Relationships between PET and blood plasma biomarkers in corticobasal syndrome.

Introduction: Corticobasal syndrome (CBS) can result from underlying Alzheimer's disease (AD) pathologies. Little is known about the utility of blood plasma metrics to predict positron emission tomography (PET) biomarker-confirmed AD in CBS.

Methods: A cohort of eighteen CBS patients (8 amyloid beta [Aβ]+; 10 Aβ-) and 8 cognitively unimpaired (CU) individuals underwent PET imaging and plasma analysis.

Clinical Utility of Tectal Plate Measurements on Magnetic Resonance Imaging in Progressive Supranuclear Palsy.

Background: Midbrain atrophy is a characteristic feature of progressive supranuclear palsy (PSP), observed in PSP-Richardson's syndrome (PSP-RS) and to a lesser extent PSP-parkinsonism (PSP-P).

Objective: Our aim was to critically evaluate the utility of manual magnetic resonance imaging measurements of the midbrain tectal plate as a diagnostic biomarker in PSP.

Methods: Length of the tectal plate and width of the superior and inferior colliculi were measured in 40 PSP (20 PSP-RS and 20 PSP-P) patients and compared with 20 Parkinson's disease and 20 healthy control subjects.

Atypical Alzheimer's disease: new insights into an overlapping spectrum between the language and visual variants.

Overlap between language and visual variants of atypical Alzheimer's disease (AD) has been reported. However, the extent, frequency of overlap, and its neuroanatomical underpinnings remain unclear. Eighty-two biomarker-confirmed AD patients who presented with either predominant language (n = 34) or visuospatial/perceptual (n = 48) deficits underwent detailed clinical examinations, MRI, and [F]flortaucipir-PET.

Plasma glial fibrillary acidic protein in the visual and language variants of Alzheimer's disease.

Introduction: Glial fibrillary acidic protein (GFAP) in plasma is a proxy for astrocytic activity and is elevated in amyloid-β (Aβ)-positive individuals, making GFAP a potential blood-based biomarker for Alzheimer's disease (AD).

Methods: We assessed plasma GFAP in 72 Aβ-positive participants diagnosed with the visual or language variant of AD who underwent Aβ- and tau-PET. Fifty-nine participants had follow-up imaging.

Longitudinal default mode sub-networks in the language and visual variants of Alzheimer's disease.

Disruption of the default mode network is a hallmark of Alzheimer's disease, which has not been extensively examined in atypical phenotypes. We investigated cross-sectional and 1-year longitudinal changes in default mode network sub-systems in the visual and language variants of Alzheimer's disease, in relation to age and tau. Sixty-one amyloid-positive Alzheimer's disease participants diagnosed with posterior cortical atrophy ( = 33) or logopenic progressive aphasia ( = 28) underwent structural MRI, resting-state functional MRI and [F]flortaucipir PET.

Altered structural and functional connectivity in Posterior Cortical Atrophy and Dementia with Lewy bodies.

Posterior cortical atrophy (PCA) and dementia with Lewy bodies (DLB) show distinct atrophy and overlapping hypometabolism profiles, but it is unknown how disruptions in structural and functional connectivity compare between these disorders and whether breakdowns in connectivity relate to either atrophy or hypometabolism. Thirty amyloid-positive PCA patients, 24 amyloid-negative DLB patients and 30 amyloid-negative cognitively unimpaired (CU) healthy individuals were recruited at Mayo Clinic, Rochester, MN, and underwent a 3T head MRI, including structural MRI, resting state functional MRI (rsfMRI) and diffusion tensor imaging (DTI) sequences, as well as [F] fluorodeoxyglucose (FDG) PET. We assessed functional connectivity within and between 12 brain networks using rsfMRI and the CONN functional connectivity toolbox and calculated regional DTI metrics using the Johns Hopkins atlas.

Behavioral and Neuropsychiatric Differences Across Two Atypical Alzheimer's Disease Variants: Logopenic Progressive Aphasia and Posterior Cortical Atrophy.

Background: Posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA) are two common atypical Alzheimer's disease (AD) variants. Little is known about behavioral and neuropsychiatric symptoms or activities of daily living (ADLs) in PCA and LPA, and whether they differ across syndromes.

Objective: To characterize the behavioral and neuropsychiatric profiles and ADLs of PCA and LPA and compare presence/absence and severity of symptoms between syndromes.

Acoustic Analysis and Neuroimaging Correlates of Diadochokinetic Rates in Mild-Moderate Primary Progressive Apraxia of Speech.

Speech rate can be judged clinically using diadochokinetic (DDK) tasks, such as alternating motion rates (AMR) and sequential motion rates (SMR). We evaluated whether acoustic AMR/SMR speech rates would differentiate primary progressive apraxia of speech (PPAOS) from healthy controls, and determined how DDK rates relate to phonetic and prosodic speech characteristics and brain metabolism on FDG-PET. Rate was calculated for each of three AMRs (repetitions of 'puh', 'tuh', and 'kuh') and for SMRs (repetitions of 'puhtuhkuh') for 27 PPAOS patients and 52 controls who underwent FDG-PET.

Longitudinal rates of atrophy and tau accumulation differ between the visual and language variants of atypical Alzheimer's disease.

Introduction: Atypical variants of Alzheimer's disease (AD) include the visual variant, known as posterior cortical atrophy (PCA), and the language variant, known as logopenic progressive aphasia (LPA). Clinically, rates of disease progression differ between them.

Methods: We evaluated 34 PCA and 29 LPA participants.

Altered within- and between-network functional connectivity in atypical Alzheimer's disease.

Posterior cortical atrophy and logopenic progressive aphasia are atypical clinical presentations of Alzheimer's disease. Resting-state functional connectivity studies have shown functional network disruptions in both phenotypes, particularly involving the language network in logopenic progressive aphasia and the visual network in posterior cortical atrophy. However, little is known about how connectivity differs both within and between brain networks in these atypical Alzheimer's disease phenotypes.

Diffusivity Changes in Posterior Cortical Atrophy and Logopenic Progressive Aphasia: A Longitudinal Diffusion Tensor Imaging Study.

Background: Posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA) are associated with characteristic patterns of structural network degeneration. Little is known about longitudinal patterns of white matter tract degeneration in these phenotypes.

Objective: To assess longitudinal patterns of white matter degeneration and identify phenotype specific cross-sectional and longitudinal diffusion tensor imaging (DTI) biomarkers in PCA and LPA.

APOE ε4 influences within and between network functional connectivity in posterior cortical atrophy and logopenic progressive aphasia.

Introduction: Presence of apolipoprotein E (APOE) ε4 has shown greater predisposition to medial temporal involvement in posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA). Little is known about its influence on memory network connectivity, a network comprised of medial temporal structures.

Methods: Fifty-eight PCA and 82 LPA patients underwent structural and resting state functional magnetic resonance imaging (MRI).

Clinicopathological associations of hemispheric dominance in primary progressive apraxia of speech.

Objective: Primary progressive apraxia of speech (PPAOS) is associated with imaging abnormalities in the lateral premotor cortex (LPC) and supplementary motor area (SMA). It is not known whether greater involvement of these regions in either hemisphere is associated with demographics, presenting, and/or longitudinal features.

Methods: In 51 prospectively recruited PPAOS patients who completed [ F]-fluorodeoxyglucose (FDG) positron emission tomography (PET), we classified patients as left-dominant, right-dominant, or symmetric, based on visual assessment of the LPC and SMA on FDG-PET.

Distinct brain iron profiles associated with logopenic progressive aphasia and posterior cortical atrophy.

Quantitative susceptibility mapping (QSM) can detect iron distribution in the brain by estimating local tissue magnetic susceptibility properties at every voxel. Iron deposition patterns are well studied in typical Alzheimer's disease (tAD), but little is known about these patterns in atypical clinical presentations of AD such as logopenic progressive aphasia (LPA) and posterior cortical atrophy (PCA). Seventeen PCA patients and eight LPA patients were recruited by the Neurodegenerative Research Group at Mayo Clinic, Rochester, MN, and underwent MRI that included a five-echo gradient echo sequence for calculation of QSM.

Atypical Alzheimer's disease phenotypes with normal or borderline PET biomarker profiles.

Posterior cortical atrophy (PCA) and logopenic progressive aphasia (LPA) are clinical syndromes that commonly have underlying Alzheimer's disease (AD), although non-AD pathologies have also been reported. PET imaging allows for identification of beta-amyloid (Aβ) and tau in AD, so we aimed to assess these in a large cohort to identify patients that do not have evidence for biomarker-defined AD. Eight-one patients, 47 PCA and 34 LPA, underwent extensive neurological and neuropsychological testing, [C] Pittsburgh compound B, [F] flortaucipir and [F] fluorodeoxyglucose PETs.

APOE ε4 influences medial temporal atrophy and tau deposition in atypical Alzheimer's disease.

Introduction: Apolipoprotein E (APOE) ε4 is an important genetic risk factor for typical Alzheimer's disease (AD), influencing brain volume and tau burden. Little is known about its influence in atypical presentations of AD.

Methods: An atypical AD cohort of 140 patients diagnosed with either posterior cortical atrophy or logopenic progressive aphasia underwent magnetic resonance imaging and positron emission tomography.

Unique spatiotemporal fMRI dynamics in the awake mouse brain.

Human imaging studies have shown that spontaneous brain activity exhibits stereotypic spatiotemporal reorganization in awake, conscious conditions with respect to minimally conscious states. However, whether and how this phenomenon can be generalized to lower mammalian species remains unclear. Leveraging a robust protocol for resting-state fMRI (rsfMRI) mapping in non-anesthetized, head-fixed mice, we investigated functional network topography and dynamic structure of spontaneous brain activity in wakeful animals.

EGCG Nanoparticles Attenuate Aluminum Chloride Induced Neurobehavioral Deficits, Beta Amyloid and Tau Pathology in a Rat Model of Alzheimer's Disease.

: Alzheimer's disease (AD) is a neurodegenerative pathology characterized by the presence of neuritic plaques and neurofibrillary tangles. Aluminum has been reported to play an important role in the etiology and pathogenesis of this disease. Hence, the present study aimed to evaluate the neuroprotective role of epigallocatechin-gallate (EGCG) loaded nanoparticles (nanoEGCG) against aluminum chloride (AlCl) induced neurobehavioral and pathological changes in AD induced rats.

Inhibition of Al(III)-Induced A Fibrillation and Reduction of Neurotoxicity by Epigallocatechin-3-Gallate Nanoparticles.

Rational: Accumulation of amyloid beta fibrils is the pathological hallmark of Alzheimer's disease. Epigallocatechin-3-gallate (EGCG) has shown to possess potent anti-amyloidogenic, metal chelation and antioxidant properties. However, its therapeutic potential is limited in-vivo due to its poor bioavailability and stability.

Potential neuroprotective properties of epigallocatechin-3-gallate (EGCG).

Neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD) enforce an overwhelming social and economic burden on society. They are primarily characterized through the accumulation of modified proteins, which further trigger biological responses such as inflammation, oxidative stress, excitotoxicity and modulation of signalling pathways. In a hope for cure, these diseases have been studied extensively over the last decade to successfully develop symptom-oriented therapies.