INTRODUCTION Alzheimer disease is the main cause of dementia associated with aging in Cuba and the world. Development of methods for early diagnosis is vital to increasing intervention effectiveness and improving patient quality of life. Recent studies have shown associations between alterations in serum levels of antineuronal antibodies and Alzheimer disease pathology. However, the specific relationship between such antineuronal antibodies and Alzheimer pathogenesis remains unclear because of the great variety of antibodies identified and their heterogeneity among patients and nondemented controls.

OBJECTIVE Assess the association between serum levels of antibodies against neuronal antigens (total brain protein, aldolase and amyloid beta protein) and cognitive performance in older Cuban adults.

METHODS A cross-sectional pilot study was conducted of adults aged ≥65 years living in Havana’s Playa Municipality and Artemisa Province (southwest of Havana). A sociodemographic and risk factor questionnaire was administered, neuropsychological assessment conducted, and physical and neurological examinations performed. A relative or caregiver was also interviewed. Laboratory tests included: complete blood count, glycemia, lipid panel, and apolipoprotein E genotype. Of 143 individuals studied, 33 were cognitively normal, 52 had mild cognitive impairment, and 58, probable Alzheimer disease. Serum antibody levels were determined by ELISA and compared using covariance analysis with a significance level of 0.05. ELISA specificity, sensitivity and predictive value were assessed by analyzing their respective diagnostic performance curves.

RESULTS Patients with probable Alzheimer disease performed least well on the mini mental state examination (cognitively normal 28.8, SD 1.2; mild cognitive impairment 27.4, SD 2.2; probable Alzheimer disease 12.9, SD 6.5; ANOVA p <0.001). The percentage of Apo E4 carriers was seven times greater in the group with probable Alzheimer disease than in the cognitively normal group. Among the antibodies studied, only those against amyloid beta peptide had levels significantly higher in the Alzheimer disease group than in the cognitively normal group (p = 0.007) and the group with mild cognitive impairment (p = 0.002).

CONCLUSIONS Results support the presence of an autoimmune component in Alzheimer disease and suggest that serum anti–amyloid-beta could be used for its diagnosis.

KEYWORDS Dementia, Alzheimer disease, mild cognitive impairment, autoantibodies, E4 apolipoprotein, Apo E4, enzyme-linked immunosorbent assay, ELISA, immunoassay, immunosorbent techniques, amyloid beta protein, Cuba

INTRODUCTION Cross-modal plasticity has been extensively studied in deaf adults with neuroimaging studies, yielding valuable results. A recent study in our laboratory with deaf–blind children found evidence of cross-modal plasticity, revealed in over-representation of median nerve somatosensory evoked potentials (SEP N20) in left hemisphere parietal, temporal and occipital regions. This finding led to asking whether SEP N20 changes are peculiar to deaf–blindness or are also present in sighted deaf children.

OBJECTIVE Assess cross-modal plasticity in deaf child cochlear implant candidates using neurophysiological techniques (visual evoked potentials and median nerve somatosensory evoked potentials).

METHODS Participants were 14 prelingually deaf children assessed in the Cuban Cochlear Implant Program. Flash visual-evoked potentials and SEP N20 were recorded at 19 scalp recording sites. Topographic maps were obtained and compared to those of control group children with normal hearing. Analysis took into account duration of hearing loss.

RESULTS Topographic maps of flash visual-evoked potentials did not show changes in deaf child cochlear implant candidates. However, SEP N20 from right median nerve stimulation did show changes from expansion of cortical activation into the left temporal region in deaf children aged ≥7 years, which was interpreted as neurophysiological evidence of cross-modal plasticity, not previously described for this technique and type of somatosensory stimulus. We interpret this finding as due in part to duration of deafness, particularly related to handedness, since expansion was selective for the left hemisphere in the children, who were all right-handed.

CONCLUSIONS Cortical over-representation of SEP N20 in the left temporal region is interpreted as evidence of cross-modal plasticity that occurs if the deaf child does not receive a cochlear implant early in life—before concluding the critical period of neural development—and relies on sign language for communication.

KEYWORDS Neuroplasticity, somatosensory evoked potentials, visual evoked potentials, cochlear implants, deafness, prelingual deafness, hearing loss, sensorineural hearing loss, neurophysiology, Cuba