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36/100
Our findings suggest that, with respect to this putative marker of central cholinergic activity, dementia in aging DS shares pathophysiological similarities to AD in the general population.
Why it matters
In 12 patients with Down syndrome, a brain stimulation test showed reduced cholinergic activity compared with healthy controls, and the measure improved after a single dose of donepezil in 5 patients. This small study suggests dementia in Down syndrome shares features with Alzheimer's disease, but it does not show that donepezil treats or prevents dementia.
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Alzheimer disease (AD) is a progressive, neurodegenerative disorder that leads to debilitating cognitive deficits.
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Ts65Dn, a well-characterized animal model for Down syndrome, has three copies of the distal end of mouse chromosome 16 and therefore has segmental trisomy for orthologs for nearly half of the genes located on human chromosome 21.
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Alterations in synaptic protein stoichiometry may contribute to neocortical synaptic dysfunction in Alzheimer disease (AD).
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In this study, we investigated the molecular basis for the altered signal transduction associated with soluble amyloid beta-protein (Abeta) oligomer-mediated neurotoxicity in the hippocampus, which is primarily linked to cognitive dysfunction in Alzheimer disease (AD).
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Neurofibrillary tangles form in a specific spatial and temporal pattern in Alzheimer's disease.
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Progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), sporadic multisystem tauopathy, and some forms of frontotemporal dementia with Parkinsonism linked to chromosome 17 are characterized by neuronal and glial lesions accumulating tau protein containing 4 conserved repeats in microtubule-binding domain (4R tau).
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The microtubule binding protein tau is implicated in neurodegenerative tauopathies, including frontotemporal dementia (FTD) with Parkinsonism caused by diverse mutations in the tau gene.
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The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites.
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From clinical studies it is known that recurrent depressive episodes associate with a reduced hippocampal volume.
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In spite of a relatively small sample size, the presence of the met-BDNF allele was found associated with a reduced volume of the hippocampal formation in healthy volunteers and may represent a vulnerability factor for the development of disease processes associated with the dysfunction of this brain region.
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Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of tauopathies.
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Many neurodegenerative diseases are caused by intracellular, aggregate-prone proteins, including polyglutamine-expanded huntingtin in Huntington's disease (HD) and mutant tau in fronto-temporal dementia/tauopathy.
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Analysis of post-mortem tissue from patients with affective disorders has revealed a decreased number of glial cells in several brain areas.
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Discovery of various mutations in the tau gene among frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) families suggests gain-of-toxic function of wild-type or mutant tau as the mechanism for extensive neuronal loss.
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We generated several cell models of tauopathy in order to study the mechanisms of neurodegeneration in diseases involving abnormal changes of tau protein.
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Daily restraint for 3 weeks was shown to atrophy dendrites of hippocampal pyramidal neurons in rats.
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Interactions between endothelial cells and mural cells (pericytes and vascular smooth muscle cells) in the blood vessel wall have recently come into focus as central processes in the regulation of vascular formation, stabilization, remodeling, and function.
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Microtubule-associated protein tau is the major component of the neurofibrillary tangles of Alzheimer disease (AD) and is genetically linked to frontotemporal dementias (FTDP-17).
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Synaptic dysfunction is one of the earliest events in the pathogenesis of Alzheimer disease (AD).
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Prematurity is associated with mild brain structural differences that persist at 8 years of age, with associated lower scores in neurocognitive assessments.
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Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of sporadic and familial tauopathies.
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Diverse oxidative pathways, such as direct oxidation of amino acids, glycoxidation, and lipoxidation could contribute to Alzheimer disease pathogenesis.
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The birth of new neurons, or neurogenesis, in the hippocampal formation has been demonstrated throughout the lifetime of multiple species including humans.
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Transgenic Tg(PG14) mice express a mutant prion protein containing 14 octapeptide repeats, whose human homologue is associated with an inherited prion dementia.
From across this topic
10 of the 4,748 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Subacute meningoencephalitis in a subset of patients with AD after Aβ42 immunization
- HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as biomarkers of neuroinflammation and progression to neurodegeneration in Alzheimer's disease
- Role of neuroinflammation in neurodegenerative diseases (Review)
- The Role of Microglia in Retinal Neurodegeneration: Alzheimer's Disease, Parkinson, and Glaucoma
- Autophagy flux in CA1 neurons of Alzheimer hippocampus: Increased induction overburdens failing lysosomes to propel neuritic dystrophy
- Serum neurotrophins--a study on the time course and influencing factors in a large old age sample
- Age‐Related Complement C3 Drives Memory Impairments and Associated Neuropathologies in a Mouse Model
- Microglia and brain macrophages: An update
- Neuroinflammation and blood–brain barrier dysfunction in cerebral small vessel disease: mechanisms, biomarkers, and therapeutic implications
- Association of Brain Volumes and White Matter Injury With Race, Ethnicity, and Cardiovascular Risk Factors: The Multi-Ethnic Study of Atherosclerosis