Aspectos clínicos y moleculares de las afasias progresivas degenerativas

Abstract

The debate between equipotentiality or specialization of the cerebral cortex as a substrate for higher neurological functions lasted until the second half of the 19th century. The classic observations of Broca, Wernicke and other authors demonstrating the language alterations due to cortical focal lesions were decisive in solving the problem and gave rise to a localization current, similar to that of the phrenologists, but not speculative but neuropathologically based. This vision of the cerebral cortex as a mosaic of autonomous specialized areas has been superseded and complemented by modern neuroscience that supports brain functions in a networked anatomical-functional model, with more or less specific areas or nodes, cortical and subcortical. Other classic authors such as Pick have already pointed out that aphasia could be, in addition to a consequence of focal vascular lesions, an early symptom of degenerative diseases. Mesulam more modernly, retrieved that idea and coined the concept of primary progressive aphasia. Later, it has been shown that primary or degenerative progressive aphasia is a heterogeneous process both clinically with at least three varieties, non-fluid, semantic and logopenic, and pathologically and in its molecular substrate, which currently includes tau pathology, TDP43. and Alzheimer. There is an imperfect correlation between the clinical variety of aphasia, the preferred location of neurodegeneration, histology, and molecular pathology. The new molecular neuroimaging techniques (amyloid-PET, PET-tau) and other markers can help to refine the clinical-pathological correlation and help to better understand the reasons for this selective vulnerability of one or other brain areas involved in the anatomy.physiology of language.