Advanced search    

Search: authors:"Mufson, Elliott J"

8 papers found.
Use AND, OR, NOT, +word, -word, "long phrase", (parentheses) to fine-tune your search.

Tau Oligomer Pathology in Nucleus Basalis Neurons During the Progression of Alzheimer Disease

Although tau is the primary constituent of neurofibrillary tangles (NFTs), evidence suggests that its toxic moiety is oligomeric in Alzheimer disease (AD). In this regard, tau oligomers correlate more strongly with neuronal loss than NFTs and exhibit neurotoxicity in preclinical AD models. Here, we investigated the spatiotemporal progression of oligomeric tau accumulation within...

Tenascin-C Is Associated with Cored Amyloid-β Plaques in Alzheimer Disease and Pathology Burdened Cognitively Normal Elderly

Tenascin-C (TN-C) is an extracellular matrix glycoprotein linked to inflammatory processes in pathological conditions including Alzheimer disease (AD). We examined the distribution of TN-C immunoreactivity (ir) in relation to amyloid-β (Aβ) plaques and vascular Aβ deposits in autopsy brain tissues from 14 patients with clinical and neuropathological AD and 10 aged-matched...

Hippocampal Endosomal, Lysosomal, and Autophagic Dysregulation in Mild Cognitive ImpairmentCorrelation With Aβ and Tau Pathology

Endosomal-lysosomal and autophagic dysregulation occurs in the hippocampus in prodromal Alzheimer disease (AD), but its relationship with β-amyloid (Aβ) and tau pathology remains unclear. To investigate this issue, we performed immunoblot analysis of hippocampal homogenates from cases with an antemortem clinical diagnosis of no cognitive impairment, mild cognitive impairment (MCI...

Hippocampal ProNGF Signaling Pathways and β-Amyloid Levels in Mild Cognitive Impairment and Alzheimer Disease

Hippocampal precursor of nerve growth factor (proNGF)/NGF signaling occurs in conjunction with β-amyloid (Aβ) accumulations in Alzheimer disease (AD). To assess the involvement of this pathway in AD progression, we quantified these proteins and their downstream pathway activators in postmortem tissues from the brains of subjects with no cognitive impairment (NCI), mild cognitive...

The Role of Nerve Growth Factor Receptors in Cholinergic Basal Forebrain Degeneration in Prodromal Alzheimer Disease

Dysfunction of nerve growth factor (NGF) and its high (TrkA) and low (p75NTR) affinity receptors has been suggested to underlie the selective degeneration of the nucleus basalis (NB) cholinergic cortical projection neurons in end stage Alzheimer disease (AD). Whether the NGF system is dysfunctional during the prodromal stages of AD has only recently been evaluated. Surprisingly...

Differential Expression of Synaptic Proteins in the Frontal and Temporal Cortex of Elderly Subjects With Mild Cognitive Impairment

Alterations in synaptic protein stoichiometry may contribute to neocortical synaptic dysfunction in Alzheimer disease (AD). Whether perturbations in synaptic protein expression occur during the earliest stages of cognitive decline remain unclear. We examined protein levels of synaptophysin (SYP), synaptotagmin (SYT), and drebrin (DRB) in 5 neocortical regions (anterior cingulate...

Increased Metabolic Activity in Nucleus Basalis of Meynert Neurons in Elderly Individuals With Mild Cognitive Impairment as Indicated by the Size of the Golgi Apparatus

In this study, we examined the metabolic activity of nucleus basalis of Meynert (NBM) neurons in individuals clinically diagnosed with no cognitive impairment (NCI, n = 8), mild cognitive impairment (MCI, n = 9), and subjects with moderate Alzheimer disease (AD, n = 7). We used Golgi apparatus (GA) size as a measure of neuronal metabolic activity. Subjects with MCI showed...