نتایج جستجو برای: amyloid deposition

تعداد نتایج: 126596  

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2016
Peng Yuan Jaime Grutzendler

UNLABELLED Aberrant neural hyperactivity has been observed in early stages of Alzheimer's disease (AD) and may be a driving force in the progression of amyloid pathology. Evidence for this includes the findings that neural activity may modulate β-amyloid (Aβ) peptide secretion and experimental stimulation of neural activity can increase amyloid deposition. However, whether long-term attenuation...

2014
Diego Real de Asúa Ramón Costa Jose María Galván María Teresa Filigheddu Davinia Trujillo Julen Cadiñanos

The term "amyloidosis" encompasses the heterogeneous group of diseases caused by the extracellular deposition of autologous fibrillar proteins. The global incidence of amyloidosis is estimated at five to nine cases per million patient-years. While amyloid light-chain (AL) amyloidosis is more frequent in developed countries, amyloid A (AA) amyloidosis is more common in some European regions and ...

Journal: :Gut 1969
T Gilat M Revach E Sohar

Amyloid may cause widespread damage to the gastrointestinal tract. Affection of blood vessels may lead to infarction and perforation of the bowel (Brody, Wertlake, and Laster, 1964; Akbarian and Fenton, 1964) as well as to bleeding or loss of protein into the lumen of the gut (Jarnum, 1965); damage to the musculature or nervous elements may cause marked alterations in motility (Gilat and Spiro,...

Journal: :Puerto Rico health sciences journal 2008
Lincoln Jiménez Marie L Rivera Susana Ferrá Lillian E Colón Eric Carro

Prolactinomas are common benign pituitary neoplasms. Amyloid deposits are rare findings that have been reported in pituitary neoplasms. We report a case of a 48-year old man with a diagnosis of prolactinoma with extensive amyloid deposition. To our knowledge, this is the first case of amyloid in a pituitary neoplasm at our institution.

Journal: :The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques 1977
J Bruni J M Bilbao K P Pritzker

The clinico-pathological features of five patients with vascular amyloid restricted to the central nervous system are presented. In three normotensive patients, intracerebral hemorrhage was the dramatic manifestation of amyloid angiopathy. In two other cases, one of amyloid in an arteriovenous malformation, the other of amyloid following therapeutic radiation, amyloid deposition was asymptomati...

Journal: :Journal of neuropathology and experimental neurology 2004
Marcin Sadowski Joanna Pankiewicz Henrieta Scholtzova Julia Tsai Yongsheng Li Richard I Carp Harry C Meeker Pierluigi Gambetti Manik Debnath Chester A Mathis Li Shao Wen-Biao Gan William E Klunk Thomas Wisniewski

The diagnosis of prion diseases in humans is challenging due to a lack of specific and sensitive non-invasive tests. Many forms of human prion disease including variant Creutzfeldt-Jakob disease (vCJD), Gerstmann-Sträussler-Scheinker (GSS) syndrome, and 10% of sporadic CJD cases are associated with amyloid deposition. Several positron emission tomography (PET) ligands have recently been develop...

2017
Stephanie L Leal Susan M Landau Rachel K Bell William J Jagust

The amyloid hypothesis suggests that beta-amyloid (Aβ) deposition leads to alterations in neural function and ultimately to cognitive decline in Alzheimer's disease. However, factors that underlie Aβ deposition are incompletely understood. One proposed model suggests that synaptic activity leads to increased Aβ deposition. More specifically, hyperactivity in the hippocampus may be detrimental a...

Journal: :Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 1998
G Ehlerding J Schaeffer W Drommer T Miyata K M Koch J Floege

BACKGROUND Beta-2-microglobulin-associated amyloidosis (AB2M) is a frequent complication of long-term dialysis treatment. Uraemic retention of beta2-microglobulin (beta2M) apparently constitutes the basis for AB2M. However, it is unclear why clinical manifestations are largely confined to osteoarticular tissues. It has been speculated that synovial inflammatory changes, induced by uraemia and/o...

2004
References Kang Han

The pathological signature of Alzheimer’s disease is the deposition of β-amyloid protein (Aβ). Its cleavage products, such as Aβ40 and Aβ42, form amyloid fibrils and plaques in the brains of affected individuals. Compounds that have affinity for Aβ have the ability to prevent neurotoxicity by inhibiting aggregation of amyloid fibrils. In addition, these molecules can also serve to quantify amyl...

Journal: :Cell 2005
Orly Lazarov John Robinson Ya-Ping Tang Ilana S. Hairston Zeljka Korade-Mirnics Virginia M.-Y. Lee Louis B. Hersh Robert M. Sapolsky Karoly Mirnics Sangram S. Sisodia

Cerebral deposition of beta-amyloid (Abeta) peptides is an invariant pathological hallmark in brains of patients with Alzheimer's disease (AD) and transgenic mice coexpressing familial AD-linked APP and PS1 variants. We now report that exposure of transgenic mice to an "enriched environment" results in pronounced reductions in cerebral Abeta levels and amyloid deposits, compared to animals rais...

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