Calb1 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
:: infobox .infobox-gene
Symbol: CALB1
Full Name: Calbindin 1
Chromosomal Location: 8q21.3
NCBI Gene ID: 793
OMIM: 114050
Ensembl ID: ENSG00000171345
UniProt: P05937
Proteins: Calbindin-D28k
Associated Diseases: Alzheimer's Disease, Huntington's Disease, Cerebellar Degeneration
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CALB1 is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of CALB1 is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
CALB1 encodes calbindin-D28k, a calcium-binding protein that buffers intracellular calcium levels. Calbindin is expressed in specific neuronal populations where it protects against calcium-mediated excitotoxicity. Loss of calbindin-expressing neurons is observed in Alzheimer's disease and Huntington's disease, making it a marker of neuronal vulnerability.
Calbindin is expressed in:
- Cerebellum (Purkinje cells)
- Hippocampus (CA1 pyramidal cells, interneurons)
- Basal ganglia (medium spiny neurons)
- Substantia nigra (some dopaminergic neurons)
- Dorsal root ganglia
The pattern of expression correlates with neuronal populations vulnerable in neurodegeneration.
- Baimbridge KG, et al. (1992). "Calcium-binding proteins in the nervous system." Trends Neurosci. PMID:1376853
- Iacopino AM, et al. (1992). "Calbindin-D28k: a calcium-binding protein with a potential role in neuronal degeneration." Mol Neurobiol. PMID:1335448
- Goodman JH, et al. (1996). "Altered calcium homeostasis in Alzheimer's disease." J Neurosci Res. PMID:8747552
The study of Calb1 Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Su Y et al.. "Identification of lung innervating sensory neurons and their target specificity." Am J Physiol Lung Cell Mol Physiol (2022). DOI: 10.1152/ajplung.00376.2021 PubMed: 34755535
- Datta D et al.. "Key Roles of CACNA1C/Cav1.2 and CALB1/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders." JAMA psychiatry (2024). DOI: 10.1001/jamapsychiatry.2024.1112 PubMed: 38776078
- Katsetos CD, Burger PC. "Medulloblastoma." Seminars in diagnostic pathology (1994). PubMed: 7809510
- Dong J et al.. "Molecularly distinct striatonigral neuron subtypes differentially regulate locomotion." Nature communications (2025). DOI: 10.1038/s41467-025-58007-x PubMed: 40108161
- Castrogiovanni P et al.. "Brain CHID1 Expression Correlates with NRGN and CALB1 in Healthy Subjects and AD Patients." Cells (2021). DOI: 10.3390/cells10040882 PubMed: 33924468
- Lei H et al.. "Improving vulnerable Calbindin1- neurons in the ventral hippocampus rescues tau-induced impairment of episodic memory." Translational neurodegeneration (2025). DOI: 10.1186/s40035-025-00473-w PubMed: 40038800
- Yu H et al.. "Infralimbic medial prefrontal cortex signalling to calbindin 1 positive neurons in posterior basolateral amygdala suppresses anxiety- and depression-like behaviours." Nature communications (2022). DOI: 10.1038/s41467-022-33139-6 PubMed: 36115848
- Sanfilippo C et al.. "CHI3L2 Expression Levels Are Correlated with AIF1, PECAM1, and CALB1 in the Brains of Alzheimer's Disease Patients." Journal of molecular neuroscience : MN (2020). DOI: 10.1007/s12031-020-01667-9 PubMed: 32705525