Letter To Editor:

Dear Editor, that the transformation of short term into longer term memory is not instantaneous was known long before the scientific era, as epitomized in the observation of the Roman orator Quintilian: “…curious fact…that the interval of a single night will greatly increase the strength of the memory…the power of recollection…undergoes a process of ripening and maturing during the time which intervenes (Quintilian, Inst. Orat. 11.2.43). Memory consolidation refers to the transformation over time of experience-dependent internal representation and their neurobiological underpinnings. The process is assumed to be embodied in synaptic and cellular modifications at brain circuits in which the memory is initially encoded and to proceed by recurrent reactivations, both wakefulness and during sleep, culminating in the distribution of information to additional locales and integration of new information into existing knowledge. The relatively fast molecular synaptic, and cellular local mechanisms likely serve as repetitive subroutines in the mechanisms that embody slower systems consolidations, in which the experience-dependent information redistributes over brain circuits. The kinetics of consolidation appears to be a function of the dissonance between the novel information and the knowledge already available; experiences that fit available knowledge schemas may consolidate faster at the systems level and even skip the engagement of brain circuits that are essential for processing unexpected information. We examined 21 male Calabrian patients: 9/21 were Alzheimer’s Disease patients (age range 54-88, mean age 72 years); 12/21 were Mild Cognitive Impairment (age range 64-83, mean age 66.5 years). 21 controls were matched for age, and sex. 8 out of 11 Alzheimer’s Disease patients showed normal color vision, 1 out of them showed a blue deficit, 1 out of them showed green deficit, 1 out of them showed and color vision. 6 out of Mild Cognitive Impairment patients showed normal color vision, 6 out of them showed red and green color vision deficit, 1 out of them showed red-green color vision deficit, 1 out of them showed red and blue color vision deficit, 1 out of them showed blue color vision deficit. 1 patient was colorblind.

At a stage of Mild Cognitive Impairment where there are no plaque deposition, hyper phosphorylated tau tangles or sign of neuronal loss in cortical and hippocampal regions involved in memory deficits has occurred, a specific apoptotic process takes place in the ventral tegmental area, causing progressive degeneration of the dopaminergic neuronal populations, so alterations in the dopaminergic system include reduced levels of dopamine and alterations in the dopamine receptors modulating the hippocampal synaptic plasticity. It is evidently that at a stage showing Alzheimer Disease presenting the plaques, patients live on memories about all the color vision that they knew during the health stage of their life.

Acknowledgement

Authors thank Fondazione Cassa di Risparmio di Calabria e Lucania for its contribution.