Map1a, short for Microtubule-associated Protein 1A, is a crucial protein in the brain. It is involved in regulating microtubule stability, which is essential for neuronal development, determining neuronal shape, and maintaining the balance between plasticity and rigidity in neuronal processes. It has been shown to interact with various molecules and is thought to function as an adaptor between microtubules and other molecules, facilitating endocytic vesicle trafficking and regulating the trafficking of signaling molecules [2,3].

In a mouse model, targeted deletion of the Map1a gene led to neurodegenerative defects such as tremors, ataxia, and loss of cerebellar Purkinje neurons in aged homozygous mice. Before neuron death, mutant Purkinje cells had abnormal focal swellings of dendritic shafts, disruptions in axon initial segment morphology, a reduced MT network in the somatodendritic and AIS compartments, and aberrant distribution of MAP1B. Additionally, PSD-93, a MAGUK protein, was reduced in Map1a(-/-) Purkinje cells, demonstrating that Map1a functions to maintain both the neuronal MT network and the level of PSD-93 in neurons [4].

In conclusion, Map1a is vital for maintaining the neuronal microtubule network and the level of certain scaffolding proteins in neurons. Studies using Map1a knockout mouse models have revealed its significance in neurodegenerative processes, providing valuable insights into the mechanisms underlying related diseases. It also plays a role in neurite outgrowth, EGF-dependent EGF receptor signaling, and is potentially a biomarker for bladder cancer, highlighting its diverse functions in biological processes and disease contexts [1,2,4,5].