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Early neurotransmission impairment in non-invasive Alzheimer Disease detection

ABSTRACT: Alzheimer Disease (AD) is a pathology suffered by millions of people worldwide and it has a great social and economic impact. Previous studies reported a relationship between alterations in different amino acids and derivatives involved in neurotransmission systems and cognitive impairment. Therefore, in this study the neurotransmission impairment associated to early AD has been evaluated. For this purpose, different amino acids and derivatives were determined in saliva samples from AD patients and healthy subjects, by means of an analytical method based on chromatography coupled to tandem mass spectrometry. Results showed statistically significant differences in salivary levels for the compounds myo-inositol, creatine and acetylcholine; and other compounds (myo-inositol, glutamine, creatine, acetylcholine) showed significant correlations with some cognitive tests scores. Therefore, these compounds were included in a multivariate analysis and the corresponding diagnosis model showed promising indices (AUC 0.806, sensitivity 61%, specificity 92%). In conclusion, some amino acids and derivatives involved in neurotransmission impairment could be potential biomarkers in early and non-invasive AD detection.

SUBMITTER: Pena-Bautista C

PROVIDER: S-EPMC7532202 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Project description:Importance:There are conflicting results claiming that Alzheimer disease signature neurodegeneration may be more, less, or similarly advanced in individuals with ?-amyloid peptide (A?)-negative (A?-) suspected non-Alzheimer disease pathophysiology (SNAP) than in A?-positive (A?+) counterparts. Objective:To examine patterns of neurodegeneration in individuals with SNAP compared with their A?+ counterparts. Design, Setting, and Participants:A longitudinal cohort study was conducted among individuals with mild cognitive impairment (MCI) and cognitively normal individuals receiving care at Alzheimer's Disease Neuroimaging Initiative sites in the United States and Canada for a mean follow-up period of 30.5 months from August 1, 2005, to June 30, 2015. Several neurodegeneration biomarkers and longitudinal cognitive function were compared between patients with distinct SNAP (A?- and neurodegeneration-positive [A?-N+]) subtypes and their A?+N+ counterparts. Main Outcomes and Measures:Participants were classified according to the results of their florbetapir F-18 (A?) positron emission tomography and their Alzheimer disease-associated neurodegeneration status (temporoparietal glucose metabolism determined by fluorodeoxyglucose F 18 [FDG]-labeled positron emission tomography and/or hippocampal volume [HV] determined by magnetic resonance imaging: participants with subthreshold HV values were regarded as exhibiting hippocampal volume atrophy [HV+], while subthreshold mean FDG values were considered as FDG hypometabolism [FDG+]). Results:The study comprised 265 cognitively normal individuals (135 women and 130 men; mean [SD] age, 75.5 [6.7] years) and 522 patients with MCI (225 women and 297 men; mean [SD] age, 72.6 [7.8] years). A total of 469 individuals with MCI had data on neurodegeneration biomarkers; of these patients, 107 were A?-N+ (22.8%; 63 FDG+, 82 HV+, and 38 FDG+HV+) and 187 were A?+N+ (39.9%; 135 FDG+, 147 HV+, and 95 FDG+HV+ cases). A total of 209 cognitively normal participants had data on neurodegeneration biomarkers; of these, 52 were A?-N+ (24.9%; 30 FDG+, 33 HV+, and 11 FDG+HV+) and 37 were A?+N+ (17.7%; 22 FDG+, 26 HV+, and 11 FDG+HV+). Compared with their A?+ counterparts, all patients with MCI SNAP subtypes displayed better preservation of temporoparietal FDG metabolism (mean [SD] FDG: A?-N+, 1.25 [0.11] vs A?+N+, 1.19 [0.11]), less severe atrophy of the lateral temporal lobe, and lower mean (SD) cerebrospinal fluid levels of tau (59.2 [32.8] vs 111.3 [56.4]). In MCI with SNAP, sustained glucose metabolism and gray matter volume were associated with disproportionately low APOE ?4 (A?-N+, 18.7% vs A?+N+, 70.6%) and disproportionately high APOE ?2 (18.7% vs 4.8%) carrier prevalence. Slower cognitive decline and lower rates of progression to Alzheimer disease (A?-N+, 6.5% vs A?+N+, 32.6%) were also seen in patients with MCI with SNAP subtypes compared with their A?+ counterparts. In cognitively normal individuals, neurodegeneration biomarkers did not differ between A?-N+ and A?+N+ cases. Conclusions and Relevance:In MCI with SNAP, low APOE ?4 and high APOE ?2 carrier prevalence may account for differences in neurodegeneration patterns between A?-N+ and A?+N+ cases independent from the neuroimaging biomarker modality used to define neurodegeneration associated with Alzheimer disease.

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Early neurotransmission impairment in non-invasive Alzheimer Disease detection

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