Association between Cerebrospinal Fluid Biomarkers for Alzheimer’s Disease, APOE Genotypes and Auditory Verbal Learning Task in Subjective Cognitive Decline, Mild Cognitive Impairment, and Alzheimer’s Disease

Abstract

In the course of Alzheimer's disease (AD), early pathological changes in the brain start decades before any clinical manifestation. The concentration levels of AD cerebrospinal fluid (CSF) biomarkers, such as amyloid-β1-42 (Aβ1-42), total tau (T-tau), and phosphorylated tau (P-tau), may reflect a cerebral pathology facilitating an early diagnosis of the disease and predicting a cognitive deterioration. The aim of this study was to estimate the prevalence of AD CSF biomarkers in those individuals with a subjective cognitive decline (SCD), a mild cognitive impairment (MCI), and Alzheimer's dementia (AD-D), together with the relationships between the biomarkers, an APOE ɛ4 presence, and a verbal episodic memory performance. We included 252 patients from the memory clinic with a diagnosis of SCD (n = 85), MCI (n = 87), and AD-D (n = 80). A verbal episodic memory performance level was assessed and was based on a delayed recall trial from the 10-word list of an auditory verbal learning task (AVLT). We found that the patients with more severe cognitive impairments had significantly lower levels of Aβ1-42 and higher levels of T-tau and P-tau. This pattern was also typical for the APOE ɛ4 carriers, who had lower levels of Aβ1-42 than the noncarriers in the AD-D and MCI groups. The levels of T-tau and P-tau were significantly higher in the APOE ɛ4 carriers than in the noncarriers, but only in the MCI patients. The AVLT performance in the whole study samples was predicted by age, Aβ1-42, and the T-tau CSF biomarkers, but not by the APOE genotyping.

Profile of 6 microRNA in blood plasma distinguish early stage Alzheimer’s disease patients from non-demented subjects

“…For detection of p-tau, the INNOTEST ® PHOSPHO-TAU(181P) was used. Cut off values of assayed CSF markers for AD diagnosis were Aβ42 < 609.54 pg/ml, t-tau > 277.02 pg/ml and p-tau > 55.08 pg/ml, as described previously in [88]. Patients’ characteristics are presented in Table 1.…”

Is Alzheimer’s Disease a Liver Disease of the Brain?

“…SILK studies have shown that the A␤ 42 :A␤ 40 turnover rate positively correlates with amyloid plaque load and demonstrate that understanding A␤ dynamics in different compartments including CSF, blood, and brain tissue is crucial to improving therapy. Thus, studies showing significantly lower levels of CSF A␤ 42 in AD patients with more severe cognitive impairment [65] are unable to provide information on changes in A␤ turnover occurring either during the circadian cycle or during the progression of disease.…”

Combined use of biochemical and volumetric biomarkers to assess the risk of conversion of mild cognitive impairment to Alzheimer’s disease

“…The study population was divided into two subgroups: subgroup 1: non-converters, who did not convert to AD (31 patients) and subgroup 2: converters, who converted to AD (9 patients). The characteristics of subgroups, including the results of CSF are shown in Table I, together with the cut-off points (established in our laboratory, described in our previous study [8]). …”