ArticleJournal of molecular neuroscience : MN2013
Analysis of gene expression pattern and neuroanatomical correlates for SLC20A2 (PiT-2) shows a molecular network with potential impact in idiopathic basal ganglia calcification ("Fahr's disease").
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Experimental Primary Brain Calcification Model and Its Application to Pathogenesis Mechanism Analysis and Therapeutic Research.Neurology international · 2025Review
- Computational molecular characterization of a novel SLC20A2 variant associated with primary familial brain calcification.Scientific reports · 2025Article
- New Evidence Suggests a Much Complex Classification for the Genetic Pattern of Inheritance in Primary Brain Calcification.Journal of molecular neuroscience : MN · 2023Article
- The Genetics of Primary Familial Brain Calcification: A Literature Review.International journal of molecular sciences · 2023Review
- Familial Idiopathic Basal Ganglia Calcification: A Father-Son Dyad Demonstrate Heterogeneity of Presentation and Disease Progression.Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists · 2022Article
- Basal ganglia calcifications (Fahr's syndrome): related conditions and clinical features.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019Review
- Article
- A NovelChinese medical journal · 2018Article
- Brain calcifications andNeurology. Genetics · 2017Article
- Brain Calcification and Movement Disorders.Current neurology and neuroscience reports · 2017Review
- Extensive bilateral striopallidodentate calcinosis: a 50 years history of hypoparathyroidism presenting like a parkinsonian syndrome.Journal of neurology · 2016Article
- Precise Anatomic Localization of Accumulated Lipids in Mfp2 Deficient Murine Brains Through Automated Registration of SIMS Images to the Allen Brain Atlas.Journal of the American Society for Mass Spectrometry · 2015Article
- Loss of PiT-1 results in abnormal endocytosis in the yolk sac visceral endoderm.Mechanisms of development · 2014Article
- A Japanese family with idiopathic basal ganglia calcification with novel SLC20A2 mutation presenting with late-onset hallucination and delusion.Journal of neurology · 2014Article
- Loss of function of Slc20a2 associated with familial idiopathic Basal Ganglia calcification in humans causes brain calcifications in mice.Journal of molecular neuroscience : MN · 2013Article
- Fahr's syndrome: literature review of current evidence.Orphanet journal of rare diseases · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Familial idiopathic basal ganglia calcification (FIBGC), also known as "Fahr's disease," is a neuropsychiatric disorder with motor and cognitive symptoms. It is characterized pathologically by bilateral calcification most commonly in the basal ganglia and also in other brain regions such as the thalamus and cerebellum. A recent report by Wang et al. (2012) discovered multiple families with FIBGC carrying mutations in the SLC20A2 gene, encoding the inorganic phosphate transporter PiT-2, which segregated in an autosomal dominant pattern. To understand further the role of SLC20A2 in FIBGC brain pathology, here we described the gene expression pattern across the whole brain for SLC20A2, using the Allen Institute Human Brain Atlas database. Microarray analysis provided evidence that the neuroanatomical pattern of expression for SLC20A2 is highest in the regions most commonly affected in FIBGC. Neuroanatomical regions that demonstrated high correlation or anti-correlation with SLC20A2 expression also showed a molecular network with potential to explain the limited neuroanatomical distribution of calcifications in IBGC. Lastly, these co-expression networks suggest additional further candidate genes for FIBGC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.