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Sayfa 1 itibaren 5973 Sonuçlar
Passive (amyloid-β) immunotherapy attenuates monoaminergic axonal degeneration in the AβPPswe/PS1dE9 mice.
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The role of amyloid-β (Aβ in the neurodegeneration of Alzheimer's disease remains controversial, to a large extent because of the lack of robust neurodegeneration in mouse models of AD. To address this question, we examined the effects of Aβ antibodies in the recently described monoaminergic
Positive florbetapir PET amyloid imaging in a subject with frequent cortical neuritic plaques and frontotemporal lobar degeneration with TDP43-positive inclusions.
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Abnormal neuronal accumulation and modification of TAR DNA binding protein 43 (TDP-43) have recently been discovered to be defining histopathological features of particular subtypes of frontotemporal dementia and amyotrophic lateral sclerosis, and are also common in aging, particularly coexisting
Selective degeneration of septal and hippocampal GABAergic neurons in a mouse model of amyloidosis and tauopathy.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by brain accumulation of amyloid-β peptide and neurofibrillary tangles, which are believed to initiate a pathological cascade that results in progressive impairment of cognitive functions and eventual neuronal death. To obtain a
Cerebrospinal fluid BACE1 activity and markers of amyloid precursor protein metabolism and axonal degeneration in Alzheimer's disease.
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OBJECTIVE
The objective of this study was to assess cerebrospinal fluid (CSF) β-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) activity in relation to Alzheimer's disease (AD) and to correlate the enzyme activity with protein markers of APP metabolism and axonal
Polyethylene glycol treatment after traumatic brain injury reduces beta-amyloid precursor protein accumulation in degenerating axons.
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Polyethylene glycol (PEG; 2,000 MW; 30% v/v) is a nontoxic molecule that can be injected intravenously and possesses well-documented neuroprotective properties in the spinal cord of the guinea pig. Recent studies have shown that intravenous PEG can also enter the rat brain parenchyma after injury
Alternative Method to Detect Neuronal Degeneration and Amyloid β Accumulation in Free-Floating Brain Sections With Fluoro-Jade.
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Fluoro-Jade is a fluorescein-derived fluorochrome which specifically binds to damaged neurons. Due to this characteristic, it is commonly used for the histochemical detection and quantification of neurodegeneration in mounted brain sections. Here, we describe an alternative and simpler
MicroRNA Expression Patterns Involved in Amyloid Beta-Induced Retinal Degeneration.
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Dry age-related macular degeneration (AMD) is characterized by the accumulation of drusen under Bruch's membrane, and amyloid beta (Aβ) is speculated to be one of the key pathologic factors. While the detrimental effects of Aβ on retinas have been widely explored, Aβ-induced epigenetic regulatory
Granulovacuolar degeneration and unfolded protein response in mouse models of tauopathy and Aβ amyloidosis.
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Histopathological studies on the brains of tauopathy cases including cases with Alzheimer's disease (AD) demonstrate that neurons with hyperphosphorylated protein tau display granulovacuolar degeneration (GVD), as evidenced by vacuolar lesions harboring a central granule, together with markers of
Atrophy of the hippocampal formation in early familial Alzheimer's disease. A longitudinal MRI study of at-risk members of a family with an amyloid precursor protein 717Val-Gly mutation.
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The hippocampal formation (HF) is known from pathological and magnetic resonance imaging (MRI) studies to become severely atrophied in established Alzheimer's disease (AD). This study examined whether changes in the HF could also be detected in very early AD by scanning subjects at risk of
Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer's disease.
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BACKGROUND
The role of mitochondrial dysfunction has long been implicated in age-related brain pathology, including Alzheimer's disease (AD). However, the mechanism by which mitochondrial dysfunction may cause neurodegeneration in AD is unclear. To model mitochondrial dysfunction in vivo, we
Early increases in soluble amyloid-β levels coincide with cholinergic degeneration in 3xTg-AD mice.
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Accumulation of amyloid-β peptides (Aβ) and cholinergic degeneration are hallmarks of Alzheimer's disease (AD). In a triple transgenic mouse model of AD (3xTg-AD), soluble Aβ42 levels were detected in the septum by 2 months of age, reaching their highest levels at 3-6 months and decreasing at 12
Lack of evidence for protein AA reactivity in amyloid deposits of lattice corneal dystrophy and amyloid corneal degeneration.
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Amyloid fibrils occurring in primary and myeloma-associated (AL), secondary (AA), and certain neuropathic hereditary forms of systemic amyloidosis can be distinguished biochemically or immunohistologically as being composed of immunoglobulin light chain, protein AA, or prealbumin respectively. All
Glutamate, beta-amyloid precursor proteins, and calcium mediated neurofibrillary degeneration.
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In this article we present evidence supporting the interaction between excitotoxicity, beta APP mismetabolism, metabolic compromise and intracellular calcium destabilization in the process of neurodegeneration associated with Alzheimer's disease (AD). AD is characterized by the presence of
Amyloid precursor protein expression is enhanced in human platelets from subjects with Alzheimer's disease and frontotemporal lobar degeneration: a real-time PCR study.
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Frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD) represent the most frequent causes of early-onset and late-onset degenerative dementia, respectively. A correct diagnosis entails the choice of appropriate therapies. In this view the present study aimed to identify biomarkers
Cerebrospinal Fluid Amyloid-β Subtypes in Confirmed Frontotemporal Lobar Degeneration Cases: A Pilot Study.
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To investigate amyloid-β (Aβ) in frontotemporal dementia (FTD), cerebrospinal fluid (CSF) Aβ38, Aβ40, and Aβ42 in frontotemporal lobar degeneration (FTLD; N = 18 genetically and/or pathologically confirmed and N = 8 FTD with concomitant amyotrophic lateral sclerosis) were compared with Alzheimer's
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