نتایج جستجو برای: amyloid plaque

تعداد نتایج: 70063  

2014
Nicholas Myers Lorenzo Pasquini Jens Göttler Timo Grimmer Kathrin Koch Marion Ortner Julia Neitzel Mark Mühlau Stefan Förster Alexander Kurz Hans Förstl Claus Zimmer Afra M. Wohlschläger Valentin Riedl Alexander Drzezga Christian Sorg

There is striking overlap between the spatial distribution of amyloid-β pathology in patients with Alzheimer's disease and the spatial distribution of high intrinsic functional connectivity in healthy persons. This overlap suggests a mechanistic link between amyloid-β and intrinsic connectivity, and indeed there is evidence in patients for the detrimental effects of amyloid-β plaque accumulatio...

2018
Tsai-Teng Tzeng Chien-Chih Chen Chin-Chu Chen Huey-Jen Tsay Li-Ya Lee Wan-Ping Chen Chien-Chang Shen Young-Ji Shiao

Hericium erinaceus was used in traditional Chinese medicine for physiologically beneficial medicines. Recently, it has become a candidate in causing positive brain health-related activities. We previously reported that Hericium erinaceus mycelium ameliorates Alzheimer's disease (AD)-related pathologies. To reveal the role of the cyanthin diterpenoid and sesterterpene constituents on this effect...

Journal: :Journal of neuropathology and experimental neurology 2013
Alberto Serrano-Pozo Alona Muzikansky Teresa Gómez-Isla John H Growdon Rebecca A Betensky Matthew P Frosch Bradley T Hyman

Although it is clear that astrocytes and microglia cluster around dense-core amyloid plaques in Alzheimer disease (AD), whether they are primarily attracted to amyloid deposits or are just reacting to plaque-associated neuritic damage remains elusive. We postulate that astrocytes and microglia may differentially respond to fibrillar amyloid β. Therefore, we quantified the size distribution of d...

2010
Benoit Melchior Angie E Garcia Bor-Kai Hsiung Katherine M Lo Jonathan M Doose J Cameron Thrash Anna K Stalder Matthias Staufenbiel Harald Neumann Monica J Carson

Vaccine-based autoimmune (anti-amyloid) treatments are currently being examined for their therapeutic potential in Alzheimer's disease. In the present study we examined, in a transgenic model of amyloid pathology, the expression of two molecules previously implicated in decreasing the severity of autoimmune responses: TREM2 (triggering receptor expressed on myeloid cells 2) and the intracellula...

Journal: :International journal of clinical and experimental pathology 2012
Krikor Dikranian Jungsu Kim Floy R Stewart Marilyn A Levy David M Holtzman

Alzheimer's disease is characterized in part by extracellular aggregation of the amyloid-β peptide in the form of diffuse and fibrillar plaques in the brain. Electron microscopy (EM) has made an important contribution in understanding of the structure of amyloid plaques in humans. Classical EM studies have revealed the architecture of the fibrillar core, characterized the progression of neuriti...

Journal: :Medical hypotheses 2006
Alan B MacDonald

Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded "plaques' in high density in brain tissue are emblematic of Alzheimer's disease (AD). Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury. In this century, in brain tissu...

Journal: :Neuron 2005
John D. Fryer David M. Holtzman

In this issue of Neuron, McGowan et al. report on a new mouse model of amyloid deposition as occurs in Alzheimer's disease. Unlike previous models in which overexpression of the amyloid precursor protein results in amyloid plaque formation, McGowan et al. have produced mice that overexpress only Abeta40 or Abeta42 and prove that Abeta42 is critical for the formation of amyloid deposits in vivo.

2016
Elena Rodriguez-Vieitez Laure Saint-Aubert Stephen F. Carter Ove Almkvist Karim Farid Michael Schöll Konstantinos Chiotis Steinunn Thordardottir Caroline Graff Anders Wall Bengt Långström Agneta Nordberg

Alzheimer's disease is a multifactorial dementia disorder characterized by early amyloid-β, tau deposition, glial activation and neurodegeneration, where the interrelationships between the different pathophysiological events are not yet well characterized. In this study, longitudinal multitracer positron emission tomography imaging of individuals with autosomal dominant or sporadic Alzheimer's ...

2016
Elena Rodriguez-Vieitez Laure Saint-Aubert Stephen F. Carter Ove Almkvist Karim Farid Michael Schöll Konstantinos Chiotis Steinunn Thordardottir Caroline Graff Anders Wall Bengt Långström Agneta Nordberg

Alzheimer’s disease is a multifactorial dementia disorder characterized by early amyloid-b, tau deposition, glial activation and neurodegeneration, where the interrelationships between the different pathophysiological events are not yet well characterized. In this study, longitudinal multitracer positron emission tomography imaging of individuals with autosomal dominant or sporadic Alzheimer’s ...

2016
Elena Rodriguez-Vieitez Laure Saint-Aubert Stephen F. Carter Ove Almkvist Karim Farid Michael Schöll Konstantinos Chiotis Steinunn Thordardottir Caroline Graff Anders Wall Bengt Långström Agneta Nordberg

Alzheimer’s disease is a multifactorial dementia disorder characterized by early amyloid-b, tau deposition, glial activation and neurodegeneration, where the interrelationships between the different pathophysiological events are not yet well characterized. In this study, longitudinal multitracer positron emission tomography imaging of individuals with autosomal dominant or sporadic Alzheimer’s ...

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