Paradigm shift: semantic memory decline as a biomarker of preclinical Alzheimer's disease.

摘要: Uncovering the presence of Alzheimer’s disease (AD) in routine neurological management middle-aged/elderly adults, and differentiating its combination symptoms from those induced by processes normal aging, neurovascular or psychiatric conditions (e.g., depression), are challenges primary importance. Usually, it is onset behavioral that encourages patients with AD caregivers to seek medical attention for first time. Research evidence, however, shows earliest changes triggered on biology brain occur several decades prior any change clinical relevance [1]. Based this large preclinicalstage/symptomatic-stage temporal discrepancy, paramount importance identify biomarkers more effective than currently used practice. An ideal biomarker should be as early diagnostic help possible disease-progression timeline, well highly sensitive specific. On note, use cognitive tests among most proficient sources information phases AD, due their validity, reliability simplicity/immediateness. A skillful interpretation neuropsychological performance may offer an indirect, yet fruitful view pathological affecting nervous system, which could result incipient AD. Although episodic memory impairment has been classically recognized main symptom prodromal stage characterized mild (MCI) [2], a temporally parallel decline semantic also described [3,4]. The basic disadvantage associated qualitatively (but certainly not quantitatively) similar ‘physiologically’ visible absence pathologies general population elderly adults. In contrast, remains fairly stable across lifespan, aspects lexical-semantic abilities even appear improve age [5]. this, using same logic argument sustains all differential diagnoses, measuring can discriminative separating healthy aging. Nevertheless, recent criteria detection manifestation [6,7] persist highlighting sole role measures retrieval. major reason behind choice subdomain ‘of reference’ lies fact prodromal, earlysymptomatic (manifesting form MCI) corresponds pathophysiological moment neurofibrillary pathology intensifies within hippocampal complex [8]. This mediotemporal structure neocortical circuitry responsible context-associated, [9]. theoretical convergence peptidic accumulation hypephosphorylated TAU protein cells, Paradigm shift: preclinical