen, Jon [Vis alle 9 forfattere av denne artikkelen] (2004). Vesicular glutamate transporters 1 and 2 target to functionally distinct synaptic release sites. Science. ISSN 0036-8075. 304(5678), s. 1815–1819. Fulltekst i vitenarkiv
• Boulland, JL; Rafiki, A; Levy, Line Margrete; Storm-Mathisen, Jon & Chaudhry, Farrukh Abbas (2003). Highly differential expression of SN1, a bidirectional glutamine transporter, in astroglia and endothelium in the developing rat brain. Glia. ISSN 0894-1491. 41, s. 260–275. Fulltekst i vitenarkiv
• Bröer, A.; Albers, A.; Setiawan, I.; Edwards, R. H.; Chaudhry, Farrukh Abbas & Lang, F. [Vis alle 8 forfattere av denne artikkelen] (2002). Regulation of the glutamine transporter SN1 by extracellular pH and intracellular sodium ions. Journal of Physiology. ISSN 0022-3751. 539, s. 3–14. Fulltekst i vitenarkiv
• Boulland, Jean-Luc; Osen, Kirsten K.; Levy, Line Margrete; Danbolt, Niels Christian; Edwards, R. H. & Storm-Mathisen, Jon [Vis alle 7 forfattere av denne artikkelen] (2002). Cell-specific expression of the glutamine transporter SN1 suggests differences in dependence on the glutamine cycle. European Journal of Neuroscience. ISSN 0953-816X. 15(10), s. 1615–1631. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Reimer, R.J. & Edwards, R. H. (2002). The glutamine commute: take the N and transfer to the A line. Journal of Cell Biology. ISSN 0021-9525. 157, s. 349–355. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Schmitz, D.; Reimer, R.J.; Larsson, P.; Gray, A.T. & Nicoll, R. [Vis alle 8 forfattere av denne artikkelen] (2002). Glutamine uptake by neurons: interaction of protons with system A transporters. Journal of Neuroscience. ISSN 0270-6474. 22, s. 62–72. Fulltekst i vitenarkiv

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• Chaudhry, Farrukh Abbas; Heiberg, Arvid & Sajjad, Torunn Arntsen (2023). Søskenbarn bør kunne gifte seg. Tidsskrift for Den norske legeforening (Tidsskriftet). ISSN 0029-2001. 143(18), s. 1–5. doi: 10.4045/tidsskr.23.0733. Fulltekst i vitenarkiv
• Sajjad, Torunn Arntsen; Chaudhry, Farrukh Abbas & Heiberg, Arvid (2023). Foreldede data. Aftenposten (morgenutg. : trykt utg.). ISSN 0804-3116. Fulltekst i vitenarkiv
• Sørensen, Christina; Qureshi, Tayyaba; Fyhn, Marianne; Hafting, Torkel & Chaudhry, Farrukh Abbas (2021). GABA er essensielt for normal hjerneutvikling og synaptisk plastisitet. NBS-nytt. ISSN 0801-3535. Fulltekst i vitenarkiv
• Nissen-Meyer, Lise Sofie Haug & Chaudhry, Farrukh Abbas (2017). Corrigendum: Protein kinase C phosphorylates the system N glutamine transporter SN1 (Slc38a3) and regulates its Membrane trafficking and Degradation [Front Endocrinol, 4, (2013) (138)] doi: 10.3389/fendo.2013.00138. Frontiers in Endocrinology. 8:190, s. 1–2. doi: 10.3389/fendo.2017.00190. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Knutsen, Leif; Kohn, Leoni Abrahamsen & Kirschner, Rolf Steinar (2016). Re: Omskjæring av gutter. Tidsskrift for Den norske legeforening (Tidsskriftet). ISSN 0029-2001. 136(2), s. 106–106. doi: 10.4045/tidsskr.15.1367. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Nissen-Meyer, Lise Sofie Haug; Popescu, Mark-Christian; Bjørkmo, Mona; Gudbrandsen, Marius & Hamdani, El Hassan (2013). SN2 (Slc38a5) resembles SN1 (Slc38a3) in electroneutral transport but partly differ in functional roles. Journal of Neurochemistry. ISSN 0022-3042. 125, s. 153–153. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2013). Nervesystemet. I Nicolaysen, Gunnar & Holck, Per (Red.), Kroppens funksjon og oppbygning. Gyldendal Akademisk. ISSN 9788205323629. s. 55–94. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2012). Glutamintilførsel ved medfødt glutaminesvikt. Tidsskrift for Den norske legeforening (Tidsskriftet). ISSN 0029-2001. 18, s. 132–132. Fulltekst i vitenarkiv
• Haberle, Johannes; Ibrahim, Khalid; Hu, L.; Frapolli, Michele; Stucki, Martin & Scheer, Ianina [Vis alle 9 forfattere av denne artikkelen] (2012). Pathofunctional roles of glutamine transporters in neurotransmission, insulin secretion and pH regulation. Molecular Genetics and Metabolism. ISSN 1096-7192. 105, s. 283–283. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2012). Glutamate and GABA recycling through glutamine – what is the significance. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2012). (Patho-)functional roles of glutamine transporters in neurotransmission, insulin secretion and pH regulation. Fulltekst i vitenarkiv
• Haberle, Johannes; Ibrahim, Khalid; Shahbeck, Noora; Hu, Liyan; Frapolli, Michele & Stucki, Martin [Vis alle 10 forfattere av denne artikkelen] (2012). Glutamine synthetase deficiency: An emerging disorder of nitrogen metabolism. Molecular Genetics and Metabolism. ISSN 1096-7192. 105(3), s. 283–283. Fulltekst i vitenarkiv
• Hossain, Shaikh Abu; Chaudhry, Farrukh Abbas; Zahedi, Kamyar; Siddiqui, Faraaz & Amlal, Hassane (2011). Cellular and molecular basis of increased ammoniagenesis in potassium deprivation. American Journal of Physiology - Renal, fluid and electrolyte physiology. ISSN 0363-6127. 301(5), s. 969–978. doi: 10.1152/ajprenal.00010.2011. Fulltekst i vitenarkiv
• Antonucci, F; Alpár, A; Kacza, J; Caleo, M; Verderio, C & Giani, A [Vis alle 15 forfattere av denne artikkelen] (2011). Cracking Down on Inhibition: Selective Removal of GABAergic Interneurons from Hippocampal Networks. Journal of Neuroscience. ISSN 0270-6474. 32(6), s. 1989–2001. Fulltekst i vitenarkiv
• Solbu, Tom Tallak; Bjørkmo, Mona; Berghuis, P; Harkany, T & Chaudhry, Farrukh Abbas (2009). SAT1, a glutamine transporter, is preferentially expressed in GABAergic neurons. Frontiers in Neuroanatomy. doi: 10.3389/neuro.05.033.2010. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2008). Neurotransmitter transport. Fulltekst i vitenarkiv
• Boulland, Jean-Luc; Jenstad, Monica; Boekel, AJ; Wouterlood, FG; Edwards, RH & Storm-Mathisen, Jon [Vis alle 7 forfattere av denne artikkelen] (2008). VGLUT2 and VGAT are targeted to different subsets of vesicles within a single terminal. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Jenstad, Monica; Boekel, AJ; Wouterlood, FG; Edwards, R. H. & Storm-Mathisen, Jon [Vis alle 7 forfattere av denne artikkelen] (2008). 331.2. VGLUT2 and VGAT reside on different subpopulations of vesicles suggesting differential release of glutamate and GABA from a single nerve terminal. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Boulland, Jean-Luc; Jenstad, M; Bredahl, May Kristin Lyamouri & Edwards, RH (2008). Pharmacology of neurotransmitter transport into secretory vesicles. Handbook of Experimental Pharmacology. ISSN 0171-2004. 184, s. 77–106. Fulltekst i vitenarkiv
• Buntup, D; Thangnipon, W; Solbu, Tom Tallak; Chaudhry, Farrukh Abbas & Storm-Mathisen, Jon (2008). Effects of -amyloid25-35 on the expression of glutamine transporters and vesicular glutamate transporters in rat cortical cell cultures. Journal of Neurochemistry. ISSN 0022-3042. s. 357–357. Fulltekst i vitenarkiv
• Jenstad, M; Quazi, Abrar Zaheer; Barnes, CA; McNaughton, BL; Storm-Mathisen, J & Chaudhry, Farrukh Abbas (2005). Increased de novo synthesis of glutamate from glutamine upon high frequency stimulation of SAT2 expressing neurons. Fulltekst i vitenarkiv
• Gundersen, V; Gammelsaeter, R; Chaudhry, Farrukh Abbas; Danbolt, NC; Regazzi, R & Storm-Mathisen, J (2005). Novel roles of glutamate transporters in the regulation of insulin secretion. Fulltekst i vitenarkiv
• Faroqui, S; Chaudhry, Farrukh Abbas & Amlal, H (2005). Coordinated upregulation of Na+-glutamine cotransporter (SN1) and ammoniagenesis enzymes in the cortex of potassium-deprived rats. Fulltekst i vitenarkiv
• Solbu, Tom Tallak; Boulland, Jean-Luc; Bredahl, May Kristin Lyamouri; Zahid, W; Kongsvik, Thomas Lasker & Storm-Mathisen, J [Vis alle 7 forfattere av denne artikkelen] (2005). SN1, a neutral amino acid transporter, is upregulated during chronic metabolic acidosis by stabilization of the mRNA. Fulltekst i vitenarkiv
• Quazi, Abrar Zaheer; Jenstad, Monica; Haglerød, Camilla Margrete; Saddique, N; Ottersen, Ole Petter & Davanger, Svend [Vis alle 11 forfattere av denne artikkelen] (2005). Glutamine shuttling by the system N and system A transporters is important for the regeneration of the neurotransmitter glutamate during high frequency firing. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2005). Perspectives in Transport Biology. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2005). New perspectives in neurotransmitter transporter biology. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2005). Molecular Approaches to Membrane Transport. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2005). Glutamate in CNS metabolism and neurotransmission: interactions at the inter- and intracellular level. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2005). Membrane transporters: bridging basic and applied sciences. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2005). Neurocircuits and the synapse. Fulltekst i vitenarkiv
• Bredahl, May Kristin Lyamouri; Solbu, Tom Tallak; Boulland, Jean-Luc; Zahid, W; Storm-Mathisen, J & Chaudhry, Farrukh Abbas (2005). SN1, a neutral amino acid transporter, is regulated in the kidney during chronic metabolic acidosis by stabilization of the mRNA. Journal of Neurochemistry. ISSN 0022-3042. s. 357–357. Fulltekst i vitenarkiv
• Solbu, Tom Tallak; Boulland, Jean-Luc; Bredahl, May Kristin Lyamouri; Zahid, W; Kongsvik, Thomas Lasker & Storm-Mathisen, J [Vis alle 7 forfattere av denne artikkelen] (2005). Stabilization of AU-RICH elements in 3'UTR upregulates the neutral amino acid transporter SN1 during chronic metabolic acidosis. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas (2004). Characterization of transporter proteins involved in the recycling of the neurotransmitters glutamate and GABA. Journal of Neurochemistry. ISSN 0022-3042. 90, s. 132–132. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Boulland, Jean-Luc; Solbu, Tom Tallak; Jenstad, Monica; Haglerød, Camilla Margrete & Zahid, W [Vis alle 7 forfattere av denne artikkelen] (2003). Glutamine transporters involved in the glutamine-glutamate/GABA cycle. Journal of Neurochemistry. ISSN 0022-3042. 87, s. 4–4. Fulltekst i vitenarkiv
• Solbu, Tom Tallak; Zahid, W.; Boulland, JL; Qureshi, T.; Storm-Mathisen, Jon & Chaudhry, Farrukh Abbas (2003). Targeting of the proton-coupled glutamine transporter, SN1, suggests roles in synaptic functions and pH. Glia. ISSN 0894-1491. s. 32–32. Fulltekst i vitenarkiv
• Gammelsæter, Runhild; Gundersen, Vidar; Storm-Mathisen, Jon & Chaudhry, Farrukh Abbas (2003). Expression of VGLUT2 and VGLUT3 in pancreatic neuroendocrine cells: preserved after transplantation of islets of Langerhans to kidney. Fulltekst i vitenarkiv
• Chaudhry, Farrukh Abbas; Boulland, Jean-Luc; Qureshi, T; Solbu, Tom Tallak; Jenstad, Monica & Kanstad, Kristin [Vis alle 10 forfattere av denne artikkelen] (2003). Glutamine and vesicular glutamate transporters involved in the glutamine-glutamate/GABA cycle. Journal of Neurochemistry. ISSN 0022-3042. 87, s. 3–3. Fulltekst i vitenarkiv
• Solbu, Tom Tallak; Jenstad, Monica; Etemad, K. K.; Zahid, W.; Boulland, Jean-Luc & Storm-Mathisen, Jon [Vis alle 8 forfattere av denne artikkelen] (2002). Glutamine transporters involved in the glutamine-glutamate/GABA cycle. Fulltekst i vitenarkiv

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