The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index; 10 of the 143 sources its claims cite were checked for support.
Parvalbumin interneuron vulnerability and brain disorders
Open accessAbstract
Parvalbumin-expressing interneurons (PV-INs) are highly vulnerable to stressors and have been implicated in many neuro-psychiatric diseases such as schizophrenia, Alzheimer's disease, autism spectrum disorder, and bipolar disorder. We examined the literature about the current knowledge of the physiological properties of PV-INs and gathered results from diverse research areas to provide insight into their vulnerability to stressors. Among the factors that confer heightened vulnerability are the substantial energy requirements, a strong excitatory drive, and a unique developmental trajectory. Understanding these stressors and elaborating on their impact on PV-IN health is a step toward developing therapies to protect these neurons in various disease states and to retain critical brain functions.
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73 Not checked yet · 15 Own interpretation · 5 No basis given · 3 Supported · 1 Supported so far · 1 Partly supported · accuracy not yet measured
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In the paper
“Mouse models relevant for both disorders, including the disrupted in schizophrenia 1 gene (Disc1) [57][58][59][60][61], or brain derived neurotrophic factor (Bdnf) [62], show abnormal PV-IN function ranging from migration deficits to reduction in IN number.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Partly supportedcites [57] Lee FH, Zai CC, Cordes SP, Roder JC, Wong AH. Abnormal interneuron development in disrupted-in-schizophrenia-1 L100P mutant mice. Mol Brain. 2013;6:20. sourceExperimental — accuracy not yet measured
The Results sections on embryonic tangential position, adult cortical PV-interneuron distribution, and mPFC cell numbers report migration-related abnormalities and fewer PV-positive interneurons in Disc1-L100P mice. The paper describes this model as relevant to schizophrenia and refers generally to other mental disorders, but does not establish its relevance to bipolar disorder. Bdnf has a separate citation in the citing sentence and is not attributed to this source. (LLM, conf=0.83)
- Partly supportedcites [62] Jones NC, Hudson M, Foreman J, Rind G, Hill R, Manning EE, et al. Brain-derived neurotrophic factor haploinsufficiency impairs high-frequency cortical oscillations in mice. Eur J Neurosci. 2018;48:2816–25. sourceExperimental — accuracy not yet measured
The Results section (‘Effects of BDNF genotype on parvalbumin levels’; page unavailable) reports reduced cortical PV immunoreactivity in BDNF-deficient mice, supporting an abnormality associated with PV interneurons. It measures protein expression, not interneuron number or migration, and the paper frames the model as relevant to schizophrenia rather than establishing relevance to bipolar disorder. The Disc1 models are attached to other citations in the sentence. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Partly supported
In the paper
“Furthermore, individuals with schizophrenia have a lower density of excitatory synapses on PV-INs [12] and exhibit alterations in gamma oscillations during a working memory task [13].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [12] Chung DW, Fish KN, Lewis DA. Pathological basis for deficient excitatory drive to cortical parvalbumin interneurons in schizophrenia. Am J Psychiatry. 2016;173:1131–9. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Injury to, or dysfunction of, parvalbumin inhibitory interneurons (PV-INs) has been proposed to contribute to the pathophysiology of several important neuro-psychiatric disorders, including schizophrenia, autism spectrum disorder (ASD), bipolar disorder (BPD), various neurodegenerative diseases, and even aging-related cognitive changes.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
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In the paper
“Furthermore, individuals with schizophrenia have a lower density of excitatory synapses on PV-INs [12] and exhibit alterations in gamma oscillations during a working memory task [13].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [13] Barr MS, Farzan F, Tran LC, Chen R, Fitzgerald PB, Daskalakis ZJ. Evidence for excessive frontal evoked gamma oscillatory activity in schizophrenia during working memory. Schizophr Res. 2010;121:146–52. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Animal models that mimic schizophrenia replicate the loss of PV-INs in the hippocampus [6,14,15], and show a loss of PV fluorescence per cell in prelimbic regions [16].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [6] Lodge DJ, Behrens MM, Grace AA. A loss of parvalbumin-containing interneurons is associated with diminished oscillatory activity in an animal model of schizophrenia. J Neurosci. 2009;29:2344–54. source
- Not checked yetcites [14] Koh MT, Shao Y, Sherwood A, Smith DR. Impaired hippocampal-dependent memory and reduced parvalbumin-positive interneurons in a ketamine mouse model of schizophrenia. Schizophr Res. 2016;171:187–94. source
- Not checked yetcites [15] Harrington AJ, Raissi A, Rajkovich K, Berto S, Kumar J, Molinaro G, et al. MEF2C regulates cortical inhibitory and excitatory synapses and behaviors relevant to neurodevelopmental disorders. eLife 2016;5:e20059. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, early intervention during the prepubertal period might prevent loss of PV-INs, as shown in the methylazoxymethanol acetate (MAM) rat model of PV-IN loss in the ventral hippocampus [17].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [17] Du Y, Grace AA. Loss of parvalbumin in the hippocampus of MAM schizophrenia model rats is attenuated by peripubertal diazepam. Int J Neuropsychopharmacol. 2016;19:pyw060. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Reductions in the number of PV-INs were reported in the hippocampus, entorhinal cortex, and subicular areas [1,[9][10][11].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [9] Wang AY, Lohmann KM, Yang CK, Zimmerman EI, Pantazopoulos H, Herring N, et al. Bipolar disorder type 1 and schizophrenia are accompanied by decreased density of parvalbumin- and somatostatin-positive interneurons in the parahippocampal region. Acta Neuropathol. 2011;122:615–26. source
- Not checked yetcites [10] Chung DW, Volk DW, Arion D, Zhang Y, Sampson AR, Lewis DA. Dysregulated ErbB4 splicing in schizophrenia: selective effects on parvalbumin expression. Am J Psychiatry. 2016;173:60–8. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“While these findings point to a pathology in PV-INs, they cannot differentiate between loss of neurons or loss of PV expression.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Animal models that mimic schizophrenia replicate the loss of PV-INs in the hippocampus [6,14,15], and show a loss of PV fluorescence per cell in prelimbic regions [16].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“For example, decreases in the number of PV-INs in the hippocampus were observed in two mouse models of AD [33,34], while an increase in hippocampal PV immunoreactivity was observed in another [35], and no change in the number of hippocampal PV-positive interneurons was observed in yet another model [36].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [33] Mahar I, Albuquerque MS, Mondragon-Rodriguez S, Cavanagh C, Davoli MA, Chabot JG, et al. Phenotypic alterations in hippocampal NPY- and PV-expressing interneurons in a presymptomatic transgenic mouse model of Alzheimer’s disease. Front Aging Neurosci. 2016;8:327.
- Not checked yetcites [34] Takahashi H, Brasnjevic I, Rutten BP, Van Der Kolk N, Perl DP, Bouras C, et al. Hippocampal interneuron loss in an APP/PS1 double mutant mouse and in Alzheimer’s disease. Brain Struct Funct. 2010;214:145–60. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, decreases in the number of PV-INs in the hippocampus were observed in two mouse models of AD [33,34], while an increase in hippocampal PV immunoreactivity was observed in another [35], and no change in the number of hippocampal PV-positive interneurons was observed in yet another model [36].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [36] Albuquerque MS, Mahar I, Davoli MA, Chabot JG, Mechawar N, Quirion R, et al. Regional and sub-regional differences in hippocampal GABAergic neuronal vulnerability in the TgCRND8 mouse model of Alzheimer’s disease. Front Aging Neurosci. 2015;7:30. source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, abnormalities in the default mode network, which is regulated in part by PV-INs [27], have been observed in AD patients [28][29][30][31][32].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [28] Jones DT, Machulda MM, Vemuri P, McDade EM, Zeng G, Senjem ML, et al. Age-related changes in the default mode network are more advanced in Alzheimer disease. Neurology. 2011;77:1524–31. source
- Not checked yetcites [29] Zhang HY, Wang SJ, Liu B, Ma ZL, Yang M, Zhang ZJ, et al. Resting brain connectivity: changes during the progress of Alzheimer disease. Radiology. 2010;256:598–606. source
- Not checked yetcites [30] Zhou J, Greicius MD, Gennatas ED, Growdon ME, Jang JY, Rabinovici GD, et al. Divergent network connectivity changes in behavioural variant frontotemporal dementia and Alzheimer’s disease. Brain. 2010;133:1352–67. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“PV-INs in the cortex are highly interconnected via electrical and chemical synapses [69].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [69] Galarreta M, Hestrin S. Electrical and chemical synapses among parvalbumin fast-spiking GABAergic interneurons in adult mouse neocortex. Proc Natl Acad Sci USA. 2002;99:12438–43. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“In AD patients, however, a decrease in PV-INs was reported in the dentate gyrus, and an increase in PV-INs was reported in the piriform cortex [34,37,38].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [34] Takahashi H, Brasnjevic I, Rutten BP, Van Der Kolk N, Perl DP, Bouras C, et al. Hippocampal interneuron loss in an APP/PS1 double mutant mouse and in Alzheimer’s disease. Brain Struct Funct. 2010;214:145–60. source
- Not checked yetcites [37] Baig S, Wilcock GK, Love S. Loss of perineuronal net N-acetylgalactosamine in Alzheimer’s disease. Acta Neuropathol. 2005;110:393–401. source
- Not checked yetcites [38] Saiz-Sanchez D, De la Rosa-Prieto C, Ubeda-Banon I, Martinez-Marcos A. Interneurons, tau and amyloid-beta in the piriform cortex in Alzheimer’s disease. Brain Struct Funct. 2015;220:2011–25. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Concurrently, PV knockout mice display behavioral phenotypes that resemble core behavioral phenotypes found in humans with ASD [53].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [53] Wohr M, Orduz D, Gregory P, Moreno H, Khan U, Vorckel KJ, et al. Lack of parvalbumin in mice leads to behavioral deficits relevant to all human autism core symptoms and related neural morphofunctional abnormalities. Transl Psychiatry. 2015;5:e525. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In other mouse models of ASD, a reduction in PV-INs or a decrease in PV immunoreactivity has been reported [20].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [20] Filice F, Vorckel KJ, Sungur AO, Wohr M, Schwaller B. Reduction in parvalbumin expression not loss of the parvalbumin-expressing GABA interneuron subpopulation in genetic parvalbumin and shank mouse models of autism. Mol Brain. 2016;9:10. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Reports of changes of PV-INs in AD are not without controversy.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
hedged- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The Df (16)A± transgenic mouse and the LgDel(±) mouse, both of which model the 22q11.2deletion in humans [5,[40][41][42][43], the contactin associated protein 2 mouse [44][45][46], the neurexin transgene model [47], Shank models [20,[48][49][50], and platelet-derived growth factor receptor-beta (Pdgfrb) knockout mouse [51,52] are examples of models for both ASD and schizophrenia, which have large”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [5] Mukherjee A, Carvalho F, Eliez S, Caroni P. Long-lasting rescue of network and cognitive dysfunction in a genetic schizophrenia model. Cell. 2019;178:1387–402 e14. source
- Not checked yetcites [40] Hamm JP, Peterka DS, Gogos JA, Yuste R. Altered cortical ensembles in mouse models of schizophrenia. Neuron. 2017;94:153–67 e8. source
- Not checked yetcites [41] Piskorowski RA, Nasrallah K, Diamantopoulou A, Mukai J, Hassan SI, Siegelbaum SA, et al. Age-dependent specific changes in area CA2 of the hippocampus and social memory deficit in a mouse model of the 22q11.2 deletion syndrome. Neuron. 2016;89:163–76. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“For this reason, the characteristic phenotype of PV-INs is fast-spiking action potentials at high energetic costs [66].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [66] Hu H, Gan J, Jonas P. Interneurons. Fast-spiking, parvalbumin(+) GABAergic interneurons: from cellular design to microcircuit function. Science. 2014;345:1255263. source
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These contradicting observations may be explained by the different mouse models used in each study.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Furthermore, abnormalities in the default mode network, which is regulated in part by PV-INs [27], have been observed in AD patients [28][29][30][31][32].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [27] Nair J, Klaassen AL, Arato J, Vyssotski AL, Harvey M, Rainer G. Basal forebrain contributes to default mode network regulation. Proc Natl Acad Sci USA. 2018;115:1352–7. source
plainconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“They help to create and maintain gamma oscillations, which are high-frequency waves between 20 and 100 Hz [66,75].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [66] Hu H, Gan J, Jonas P. Interneurons. Fast-spiking, parvalbumin(+) GABAergic interneurons: from cellular design to microcircuit function. Science. 2014;345:1255263. source
- Not checked yetcites [75] Buzsaki G, Wang XJ. Mechanisms of gamma oscillations. Annu Rev Neurosci. 2012;35:203–25. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, amyloid plaques were reduced when hippocampal PV-INs artificially produced gamma oscillations in optogenetics paradigms [21].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [21] Iaccarino HF, Singer AC, Martorell AJ, Rudenko A, Gao F, Gillingham TZ, et al. Gamma frequency entrainment attenuates amyloid load and modifies microglia. Nature. 2016;540:230–5. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Alzheimer's disease (AD) is also associated with changes in fastspiking interneurons (Table 2).”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In AD patients, however, a decrease in PV-INs was reported in the dentate gyrus, and an increase in PV-INs was reported in the piriform cortex [34,37,38].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [34] Takahashi H, Brasnjevic I, Rutten BP, Van Der Kolk N, Perl DP, Bouras C, et al. Hippocampal interneuron loss in an APP/PS1 double mutant mouse and in Alzheimer’s disease. Brain Struct Funct. 2010;214:145–60. source
- Not checked yetcites [37] Baig S, Wilcock GK, Love S. Loss of perineuronal net N-acetylgalactosamine in Alzheimer’s disease. Acta Neuropathol. 2005;110:393–401. source
- Not checked yetcites [38] Saiz-Sanchez D, De la Rosa-Prieto C, Ubeda-Banon I, Martinez-Marcos A. Interneurons, tau and amyloid-beta in the piriform cortex in Alzheimer’s disease. Brain Struct Funct. 2015;220:2011–25. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Theta-gamma oscillation phaseamplitude cross-frequency coupling was impaired prior to neuronal loss or maximum tau pathology in a tau seeding model with AD-like pathology [23].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [23] Ahnaou A, Moechars D, Raeymaekers L, Biermans R, Manyakov NV, Bottelbergs A, et al. Emergence of early alterations in network oscillations and functional connectivity in a tau seeding mouse model of Alzheimer’s disease pathology. Sci Rep. 2017;7:14189. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“These networks are associated with plasticity from early life throughout adulthood [70][71][72][73].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [70] Donato F, Rompani SB, Caroni P. Parvalbumin-expressing basket-cell network plasticity induced by experience regulates adult learning. Nature. 2013;504:272–6. source
- Not checked yetcites [71] Yazaki-Sugiyama Y, Kang S, Cateau H, Fukai T, Hensch TK. Bidirectional plasticity in fast-spiking GABA circuits by visual experience. Nature. 2009;462:218–21. source
- Not checked yetcites [72] Kuhlman SJ, Olivas ND, Tring E, Ikrar T, Xu X, Trachtenberg JT. A disinhibitory microcircuit initiates critical-period plasticity in the visual cortex. Nature. 2013;501:543–6. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“One of the best described ASD models, knockout of the gene responsible for Rett syndrome, methyl CpG binding protein 2 (Mecp2), shows repetitive behaviors and stereotypies even if the gene is selectively removed from INs only [54].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [54] Chao HT, Chen H, Samaco RC, Xue M, Chahrour M, Yoo J, et al. Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes. Nature. 2010;468:263–9. source
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In the paper
“Evoked gamma oscillations to auditory stimuli were also disrupted in this model [23].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [23] Ahnaou A, Moechars D, Raeymaekers L, Biermans R, Manyakov NV, Bottelbergs A, et al. Emergence of early alterations in network oscillations and functional connectivity in a tau seeding mouse model of Alzheimer’s disease pathology. Sci Rep. 2017;7:14189. source
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In the paper
“The different findings reported in each study could be due to the different brain regions examined.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
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In the paper
“For example, decreases in the number of PV-INs in the hippocampus were observed in two mouse models of AD [33,34], while an increase in hippocampal PV immunoreactivity was observed in another [35], and no change in the number of hippocampal PV-positive interneurons was observed in yet another model [36].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [35] Verdaguer E, Brox S, Petrov D, Olloquequi J, Romero R, de Lemos ML, et al. Vulnerability of calbindin, calretinin and parvalbumin in a transgenic/knock-in APPswe/PS1dE9 mouse model of Alzheimer disease together with disruption of hippocampal neurogenesis. Exp Gerontol. 2015;69:176–88. source
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In the paper
“The large amounts of ATP needed to sustain gamma oscillations are supplied by a high density of mitochondria [81][82][83].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
- Not checked yetcites [82] Inan M, Zhao M, Manuszak M, Karakaya C, Rajadhyaksha AM, Pickel VM, et al. Energy deficit in parvalbumin neurons leads to circuit dysfunction, impaired sensory gating and social disability. Neurobiol Dis. 2016;93:35–46. source
- Not checked yetcites [83] Kann O, Huchzermeyer C, Kovacs R, Wirtz S, Schuelke M. Gamma oscillations in the hippocampus require high complex I gene expression and strong functional performance of mitochondria. Brain. 2011;134:345–58. source
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In the paper
“The combination of large Ca 2+ waves, high mitochondrial density, and dependence on uninterrupted ATP supply creates a delicate balance in PV-INs that can rapidly turn into pathology.”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
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In the paper
“In addition, PV-INs connect to many principal neurons [74,75,87,88].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [74] Packer AM, Yuste R. Dense, unspecific connectivity of neocortical parvalbumin-positive interneurons: a canonical microcircuit for inhibition? J Neurosci. 2011;31:13260–71. source
- Not checked yetcites [75] Buzsaki G, Wang XJ. Mechanisms of gamma oscillations. Annu Rev Neurosci. 2012;35:203–25. source
- Not checked yetcites [87] Kisvarday ZF, Beaulieu C, Eysel UT. Network of GABAergic large basket cells in cat visual cortex (area 18): implication for lateral disinhibition. J Comp Neurol. 1993;327:398–415. source
- Not checked yetcites [88] Sik A, Penttonen M, Ylinen A, Buzsaki G. Hippocampal CA1 interneurons: an in vivo intracellular labeling study. J Neurosci. 1995;15:6651–65. source
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In the paper
“In CA1 of the rat hippocampus, PV-INs have larger dendritic trees and thicker dendrites than calbindin-or calretinin-positive interneurons [80].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
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In the paper
“Studies have shown that the rate of oxygen consumption during hippocampal gamma oscillations can be equivalent to the rate of oxygen spent during a seizure [83,84].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [83] Kann O, Huchzermeyer C, Kovacs R, Wirtz S, Schuelke M. Gamma oscillations in the hippocampus require high complex I gene expression and strong functional performance of mitochondria. Brain. 2011;134:345–58. source
- Not checked yetcites [84] Huchzermeyer C, Berndt N, Holzhutter HG, Kann O. Oxygen consumption rates during three different neuronal activity states in the hippocampal CA3 network. J Cereb Blood Flow Metab. 2013;33:263–71. source
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In the paper
“In the MAM model of schizophrenia, reduced expression of PV-INs has been correlated with a reduction in coordinated neuronal activity during task performance in rats [6].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [6] Lodge DJ, Behrens MM, Grace AA. A loss of parvalbumin-containing interneurons is associated with diminished oscillatory activity in an animal model of schizophrenia. J Neurosci. 2009;29:2344–54. source
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In the paper
“The energy requirements of PV-INs also make them highly susceptible to inflammation.”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
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In the paper
“Zinc is more potent than Ca 2+ in its ability to disrupt mitochondrial function [109].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [109] Kwak S, Weiss JH. Calcium-permeable AMPA channels in neurodegenerative disease and ischemia. Curr Opin Neurobiol. 2006;16:281–7. source
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In the paper
“In rodent models that recapitulate aspects of brain disorders, higher oxidative stress consistently correlates with decreased PV-positive cortical interneurons [92,93].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [92] Steullet P, Cabungcal JH, Coyle J, Didriksen M, Gill K, Grace AA, et al. Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia. Mol Psychiatry. 2017. source
- Not checked yetcites [93] Cabungcal JH, Nicolas D, Kraftsik R, Cuenod M, Do KQ, Hornung JP. Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: relevance to schizophrenia. Neurobiol Dis. 2006;22:624–37. source
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In the paper
“IL-6 is likely signaling through STAT3 [96].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [96] Dugan LL, Ali SS, Shekhtman G, Roberts AJ, Lucero J, Quick KL, et al. IL-6 mediated degeneration of forebrain GABAergic interneurons and cognitive impairment in aged mice through activation of neuronal NADPH oxidase. PLoS ONE. 2009;4:e5518. source
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In the paper
“Unlike Ca 2+ , the influx of zinc through Ca 2+ -permeable AMPA receptors can lead to a longlasting production of superoxide in mitochondria [112].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [112] Sensi SL, Yin HZ, Carriedo SG, Rao SS, Weiss JH. Preferential Zn2+ influx through Ca2+-permeable AMPA/kainate channels triggers prolonged mitochondrial superoxide production. Proc Natl Acad Sci USA. 1999;96:2414–9. source
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In the paper
“Ca 2+ -permeable AMPA receptors are a major entry point of zinc [111-113].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [111] Yin HZ, Sensi SL, Ogoshi F, Weiss JH. Blockade of Ca2+-permeable AMPA/kainate channels decreases oxygen-glucose deprivation-induced Zn2+ accumulation and neuronal loss in hippocampal pyramidal neurons. J Neurosci. 2002;22:1273–9. source
- Not checked yetcites [112] Sensi SL, Yin HZ, Carriedo SG, Rao SS, Weiss JH. Preferential Zn2+ influx through Ca2+-permeable AMPA/kainate channels triggers prolonged mitochondrial superoxide production. Proc Natl Acad Sci USA. 1999;96:2414–9. source
- Not checked yetcites [113] Jia Y, Jeng JM, Sensi SL, Weiss JH. Zn2+ currents are mediated by calcium-permeable AMPA/kainate channels in cultured murine hippocampal neurones. J Physiol. 2002;543:35–48. source
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In the paper
“The dependence of most PV-INs on NMDA receptor function presents another vulnerability.”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
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In the paper
“Conversely, in animal models where no change in oxidative stress was observed, PV-positive interneuron number was not changed [92].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [92] Steullet P, Cabungcal JH, Coyle J, Didriksen M, Gill K, Grace AA, et al. Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia. Mol Psychiatry. 2017. source
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In the paper
“This injury is connected to IL-6mediated Nox2-dependent NADPH oxidase activation and production of superoxide [16,95].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [95] Behrens MM, Ali SS, Dugan LL. Interleukin-6 mediates the increase in NADPH-oxidase in the ketamine model of schizophrenia. J Neurosci. 2008;28:13957–66. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The majority of PV-INs in humans and monkeys express NMDA receptors [118, 119].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [118] Huntley GW, Vickers JC, Morrison JH. Quantitative localization of NMDAR1 receptor subunit immunoreactivity in inferotemporal and prefrontal association cortices of monkey and human. Brain Res. 1997;749:245–62. source
- Not checked yetcites [119] Huntley GW, Vickers JC, Janssen W, Brose N, Heinemann SF, Morrison JH. Distribution and synaptic localization of immunocytochemically identified NMDA receptor subunit proteins in sensory-motor and visual cortices of monkey and human. J Neurosci. 1994;14:3603–19. source
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In the paper
“PARP-1 leads to the release of apoptosis-inducing factor (AIF) via a nuclear signal that proliferates to mitochondria [110].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [110] Hong SJ, Dawson TM, Dawson VL. Nuclear and mitochondrial conversations in cell death: PARP-1 and AIF signaling. Trends Pharmacol Sci. 2004;25:259–64. source
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In the paper
“Even slower, consistent Ca 2+ influx through Ca 2+ -permeable AMPA receptors can be damaging via activation of neuronal nitric oxide synthase and generation of nitric oxide and resultant activation of Poly(ADP-ribose) polymerase 1 (PARP-1), (Fig. 1b), [109, 110].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [109] Kwak S, Weiss JH. Calcium-permeable AMPA channels in neurodegenerative disease and ischemia. Curr Opin Neurobiol. 2006;16:281–7. source
- Not checked yetcites [110] Hong SJ, Dawson TM, Dawson VL. Nuclear and mitochondrial conversations in cell death: PARP-1 and AIF signaling. Trends Pharmacol Sci. 2004;25:259–64. source
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In the paper
“At equivalent concentrations, zinc induces a larger increase in cytochrome c and AIF than Ca 2+ [115].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [115] Jiang D, Sullivan PG, Sensi SL, Steward O, Weiss JH. Zn(2+) induces permeability transition pore opening and release of pro-apoptotic peptides from neuronal mitochondria. J Biol Chem. 2001;276:47524–9. source
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In the paper
“Once postmitotic, cells migrate tangentially toward cortical areas and then radially into predetermined cortical layers (Fig. 2, steps 1a, 1b, and 2), [129, 130].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Not checked yetcites [129] Hu JS, Vogt D, Sandberg M, Rubenstein JL. Cortical interneuron development: a tale of time and space. Development. 2017;144:3867–78. source
- Not checked yetcites [130] Lim L, Mi D, Llorca A, Marin O. Development and functional diversification of cortical interneurons. Neuron. 2018;100:294–313. source
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In the paper
“The preponderance of interneuron pathologies in the hippocampus and adjacent cortical areas, such as the interneuron pathologies observed in schizophrenia and BPD, might be, at least in part, a reflection of this extended developmental vulnerability [1, 9, 122, 140-142].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [9] Wang AY, Lohmann KM, Yang CK, Zimmerman EI, Pantazopoulos H, Herring N, et al. Bipolar disorder type 1 and schizophrenia are accompanied by decreased density of parvalbumin- and somatostatin-positive interneurons in the parahippocampal region. Acta Neuropathol. 2011;122:615–26. source
- Not checked yetcites [122] Konradi C, Heckers S. Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharm Ther. 2003;97:153–79. source
- Not checked yetcites [140] Heckers S, Konradi C. GABAergic mechanisms of hippocampal hyperactivity in schizophrenia. Schizophr Res. 2015;167:4–11. source
- Not checked yetcites [141] Konradi C, Zimmerman EI, Yang CK, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons in bipolar disorder. Arch Gen Psychiatry. 2011;68:340–50. source
- Not checked yetcites [142] Heckers S, Stone D, Walsh J, Shick J, Koul P, Benes FM. Differential hippocampal expression of glutamic acid decarboxylase 65 and 67 messenger RNA in bipolar disorder and schizophrenia. Arch Gen Psychiatry. 2002;59:521–9. source
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- The authors state this as an assumption: The developmental process by which interneurons migrate and integrate into cortical networks has vulnerabilities.
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In the paper
“As interneurons assume their final position within a specific region and layer of the cortex and hippocampus, they have to switch to a molecular program designed to establish axon pathfinding and synaptic connections with local excitatory neurons born in the subventricular zone, and with other interneurons that had migrated from areas deep inside the developing brain”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
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In the paper
“Their 'parvalbumin' fate seems to be established at their origin, as the progenitors leave the cell cycle [127, 128].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Not checked yetcites [127] Wonders CP, Anderson SA. The origin and specification of cortical interneurons. Nat Rev Neurosci. 2006;7:687–96. source
- Not checked yetcites [128] Bandler RC, Mayer C, Fishell G. Cortical interneuron specification: the juncture of genes, time and geometry. Curr Opin Neurobiol. 2017;42:17–24. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Intracellularly, an expression of responsive receptors on the neurons must be timed with the transmission of guidance factors from remote brain tissues.”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This vulnerability contributes to their role in numerous brain disorders.”
§ Parvalbumin interneuron vulnerability and brain disorders > CONCLUSION AND FUTURE DIRECTIONS
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Their ontogeny and physiological properties render them uniquely susceptible to environmental disturbances.”
§ Parvalbumin interneuron vulnerability and brain disorders > CONCLUSION AND FUTURE DIRECTIONS
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- It may state two separate claims as one. 34
- Probably not a substantial claim. 9
Every source the paper cites for this claim was checked and supports it.
In the paper
“STAT3 can directly regulate mitochondrial function [97,98], and Nox2 can modulate mitochondrial activity [99][100][101]”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Supportedcites [97] Gough DJ, Corlett A, Schlessinger K, Wegrzyn J, Larner AC, Levy DE. Mitochondrial STAT3 supports Ras-dependent oncogenic transformation. Science. 2009;324:1713–6. source
The paper’s Abstract states that STAT3 regulates a metabolic function in mitochondria. Its experimental account reports that mitochondrial function was impaired without STAT3, including reduced activity of electron-transport-chain complexes II and V. The Nox2 clause has separate citations and is not attributed to this source. (LLM, conf=0.93)
- Supportedcites [98] Wegrzyn J, Potla R, Chwae YJ, Sepuri NB, Zhang Q, Koeck T, et al. Function of mitochondrial Stat3 in cellular respiration. Science. 2009;323:793–7. source
This source is cited for the STAT3 portion of the sentence, not the separately cited Nox2 portion. In the supplied passages (section labeled Abstract; no page given), mitochondria-targeted STAT3 restored electron transport chain activity in STAT3-deficient cells, supporting a direct role in mitochondrial function. (LLM, conf=0.94)
- Supportedcites [99] Kim YM, Kim SJ, Tatsunami R, Yamamura H, Fukai T, Ushio-Fukai M. ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis. Am J Physiol Cell Physiol. 2017;312:C749–64. source
The citation to this paper is attached to the Nox2 clause, not the STAT3 clause. The paper’s conclusion states that Nox2 promotes mitochondrial ROS production in endothelial cells, supporting the claim that Nox2 can modulate mitochondrial activity. (LLM, conf=0.90)
- Supportedcites [100] Joseph LC, Barca E, Subramanyam P, Komrowski M, Pajvani U, Colecraft HM, et al. Inhibition of NAPDH oxidase 2 (NOX2) prevents oxidative stress and mitochondrial abnormalities caused by saturated fat in cardiomyocytes. PLoS ONE. 2016;11:e0145750. source
The citation to this paper is attached to the Nox2 clause, not the STAT3 clause. In the Results section, NOX2 inhibition prevented palmitate-induced mitochondrial ROS, depolarization, and calcium overload in cardiomyocytes, supporting the claim that Nox2 can modulate mitochondrial activity. (LLM, conf=0.94)
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It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These receptors activate intraneuronal signaling cascades that dynamically remodel microtubule and actin cytoskeletal components to extend and retract processes that move the cells toward their destination [133].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Supportedcites [133] Peyre E, Silva CG, Nguyen L. Crosstalk between intracellular and extracellular signals regulating interneuron production, migration and integration into the cortex. Front Cell Neurosci. 2015;9:129. source
In “Migration of cINs: extracellular cues guide cINs movement” (page not provided), the paper says extracellular cues are transduced at the cytoskeleton, causing extension or retraction of leading processes. “Molecular regulation of the cytoskeleton in migrating cINs” describes receptor-triggered intracellular signaling that changes both actin and microtubule organization during branching and migration. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In schizophrenia, NMDA receptors are believed to be hypo-functioning, and the inhibition of NMDA receptors recapitulates many of the symptoms of schizophrenia [104, 122, 123].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [104] Timofeeva OA, Levin ED. Glutamate and nicotinic receptor interactions in working memory: importance for the cognitive impairment of schizophrenia. Neuroscience. 2011;195:21–36. source
- Supportedcites [122] Konradi C, Heckers S. Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharm Ther. 2003;97:153–79. source
The Introduction describes decreased NMDA receptor activity as a hypothesis of schizophrenia, and Section 2.3 says NMDA receptor hypofunction seems central to its pathology. Section 2.3 also reports that NMDA receptor inhibition with PCP or ketamine causes schizophrenia-like psychoses and mimics both positive and negative symptoms. (LLM, conf=0.94)
- Supportedcites [123] Lisman JE, Coyle JT, Green RW, Javitt DC, Benes FM, Heckers S, et al. Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends Neurosci. 2008;31:234–42. source
The Introduction’s “NMDA hypofunction” section describes reduced NMDA receptor function as a theory of schizophrenia. It also states that NMDA antagonists reproduce positive and negative symptoms and many associated cognitive deficits. The cited paper therefore supports both parts of the paraphrase. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“During migration, cellintrinsic programs and external cues must be coordinated in a time-and location-sensitive manner [131].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Supportedcites [131] Guo J, Anton ES. Decision making during interneuron migration in the developing cerebral cortex. Trends Cell Biol. 2014;24:342–51. source
The section on choices of migratory streams says intrinsic characteristics combine with regionally localized extracellular cues to determine interneuron routes. The intracortical-dispersion section adds that interneurons and their environment may mature in a stage-dependent, synchronized way, supporting the claim’s time-sensitive aspect. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
None of the sources cited for this claim have been checked yet.
In the paper
“Parvalbumin-expressing interneurons (PV-INs) are highly vulnerable to stressors and have been implicated in many neuropsychiatric diseases such as schizophrenia, Alzheimer's disease, autism spectrum disorder, and bipolar disorder.”
§ Parvalbumin interneuron vulnerability and brain disorders > Abstract
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [2] Lewis DA, Curley AA, Glausier JR, Volk DW. Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia. Trends Neurosci. 2012;35:57–67. source
- Not checked yetcites [3] Marin O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012;13:107–20. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Among the factors that confer heightened vulnerability are the substantial energy requirements, a strong excitatory drive, and a unique developmental trajectory.”
§ Parvalbumin interneuron vulnerability and brain disorders > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In schizophrenia, lower levels of PVALB mRNA, the gene coding for PV, were seen in the hippocampus and layer 4 of the dorsolateral prefrontal cortex, which might be partially explained by DNA hypermethylation [1,8].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [8] Fachim HA, Srisawat U, Dalton CF, Reynolds GP. Parvalbumin promoter hypermethylation in postmortem brain in schizophrenia. Epigenomics. 2018;10:519–24. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Extensive accounts in the literature point to PV-IN-related changes in individuals with schizophrenia [1][2][3][4], a finding that is supported by various animal models that recapitulate aspects of the disease [5][6][7] (Table 1).”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [1] Konradi C, Yang CK, Zimmerman EI, Lohmann KM, Gresch P, Pantazopoulos H, et al. Hippocampal interneurons are abnormal in schizophrenia. Schizophr Res. 2011;131:165–73. source
- Not checked yetcites [2] Lewis DA, Curley AA, Glausier JR, Volk DW. Cortical parvalbumin interneurons and cognitive dysfunction in schizophrenia. Trends Neurosci. 2012;35:57–67. source
- Not checked yetcites [3] Marin O. Interneuron dysfunction in psychiatric disorders. Nat Rev Neurosci. 2012;13:107–20. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Some human and animal model data suggest that formerly PV-INs are still present but cease to express PV, though a definitive conclusion cannot be drawn at this point [7,[18][19][20].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [7] Gill KM, Grace AA. Corresponding decrease in neuronal markers signals progressive parvalbumin neuron loss in MAM schizophrenia model. Int J Neuropsychopharmacol. 2014;17:1609–19. source
- Not checked yetcites [18] Powell SB, Sejnowski TJ, Behrens MM. Behavioral and neurochemical consequences of cortical oxidative stress on parvalbumin-interneuron maturation in rodent models of schizophrenia. Neuropharmacology. 2012;62:1322–31. source
- Not checked yetcites [19] Enwright JF, Sanapala S, Foglio A, Berry R, Fish KN, Lewis DA. Reduced labeling of parvalbumin neurons and perineuronal nets in the dorsolateral prefrontal cortex of subjects with schizophrenia. Neuropsychopharmacology. 2016;41:2206–14. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Stimulation of PV-INs leads to an increase in gamma oscillation patterns, while inhibition of PV-INs or downregulation of PV at cortical synapses reduces gamma oscillations [76][77][78].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [76] Cardin JA, Carlen M, Meletis K, Knoblich U, Zhang F, Deisseroth K, et al. Driving fast-spiking cells induces gamma rhythm and controls sensory responses. Nature. 2009;459:663–7. source
- Not checked yetcites [77] Sohal VS, Zhang F, Yizhar O, Deisseroth K. Parvalbumin neurons and gamma rhythms enhance cortical circuit performance. Nature. 2009;459:698–702. source
- Not checked yetcites [78] Volman V, Behrens MM, Sejnowski TJ. Downregulation of parvalbumin at cortical GABA synapses reduces network gamma oscillatory activity. J Neurosci. 2011;31:18137–48. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Transgenic mice with AD-like pathology were found to have reduced gamma power that, in one model, precedes cognitive impairment and amyloid plaque formation [21,22].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [21] Iaccarino HF, Singer AC, Martorell AJ, Rudenko A, Gao F, Gillingham TZ, et al. Gamma frequency entrainment attenuates amyloid load and modifies microglia. Nature. 2016;540:230–5. source
- Not checked yetcites [22] Rubio SE, Vega-Flores G, Martinez A, Bosch C, Perez-Mediavilla A, del Rio J, et al. Accelerated aging of the GABAergic septohippocampal pathway and decreased hippocampal rhythms in a mouse model of Alzheimer’s disease. FASEB J. 2012;26:4458–67. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Since PV rapidly sequesters Ca 2+ , it strongly attenuates the Ca 2+ -activated potassium conductance responsible for postspike hyperpolarization, which explains in part why PV-INs repolarize faster and fire faster than other neurons.”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Individual PV-INs contact nearly every local pyramidal neuron which enables them to synchronize networks [74].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [74] Packer AM, Yuste R. Dense, unspecific connectivity of neocortical parvalbumin-positive interneurons: a canonical microcircuit for inhibition? J Neurosci. 2011;31:13260–71. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PV-INs have roles in both feedforward and feedback inhibition, regulation of sensory responses, and in learning and plasticity [66].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [66] Hu H, Gan J, Jonas P. Interneurons. Fast-spiking, parvalbumin(+) GABAergic interneurons: from cellular design to microcircuit function. Science. 2014;345:1255263. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There is therefore ample evidence that PV-INs are vital for brain function and intricately linked to brain malfunction.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Epilepsy [63,64] and prion disease [65] are among other disorders that are associated with alterations in PV-INs.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [63] Sloviter RS, Sollas AL, Barbaro NM, Laxer KD. Calcium-binding protein (calbindin-D28K) and parvalbumin immunocytochemistry in the normal and epileptic human hippocampus. J Comp Neurol. 1991;308:381–96. source
- Not checked yetcites [64] Garbelli R, Meroni A, Magnaghi G, Beolchi MS, Ferrario A, Tassi L, et al. Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy. Epilepsia. 2006;47:1074–8. source
- Not checked yetcites [65] Guentchev M, Hainfellner JA, Trabattoni GR, Budka H. Distribution of parvalbumin-immunoreactive neurons in brain correlates with hippocampal and temporal cortical pathology in Creutzfeldt-Jakob disease. J Neuropathol Exp Neurol. 1997;56:1119–24. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Schizophrenia also shares significant overlap with BPD [55,56], including PV-IN pathology.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [55] Consortium C-DGotPG, Lee SH, Ripke S, Neale BM, Faraone SV, Purcell SM, et al. Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs. Nat Genet. 2013;45:984–94. source
- Not checked yetcites [56] Cardno AG, Rijsdijk FV, Sham PC, Murray RM, McGuffin P. A twin study of genetic relationships between psychotic symptoms. Am J Psychiatry. 2002;159:539–45. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PV increases the rate of Ca 2+ sequestration, reduces presynaptic Ca 2+ levels, modulates short-term synaptic plasticity, and prevents cumulative facilitation (Fig. 1), [67,68].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [67] Caillard O, Moreno H, Schwaller B, Llano I, Celio MR, Marty A. Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity. Proc Natl Acad Sci USA. 2000;97:13372–7. source
- Not checked yetcites [68] Wahr PA, Michele DE, Metzger JM. Parvalbumin gene transfer corrects diastolic dysfunction in diseased cardiac myocytes. Proc Natl Acad Sci USA. 1999;96:11982–5. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Separately, a voltage-gated sodium channel (Na v 1.1) that is largely found on axons of PV-INs was decreased in a mouse model with amyloid pathology, and in AD patients [24][25][26].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [24] Ogiwara I, Miyamoto H, Morita N, Atapour N, Mazaki E, Inoue I, et al. Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation. J Neurosci. 2007;27:5903–14. source
- Not checked yetcites [25] Wang W, Takashima S, Segawa Y, Itoh M, Shi X, Hwang SK, et al. The developmental changes of Na(v)1.1 and Na(v)1.2 expression in the human hippocampus and temporal lobe. Brain Res. 2011;1389:61–70. source
- Not checked yetcites [26] Verret L, Mann EO, Hang GB, Barth AM, Cobos I, Ho K, et al. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell. 2012;149:708–21. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“ASD shares many overlaps with schizophrenia, not just on a clinical scale, but also with similar PV-IN abnormalities [39].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [39] De Crescenzo F, Postorino V, Siracusano M, Riccioni A, Armando M, Curatolo P, et al. Autistic symptoms in schizophrenia spectrum disorders: a systematic review and meta-analysis. Front Psychiatry. 2019;10:78. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Gamma oscillations in humans are also associated with increased working memory load [79].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [79] Howard MW, Rizzuto DS, Caplan JB, Madsen JR, Lisman J, Aschenbrenner-Scheibe R, et al. Gamma oscillations correlate with working memory load in humans. Cereb Cortex. 2003;13:1369–74. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Indeed, it would be surprising to find that PV-IN densities in disease are uniform across every brain region given that fast-spiking interneurons have different functions in different brain areas.”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Restoration of the levels of this voltage-gated sodium channel increased gamma oscillations, while memory deficits and premature deaths decreased [26].”
§ Parvalbumin interneuron vulnerability and brain disorders > PARVALBUMIN INTERNEURONS ARE IMPLICATED IN A VARIETY OF NEURO-PSYCHIATRIC DISEASE STATES
What the sources say
- Not checked yetcites [26] Verret L, Mann EO, Hang GB, Barth AM, Cobos I, Ho K, et al. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell. 2012;149:708–21. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“PV-INs have extraordinary energy requirements to support a high metabolic activity and to protect against significant glutamatergic stress [16,80,81].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A substantial quantity of cytochrome c and cytochrome c oxidase supports the high bioenergetic needs of PV-INs [81,85], but comes at a price as cytochrome c is also central to the induction of apoptosis [86].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
- Not checked yetcites [85] Gulyas AI, Buzsaki G, Freund TF, Hirase H. Populations of hippocampal inhibitory neurons express different levels of cytochrome c. Eur J Neurosci. 2006;23:2581–94. source
- Not checked yetcites [86] Liu X, Kim CN, Yang J, Jemmerson R, Wang X. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell. 1996;86:147–57. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The energy requirements of PV-INs make them highly susceptible to the loss of mitochondrial membrane potential (a component of, and a proxy for, a decrease in mitochondrial function), and to metabolic and oxidative stress that accompanies disease states [81,91].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [81] Kann O, Papageorgiou IE, Draguhn A. Highly energized inhibitory interneurons are a central element for information processing in cortical networks. J Cereb Blood Flow Metab. 2014;34:1270–82. source
- Not checked yetcites [91] Whittaker RG, Turnbull DM, Whittington MA, Cunningham MO. Impaired mitochondrial function abolishes gamma oscillations in the hippocampus through an effect on fast-spiking interneurons. Brain. 2011;134:e180. author reply e81 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“If the pathological threshold is crossed, the electron transfer chain is disrupted, reactive oxygen species accumulate, the permeability transition pore opens, the outer mitochondrial membrane ruptures, cytochrome c is released, and an apoptotic cell death program is activated [86,109].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [86] Liu X, Kim CN, Yang J, Jemmerson R, Wang X. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell. 1996;86:147–57. source
- Not checked yetcites [109] Kwak S, Weiss JH. Calcium-permeable AMPA channels in neurodegenerative disease and ischemia. Curr Opin Neurobiol. 2006;16:281–7. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PV-INs have a higher density of inputs, more excitatory and inhibitory synapses, and a higher ratio of inhibitory to excitatory inputs than calbindin-and calretinin-positive interneurons [80].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV-INS HAVE UNIQUE ENERGY REQUIREMENTS THAT RENDER THEM VULNERABLE TO MANY STRESSORS
What the sources say
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Consistent with the notion that the presence of Ca 2+ -permeable AMPA receptors contributes to the vulnerability of PV-INs, blocking of these receptors attenuates cortical neuron death in an in vitro model of traumatic brain injury; attenuates hippocampal pyramidal neuron loss in a mouse hippocampal slice model of oxygen-glucose deprivation; and attenuates retinal ganglion cells loss in a rat”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [111] Yin HZ, Sensi SL, Ogoshi F, Weiss JH. Blockade of Ca2+-permeable AMPA/kainate channels decreases oxygen-glucose deprivation-induced Zn2+ accumulation and neuronal loss in hippocampal pyramidal neurons. J Neurosci. 2002;22:1273–9. source
- Not checked yetcites [116] Cueva Vargas JL, Osswald IK, Unsain N, Aurousseau MR, Barker PA, Bowie D, et al. Soluble tumor necrosis factor alpha promotes retinal ganglion cell death in glaucoma via calcium-permeable AMPA receptor activation. J Neurosci. 2015;35:12088–102. source
- Not checked yetcites [117] Spaethling JM, Klein DM, Singh P, Meaney DF. Calcium-permeable AMPA receptors appear in cortical neurons after traumatic mechanical injury and contribute to neuronal fate. J Neurotrauma. 2008;25:1207–16. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the hippocampus, oxidative stress was associated with a decrease in PV-INs as well as a reduction in gamma oscillations [94].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [94] Steullet P, Cabungcal JH, Kulak A, Kraftsik R, Chen Y, Dalton TP, et al. Redox dysregulation affects the ventral but not dorsal hippocampus: impairment of parvalbumin neurons, gamma oscillations, and related behaviors. J Neurosci. 2010;30:2547–58. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Animal studies suggest that a key mechanism of neural oscillations is through glutamatergic regulation.”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Importantly, NMDA receptors in PV-INs are regulating gamma rhythms and cognitive behaviors [121].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [121] Carlen M, Meletis K, Siegle JH, Cardin JA, Futai K, Vierling-Claassen D, et al. A critical role for NMDA receptors in parvalbumin interneurons for gamma rhythm induction and behavior. Mol Psychiatry. 2012;17:537–48. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Indeed, PV-INs receive the greatest excitatory input of any population of inhibitory neurons in the cortex, which puts them under intense stress [16,80].”
§ Parvalbumin interneuron vulnerability and brain disorders > CHARACTERISTICS OF PV-INS
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [80] Gulyas AI, Megias M, Emri Z, Freund TF. Total number and ratio of excitatory and inhibitory synapses converging onto single interneurons of different types in the CA1 area of the rat hippocampus. J Neurosci. 1999;19:10082–97. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, the NMDA receptor antagonist ketamine, a pro-inflammatory stimulus, injures PV-INs in vitro and in vivo [16,95].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [16] Behrens MM, Ali SS, Dao DN, Lucero J, Shekhtman G, Quick KL, et al. Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. Science. 2007;318:1645–7. source
- Not checked yetcites [95] Behrens MM, Ali SS, Dugan LL. Interleukin-6 mediates the increase in NADPH-oxidase in the ketamine model of schizophrenia. J Neurosci. 2008;28:13957–66. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Like Ca 2+ influx, zinc influx into neurons leads to the generation of nitric oxide and subsequent activation of PARP-1 and cell death [114].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [114] Kim YH, Koh JY. The role of NADPH oxidase and neuronal nitric oxide synthase in zinc-induced poly(ADP-ribose) polymerase activation and cell death in cortical culture. Exp Neurol. 2002;177:407–18. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Working memory is notably impaired in schizophrenia and in other neuro-psychiatric diseases likely due to the expected change in gamma oscillation power resulting from disinhibition”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Like other interneurons, PV-INs are derived from progenitor cells in the embryonic ganglionic eminences of the ventral telencephalon of the developing brain (Fig. 2).”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PV-INs are implicated in neurodevelopmental diseases such as early-onset psychiatric disorders and in neurodegenerative diseases such as AD, demonstrating the vulnerability of this interneuron subset throughout life.”
§ Parvalbumin interneuron vulnerability and brain disorders > CONCLUSION AND FUTURE DIRECTIONS
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Externally, an exquisite coordination of attractant and repellant guidance factors transmitted from various brain regions guide migrating neurons to their ultimate destination [132].”
§ Parvalbumin interneuron vulnerability and brain disorders > THE DEVELOPMENTAL TRAJECTORY OF INTERNEURONS INTRODUCES UNIQUE VULNERABILITIES
What the sources say
- Not checked yetcites [132] Marin O, Valiente M, Ge X, Tsai LH. Guiding neuronal cell migrations. Cold Spring Harb Perspect Biol. 2010;2:a001834. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“PV-INs are important for proper brain function.”
§ Parvalbumin interneuron vulnerability and brain disorders > CONCLUSION AND FUTURE DIRECTIONS
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“NMDA receptor antagonists, such as ketamine and phencyclidine, can transiently reproduce key clinical features of schizophrenia, and are believed to reduce PV-IN excitation [123].”
§ Parvalbumin interneuron vulnerability and brain disorders > PV alteration Described in References
What the sources say
- Not checked yetcites [123] Lisman JE, Coyle JT, Green RW, Javitt DC, Benes FM, Heckers S, et al. Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends Neurosci. 2008;31:234–42. source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The authors state this as an assumption.
The developmental process by which interneurons migrate and integrate into cortical networks has vulnerabilities.
“While there likely is some space to correct for minor variabilities, it seems reasonable to assume that the process also has some vulnerabilities.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Dysfunction and/or deficient inhibitory output from PV interneurons may be a common mechanism of multiple psychiatric disorders, such as schizophrenia (SCZ) (Lewis et al. 2005), autism spectrum disorders (ASD) (Gao and Penzes 2015) and bipolar disorder (BD) (Ruden et al. 2021).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Ruden et al. 2021
Citations
Cites
1 retracted
Chen, L. Y., Jiang, M., Zhang, B., Gökçe, Ö., & Südhof, T. C. (2017) · Neuron · doi:10.1016/j.neuron.2017.04.011 · Cited by 209
RetractedShrestha, S., & Offer, S. M. (2016) · Medical Epigenetics · doi:10.1159/000444713 · Cited by 8,951
Induction of Apoptotic Program in Cell-Free Extracts: Requirement for dATP and Cytochrome c
Liu, X., Kim, C. N., Yang, J., Jemmerson, R., & Wang, X. (1996) · Cell · doi:10.1016/s0092-8674(00)80085-9 · Cited by 5,167
Greicius, M. D., Srivastava, G., Reiss, A. L., & Menon, V. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0308627101 · Cited by 3,684
Mechanisms of Gamma Oscillations
Buzsáki, G., & Wang, X.-J. (2012) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-062111-150444 · Cited by 2,796
Parvalbumin neurons and gamma rhythms enhance cortical circuit performance
Sohal, V. S., Zhang, F., Yizhar, O., & Deisseroth, K. (2009) · Nature · doi:10.1038/nature07991 · Cited by 2,606
Driving fast-spiking cells induces gamma rhythm and controls sensory responses
Cardin, J. A., Carlén, M., Meletis, K., Knoblich, U., Zhang, F., Deisseroth, K., Tsai, L.-H., & Moore, C. I. (2009) · Nature · doi:10.1038/nature08002 · Cited by 2,603
Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs
Cross-Disorder Group of the Psychiatric Genomics Consortium (2013) · Nature Genetics · doi:10.1038/ng.2711 · Cited by 2,263
GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits
Tremblay, R., Lee, S., & Rudy, B. (2016) · Neuron · doi:10.1016/j.neuron.2016.06.033 · Cited by 2,033
Gamma frequency entrainment attenuates amyloid load and modifies microglia
Iaccarino, H. F., Singer, A. C., Martorell, A. J., Rudenko, A., Gao, F., Gillingham, T. Z., Mathys, H., Seo, J., Kritskiy, O., Abdurrob, F., et al. (2016) · Nature · doi:10.1038/nature20587 · Cited by 1,328
Cited by
Sorted by citations
Cognitive impairment in schizophrenia: aetiology, pathophysiology, and treatment
McCutcheon, R. A., Keefe, R. S. E., & McGuire, P. K. (2023) · Molecular Psychiatry · doi:10.1038/s41380-023-01949-9 · Cited by 861
“For example, because parvalbumin interneurons have extremely high energy requirements, oxidative and metabolic stressors can have a disproportionate impact on these neurons, and their effects may be greatest in regions where they are present at high densities [265].”
BackgroundCortical interneurons in autism
Contractor, A., Ethell, I. M., & Portera‐Cailliau, C. (2021) · Nature Neuroscience · doi:10.1038/s41593-021-00967-6 · Cited by 186
Gómez de San José, N., Massa, F., Halbgebauer, S., Oeckl, P., Steinacker, P., & Otto, M. (2022) · Journal of Neural Transmission · doi:10.1007/s00702-021-02411-2 · Cited by 112
Brown, D. A., Altermatt, M., Dobreva, T., Chen, S., Wang, A. Z., Thomson, M. W., & Gradinaru, V. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.730825 · Cited by 61
Canetta, S. E., Holt, E. S., Benoit, L. J., Teboul, E., Sahyoun, G. M., Ogden, R. T., Harris, A. Z., & Kellendonk, C. (2022) · eLife · doi:10.7554/elife.80324 · Cited by 59
“The importance of this cell population for cortical development is underscored by the fact that they show histological abnormalities in multiple neurological and psychiatric disorders with a presumed neurodevelopmental origin, most classically schizophrenia (Lewis, 2014, Ruden et al., 2021).”
Background
Metadata
- Authors
- Ruden, J. B., Dugan, L. L., & Konradi, C.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Konradi, Christine
- Venue
- Neuropsychopharmacology
- Published
- 2020-07-28
- Volume
- 46
- Issue
- 2
- Pages
- 279-287
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC7852528
- OpenAlex
- W3044343625
- Semantic Scholar
- 2c4e5394f3b88323dda4206c07141d738c058a9c
- Cited by
- 194
- References
- 148
- Citations by year
- 2026: 33 · 2025: 50 · 2024: 36 · 2023: 31 · 2022: 28 · 2021: 16
- FWCI
- 2.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX004321)
- Vanderbilt University
- Vanderbilt Institute for Clinical and Translational Research
- Geriatric Research Education and Clinical Center
- National Institute on Aging (R01AG058856)
- National Center for Research Resources (KL2RR024977)
- NIH Clinical Center
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- parvalbumin interneurons, neuronal vulnerability, stressors, schizophrenia, Alzheimer's disease, autism spectrum disorder, bipolar disorder, excitatory drive, energy requirements, interneuron development, neuroprotection
- MeSH terms
- Autism Spectrum Disorder, Alzheimer Disease, Humans, Interneurons, Neurons, Parvalbumins
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