MAP1A and Associated Diseases

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Backgrounds of MAP1A

MAP1A is one of the most abundant MAPs in the adult brain and plays an important role in neuronal microtubule organization, synaptic protein regulation, and neuronal survival. Microtubule-associated protein MAP1A is highly expressed in mature neurons. MAP1A is a high molecular weight MAP¹ that plays an important role in determining neuronal morphology and in determining the balance between plasticity and stability of neuritis. This gene encodes a pro polypeptide, which is further hydrolyzed to form the heavy chain and light chain of MAP1A. MAP1A expression increases continually during the postneonatal period and is maintained at a high level throughout adulthood. MAP1A was highly enriched in AIS from adult cerebellar Purkinje cells in addition to growth dendrite compartments.

Fig.1 MAP1A expression and localization in neuron cultures. (Clemmensen, 2012)

Functions of MAP1A

MAP1A appears to play a role not only in stabilizing the microtubule but also in regulating the distribution of related molecules as a linker between them and the microtubule-based cytoskeleton. MAP1A may play a beneficial role in preserving the survival of PV+ neurons, and that inhibition of the impairment of NR2B/PSD-95/MAP1A pathway may be a novel and preferential option to ameliorate α-syn-induced neurodegeneration. Two RFX binding sites in the MAP1A gene play an inhibitory role in non-neuronal cells. MAP1A may play a key role in synaptic plasticity because cultures of neurons transfected with MAP1A siRNA show an inhibitory activity-induced contraction of dendrite branches and existing branches.

Expression of MAP1A in Diseases

Mutation studies have shown the importance of structural MAPs in mammalian brains. Loss of MAP1A may lead to neuronal death. A lack of MAP1A leads to a reduction in PSD-93 (also known as chapsyn-110 or Dlg2) in Purkinje cells, suggesting that MAP1A is necessary to maintain normal levels of this MAGUK protein. Modifications of MAP1A can contribute to the perturbation of the microtubule network in AD and ultimately lead to neuronal degeneration without the accumulation of amyloid deposits. The disruption of MAP1A could be a very early manifestation of Ab-mediated synaptic dysfunction-one that presages the clinical onset of AD by years.

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Reference

1. Clemmensen, C.; et al. The microtubule-associated protein 1A (MAP1A) is an early molecular target of soluble Aβ-peptide. Cellular and molecular neurobiology. 2012, 32(4): 561-566.