Semantic processing and neurobiology in Alzheimer?s disease and Mild Cognitive Impairment

In the present theoretical review we will perform a critical surveillance of linguistic and semantic processing in Mild Cognitive Impairment and Alzheimer???s disease, explicitly favouring a neurobiological prism. We conjecture that most linguistic alterations arise from semantic indiscrimination through inhibitory hypofunction. Specif-ically, a conjoint cluster of cholinergic dysfunction, A?? load and somatostatin-positive cell loss renders the se-mantic network disinhibited and overly noisy: fine discriminatory processes in temporal and medial-frontal regions cannot differentiate semantic representations from baseline unconscious activity, which leads to failures in faithful retrieval (preferentially idiosyncratic lexical-semantic links, e.g., proper names), verbal fluency anomalies, semantic interference, dampened N400 effects, and various semiological deviances.

Automated summary

This theoretical review critically examines linguistic and semantic processing in Mild Cognitive Impairment and Alzheimer's disease, focusing on a neurobiological perspective. The authors propose that most linguistic alterations result from inhibited semantic discrimination, caused by a cluster of cholinergic dysfunction, A?? load, and somatostatin-positive cell loss. These changes lead to failures in accurate retrieval, verbal fluency anomalies, semantic interference, dampened N400 effects, and other semantic deviations.