Memory Disorders

Memory disorders refer to an individual's inability to remember or recall information or skills, it may be a permanent or temporary memory impairment caused by pathophysiological or situational reasons. Clinical characteristics can be classified into memory loss, forgetting, misconception, fictitious memory, and other conditions.

Causes of Lexical Retrieval Impairments

Neuropsychological research clearly shows that damage to the brain's extended memory system (medial temporal lobe, diencephalon, and basal forebrain) produces anterograde amnesia while leaving other aspects of memory (retrieving common sense, vocabulary, names) relatively complete. It is found that this memory impairment is usually accompanied by related sleep disorders, neurobehavioral disorders such as depression, anxiety, aggression, vascular dementia, and neurodegenerative diseases such as Parkinson's (PD), Alzheimer's disease (AD).

Potential Targets for Lexical Retrieval Treatment

Finding the main biomarkers of memory impairment will help to develop targeted treatment products and reduce the development of diseases and complications.

A large amount of experimental evidence showed that cAMP response element binding protein (CREB) was the main regulator of memory formation. The intervention of CREB and upstream signaling pathways leads to its activation of learning-related plasticity, making it an attractive target for drugs to improve memory function in disease and healthy individuals.

Fig.1 Activation of CREB signaling pathway. (Barco, 2003)

Different external stimuli, such as the activation of a receptor coupled with adenylate cyclase (AC) or the opening of the Ca²⁺ channel, will activate the protein kinase pathway gathered at the 133 sites of CREB phosphorylation. Phosphorylation of this residue promotes the recruitment of the co-activator CREB binding protein (CBP) and initiates the transcription of target genes. In addition, studies have shown that serum protease Kallikrein 8 (KLK8) can regulate microtubule-associated protein 2c (MAP2c) defects, thereby inactivating protein kinase A (PKA) and downstream transcription factors phosphorylated CREB (pCREB), resulting in decreased regulation of memory-related genes, so targeting KLK8 may be a new pathway to treat memory disorders.

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Reference

1. Barco, A.; et al. CREB, memory enhancement and the treatment of memory disorders: promises, pitfalls, and prospects. Expert opinion on therapeutic targets. 2003, 7(1): 101-114.