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Efficient identification of cognitive decline and Alzheimer's disease (AD) risk in early stages of the AD disease continuum is a critical unmet need. Subjective cognitive decline is increasingly recognized as an early symptomatic stage of AD. Dyadic cognitive report, including subjective cognitive complaints (SCC) from a participant and an informant/study partner who knows the participant well, represents an accurate, reliable, and efficient source of data for assessing risk. However, the separate and combined contributions of self‐ and study partner report, and the dynamic relationship between the two, remains unclear. The Subjective Cognitive Decline Professional Interest Area within the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment convened a working group focused on dyadic patterns of subjective report. Group members identified aspects of dyadic‐report information important to the AD research field, gaps in knowledge, and recommendations. By reviewing existing data on this topic, we found evidence that dyadic measures are associated with objective measures of cognition and provide unique information in preclinical and prodromal AD about disease stage and progression and AD biomarker status. External factors including dyad (participant–study partner pair) relationship and sociocultural factors contribute to these associations. We recommend greater dyad report use in research settings to identify AD risk. Priority areas for future research include (1) elucidation of the contributions of demographic and sociocultural factors, dyad type, and dyad relationship to dyad report; (2) exploration of agreement and discordance between self‐ and study partner report across the AD syndromic and disease continuum; (3) identification of domains (e.g., memory, executive function, neuropsychiatric) that predict AD risk outcomes and differentiate cognitive impairment due to AD from other impairment; (4) development of best practices for study partner engagement; (5) exploration of study partner report as AD clinical trial endpoints; (6) continued development, validation, and optimization, of study partner report instruments tailored to the goals of the research and population.

Decay of the temporoparietal cortex is associated with prodromal Alzheimer’s disease (AD). Additionally, shrinkage of the temporoparietal cerebral area has been connected with an increase in α3/α2 electroencephalogram (EEG) power ratio in prodromal AD. Furthermore, a lower regional blood perfusion has been exhibited in patients with a higher α3/α2 proportion when contrasted with low α3/α2 proportion. Furthermore, a lower regional blood perfusion and reduced hippocampal volume has been exhibited in patients with higher α3/α2 when contrasted with lower α3/α2 EEG power ratio. Neuropsychological evaluation, EEG recording, and magnetic resonance imaging were conducted in 74 patients with mild cognitive impairment (MCI). Estimation of cortical thickness and α3/α2 frequency power ratio was conducted for each patient. A subgroup of 27 patients also underwent single-photon emission computed tomography evaluation. In view of α3/α2 power ratio, the patients were divided into three groups. The connections among cortical decay, cerebral perfusion, and memory loss were evaluated by Pearson’s r coefficient. Results demonstrated that higher α3/α2 frequency power ratio group was identified with brain shrinkage and cutdown perfusion inside the temporoparietal projections. In addition, decay and cutdown perfusion rate were connected with memory shortfalls in patients with MCI. MCI subgroup with higher α3/α2 EEG power ratio are at a greater risk to develop AD dementia.

The results of the present study suggest that both SL and LORETA approaches can be usefully applied in the clinical context, by using quasi-realistic head modeling and a standard 10-20 system as electrode montage (19 electrodes). These results represent a reciprocal cross-validation of the two mathematically independent techniques in a clinical environment.

BackgroundAn increase in the EEG upper/low α power ratio has been associated with mild cognitive impairment (MCI) due to Alzheimer’s disease (AD) and to the atrophy of temporoparietal brain areas. Subjects with a higher α3/α2 frequency power ratio showed lower brain perfusion than in the low α3/α2 group. The two groups show significantly different hippocampal volumes and correlation with θ frequency activity.MethodsSeventy-four adult subjects with MCI underwent clinical and neuropsychological evaluation, electroencephalogram (EEG) recording, and high resolution 3D magnetic resonance imaging (MRI). Twenty-seven of them underwent EEG recording and perfusion single-photon emission computed tomography (SPECT) evaluation. The α3/α2 power ratio and cortical thickness were computed for each subject. The difference in cortical thickness between the groups was estimated.ResultsIn the higher upper/low α group, memory impairment was more pronounced in both the MRI group and the SPECT MCI groups. An increase in the production of θ oscillations was associated with greater interhemisperic coupling between temporal areas. It also correlated with greater cortical atrophy and lower perfusional rate in the temporoparietal cortex.ConclusionHigh EEG upper/low α power ratio was associated with cortical thinning and lower perfusion in temporoparietal areas. Moreover, both atrophy and lower perfusion rate significantly correlated with memory impairment in MCI subjects. Therefore, the increase in the EEG upper/low α frequency power ratio could be useful in identifying individuals at risk for progression to AD dementia in a clinical context.

Changes induced by cerebrovascular damage (CVD) and amigdalo-hippocampal atrophy (AHC) on brain rhythmicity as revelaled by scalp electroencephalography (EEG) were evaluated in a cohort of subjects with mild cognitive impairment (MCI) in order to detect different EEG patterns due to the vascular or degenerative impairment. All subjects underwent EEG recording and magnetic resonance imaging (MRI). EEGs were recorded at rest. Relative power was separately computed for delta, theta, alpha1, alpha2, and alpha 3 frequency bands. Increased delta power and decreased alpha2 power were associated with the load of cerebrovascular damage (CVD). Moreover, the theta/alpha 1 ratio could be a reliable index for the estimation of the individual extent of CV damage. No association of vascular damage was observed with alpha3 power. On the other side, moderate hippocampal atrophy was related to an increase of alpha2 and alpha3 frequency power ratio. Our results show that different EEG markers are associated to vascular dementia and Alzheimer's disease (AD). EEG markers could be expression of different global network pathological changes, helping in differentiation of prodromal AD from vascular demented patients. MCI stated that EEG markers could have a prospective value in differential diagnosis between vascular and degenerative MCI. Keywords EEG, Dementia, Brain Rhythms Shared Procedures EEG RecordingsAll recordings were obtained in the morning with subjects resting comfortably. Vigilance was continuously monitored in order to avoid drowsiness.The EEG activity was recorded continuously from 19 sites by using electrodes set in an elastic cap (Electro-Cap International, Inc.) and positioned according to the 10 -20 International system (Fp1, Fp2, F7, F3, Fz, F4, F8, T3, C3, Cz, C4, T4, T5, P3, Pz, P4, T6, O1, O2). The ground electrode was placed in front of Fz. The left and right mastoids served as reference for all electrodes. The recordings were used off-line to re-reference the scalp recordings to the common average. Data were recorded with a band-pass filter of 0.3 -70 Hz, and digitized at a sampling rate of 250 Hz (BrainAmp, BrainProducts, Germany). Electrodes-skin impedance was set below 5 kW. Horizontal and vertical eye movements were detected by recording the electrooculogram (EOG). The recording lasted 5 minutes, with subjects with closed eyes. Longer recordings would have reduced the variability of the data, but they would also have increased the possibility of slowing of EEG oscillations due to reduced vigilance and arousal. EEG data were then analyzed and fragmented off-line in consecutive epochs of 2 seconds, with a frequency resolution of 0.5 Hz. The average number of epochs analyzed was 140 ranging from 130 to 150. The EEG epochs with ocular, muscular and other types of artifacts were discarded.