<b>Conclusions:</b> Linguistic features of spontaneous speech transcribed and analyzed by NLP techniques show significant differences between controls and pathological states (not only eD but also MCI) and seems to be a promising approach for the identification of preclinical stages of dementia.
<b>Methods:</b> We enrolled 107 participants (45 amyloid-β-negative cognitively unimpaired [CU-], 7 amyloid-β-positive cognitively unimpaired [CU+], 31 with prodromal AD [mild cognitive impairment; MCI+], and 24 with AD dementia [DEM+]) who completed 2 baseline PET scans (<sup>18</sup>F-flortaucipir and <sup>18</sup>F-florbetaben), MRI, and neuropsychologic tests.
150 individuals with ET (109 Normal Cognition (ET-NC group), and 30 with MCI and 11 dementia (ET-CI group)) completed self-ratings and objective assessments of memory, language, and executive functioning.
A multivariate model based on the Disease State Index classifier incorporated the available baseline tests to predict progression to MCI or dementia over time.
According to cognitive function, the patients were divided into a group of normal cognitive function, a mild cognitive impairment group (MCI group) and a dementia group.
Age (hazard ratio (HR) 1.05 per year, 95% CI: 1.01-1.08, p = 0.007), presence of MCI status (HR 3.40, 95% CI: 1.97-6.92, p < 0.001), MTA (HR 1.71 per point, 95% CI: 1.26-2.32, p = 0.001), and SVD score (HR 1.23 per point, 95% CI: 1.20-1.48, p = 0.030) at baseline were independent predictors for dementia conversion in these patients.
Although PD-MCI is a risk factor for developing Parkinson's disease dementia there is evidence to suggest that PD-MCI might consist of distinct subtypes with different pathophysiologies and prognoses.
Altogether, these findings indicate that evaluating executive functions with the IFS can be valuable for the identification of MCI, a high-risk group for dementia, and for differentiating this condition from healthy aging and AD.
Among 200 outpatients with dementia and MCI whose NGF SNP rs6330 genotype was identified, those with A-MCI (n = 35) and early-stage AD (n = 67) were recruited and divided into three groups according to genotype (C/C: n = 58, C/T: n = 39, T/T: n = 5).
Among 200 outpatients with dementia and MCI, 146 outpatients with mild AD or A-MCI were recruited and divided into two genotypic groups, valine homozygosity (Val/Val) and methionine (Met) carriers, based on the representative BDNF functional polymorphism Val66Met.
Among 215 outpatients with dementia and MCI, 155 with mild AD (n = 108) or A-MCI (n = 47) were recruited and divided into three genotypic groups based on the representative NT-3 functional polymorphisms rs6332 and rs6489630.
At follow-up, 8 out of 41 patients (19.5%) with MCI had progressed to dementia, 8 patients (19.5%) had improved to normal levels of cognitive functioning, 25 patients (61%) had remained stable within the MCI group.
CCM demonstrates corneal nerve fiber loss, which is associated with a decline in cognitive function and functional independence in patients with MCI and dementia.
Cognitive decline (defined as the incidence of either Parkinson's disease mild cognitive impairment [PD-MCI] or dementia [PDD], diagnosed according to published criteria and blinded to genotype) was studied as the primary outcome.
Cognitive function was assessed using two computer-based questionnaires (touch panel-type dementia assessment scale [TDAS] and mild cognitive impairment [MCI] screen).
CSF Apo-E levels were associated with longitudinal cognitive decline, MCI conversion to dementia, and gray matter atrophy rate in total tau/Aβ1-42 ratio and APOE genotype-adjusted analyses.