Distinct cerebral small vessel disease impairment in early- and late-onset Alzheimer's disease.

Objective: This study investigated cerebral small vessel disease (CSVD) damage patterns in early-onset and late-onset Alzheimer's disease (EOAD and LOAD) and their effects on cognitive function.

Methods: This study included 93 participants, 45 AD patients (14 EOAD and 31 LOAD), and 48 normal controls (13 YNC and 35 ONC) from the ADNI database. All participants had diffusion tensor imaging data; some had amyloid PET and plasma p-tau data.

Distinct resting-state functional connectivity patterns of Anterior Insula affected by smoking in mild cognitive impairment.

Smoking is a modifiable risk factor for Alzheimer's disease (AD). The insula plays a vital role in both smoking and cognition. However, the smoking effects on insula-related networks in cognitively normal controls (CN) and mild cognitive impairment (MCI) patients remain unknown.

Neuropsychiatric symptoms associated multimodal brain networks in Alzheimer's disease.

Concomitant neuropsychiatric symptoms (NPS) are associated with accelerated Alzheimer's disease (AD) progression. Identifying multimodal brain imaging patterns associated with NPS may help understand pathophysiology correlates AD. Based on the AD continuum, a supervised learning strategy was used to guide four-way multimodal neuroimaging fusion (Amyloid, Tau, gray matter volume, brain function) by using NPS total score as the reference.

The association of enlarged perivascular space with microglia-related inflammation and Alzheimer's pathology in cognitively normal elderly.

Background: Glymphatic dysfunction may contribute to the accumulation of Alzheimer's disease (AD) pathologies. Conversely, AD pathologic change might also cause neuroinflammation and aggravate glymphatic dysfunction, forming a loop that accelerates AD progression. In vivo validations are needed to confirm their relationships.

Effects of Anosognosia on Static and Dynamic Amplitudes of Low-Frequency Fluctuation in Mild Cognitive Impairment.

Anosognosia is a significant symptom in patients with mild cognitive impairment (MCI) while the underlying neurological mechanism behind it is still unclear. A total of 121 subjects were included and classified into three groups, including 39 normal controls (NCs), 42 individuals with MCI without anosognosia (MCI-NA), and 40 individuals with MCI with anosognosia (MCI-A), based on their everyday cognition (ECog) questionnaire (discrepancy score). Resting-state functional MRIs were acquired from all the subjects, and the static amplitudes of low-frequency fluctuation (sALFF) and dynamic ALFF (dALFF) variance were investigated to evaluate the intrinsic functional network strength and stability, respectively, and both were corrected by age, sex, education, and gray matter volume.

Intrinsic Brain Activity of Inferior Temporal Region Increased in Prodromal Alzheimer's Disease With Hearing Loss.

Background And Objective: Hearing loss (HL) is one of the modifiable risk factors for Alzheimer's disease (AD). However, the underlying mechanism behind HL in AD remains elusive. A possible mechanism is cognitive load hypothesis, which postulates that over-processing of degraded auditory signals in the auditory cortex leads to deficits in other cognitive functions.

Exploration of the Mechanism Underlying the Association of Incident Microinfarct and Motor Deficit: A Preliminary Functional MRI Study.

Background: Cerebral microinfarcts (CMIs) might cause measurable disruption to brain connections and are associated with cognitive decline, but the association between CMIs and motor impairment is still unclear.

Objective: To assess the CMIs effect on motor function in vivo and explore the potential neuropathological mechanism based on graph-based network method.

Methods: We identified 133 non-demented middle-aged and elderly participants who underwent MRI scanning, cognitive, and motor assessment.

Effects of APOE ε2 on the Fractional Amplitude of Low-Frequency Fluctuation in Mild Cognitive Impairment: A Study Based on the Resting-State Functional MRI.

Background: Apolipoprotein E (APOE) ε2 is a protective genetic factor for Alzheimer's disease (AD). However, the potential interaction effects between the APOE ε2 allele and disease status on the intrinsic brain activity remain elusive.

Methods: We identified 73 healthy control (HC) with APOE ε3/ε3, 61 mild cognitive impairment (MCI) subjects with APOE ε3/ε3, 24 HC with APOE ε2/ε3, and 10 MCI subjects with APOE ε2/ε3 from the ADNI database.

Distinct impaired patterns of intrinsic functional network centrality in patients with early- and late-onset Alzheimer's disease.

Early-onset Alzheimer's disease (EOAD) involves multiple cognitive domains and shows more rapid progression than late-onset Alzheimer's disease (LOAD). However, the difference in pathogenesis between EOAD and LOAD is still unclear. Accordingly, we applied intrinsic network analysis to explore the potential neuropathological mechanism underlying distinct clinical phenotypes.

Effects of Smoking on Regional Homogeneity in Mild Cognitive Impairment: A Resting-State Functional MRI Study.

Background: Smoking is a modifiable risk factor for Alzheimer's disease (AD). However, smoking-related effects on intrinsic brain activity in high-risk AD population are still unclear.

Objective: We aimed to explore differences in smoking effects on brain function between healthy elderly and amnestic mild cognitive impairment (aMCI) patients using ReHo mapping.

Distinct Atrophy Pattern of Hippocampal Subfields in Patients with Progressive and Stable Mild Cognitive Impairment: A Longitudinal MRI Study.

Background: Predicting the prognosis of mild cognitive impairment (MCI) has outstanding clinical value, and the hippocampal volume is a reliable imaging biomarker of AD diagnosis.

Objective: We aimed to longitudinally assess hippocampal sub-regional difference (volume and asymmetry) among progressive MCI (pMCI), stable MCI (sMCI) patients, and normal elderly.

Methods: We identified 29 pMCI, 52 sMCI, and 102 normal controls (NC) from the ADNI database.

Progressive Memory Circuit Impairments along with Alzheimer's Disease Neuropathology Spread: Evidence from in vivo Neuroimaging.

During the progression of Alzheimer's disease (AD), neuropathology may propagate transneuronally, cause disruption in memory circuit, and lead to memory impairment. However, there is a lack of in vivo evidence regarding this process. Thus, we aim to simulate and observe the progression of neuropathology in AD continuum.