Results 51 to 60 of about 94,035 (378)

Calcium in the initiation, progression and as an effector of Alzheimer's disease pathology. [PDF]

open access: yes, 2009
The cause(s) of sporadic Alzheimer's disease (sAD) are complex and currently poorly understood. They likely result from a combination of genetic, environmental, proteomic and lipidomic factors that crucially occur only in the aged brain.
Green, Kim N
core   +1 more source

Neurotoxic amyloid β‐peptide and tau produce cytokine‐like effects on PMCA in glioblastoma cell lines, enhancing its activity and isoforms expression

open access: yesFEBS Open Bio, EarlyView.
Two biomarkers of Alzheimer's disease, amyloid β‐peptide (Aβ) and tau, induce the transformation of U‐251 and other glioblastoma cell lines into neurotoxic A1‐like reactive astrocytes. This transformation is produced by cytokines and is followed by upregulation of PMCA activity and isoform expression, and is closely associated with inflammation, as ...
María Berrocal   +2 more
wiley   +1 more source

Atrial amyloidosis: mechanisms and clinical manifestations

open access: yesEuropean Journal of Heart Failure, Volume 24, Issue 11, Page 2019-2028, November 2022., 2022
Atrial amyloidosis: pathophysiology and clinical manifestations. Atrial amyloidosis can manifest as part of a systemic disorder (as in amyloid light‐chain [AL] or transthyretin [ATTR] amyloidosis), or be isolated (in the form due to atrial natriuretic type [ANP] accumulation); this last form is often associated with permanent or persistent atrial ...
Giuseppe Vergaro   +11 more
wiley   +1 more source

SPON1 Can Reduce Amyloid Beta and Reverse Cognitive Impairment and Memory Dysfunction in Alzheimer’s Disease Mouse Model

open access: yesCells, 2020
Alzheimer’s disease (AD) is a complex, age-related neurodegenerative disease that is the most common form of dementia. However, the cure for AD has not yet been founded. The accumulation of amyloid beta (Aβ) is considered to be a hallmark of AD.
Soo Yong Park   +5 more
doaj   +1 more source

Model Hirano bodies protect against tau-independent and tau-dependent cell death initiated by the amyloid precursor protein intracellular domain. [PDF]

open access: yesPLoS ONE, 2012
The main pathological hallmarks of Alzheimer's disease are amyloid-beta plaques and neurofibrillary tangles, which are primarily composed of amyloid precursor protein (APP) and tau, respectively.
Matthew Furgerson   +2 more
doaj   +1 more source

Label free visualization of amyloid plaques in Alzheimer's disease with polarization-sensitive photoacoustic Mueller matrix tomography [PDF]

open access: yesarXiv, 2022
The formation of amyloid plaques in the cortical and hippocampal brain regions caused by abnormal deposition of extracellular amyloid \b{eta}-protein (A\b{eta}) is a characteristic pathological hallmark of early Alzheimer's disease (AD), while label-free graphic rendering of diseased amyloid plaques in vivo is still a highly challenging task.
arxiv  

Calcium modulating ligand confers risk for Parkinson's disease and impacts lysosomes

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
Abstract Objective Several genetic loci known to confer risk for Parkinson's disease (PD) function in lysosomal pathways. We systematically screened common variants linked to PD risk by genome‐wide association studies (GWAS) for impact on cerebrospinal fluid (CSF) proteins reflecting lysosomal function.
Hanwen Zhang   +16 more
wiley   +1 more source

Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?

open access: yesDementia & Neuropsychologia
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, including memory loss, behavioral and psychological symptoms and personality changes.
Vanessa de Jesus R. de Paula   +3 more
doaj   +1 more source

Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues

open access: yesFrontiers in Neuroscience, 2020
Severe traumatic brain injury (TBI) is a risk factor for neurodegenerative diseases. Yet, the molecular events involving dysregulated miRNAs that may be associated with protein degradation in the brain remains elusive.
Bharani Thangavelu   +5 more
doaj   +1 more source

Parenchymal and vascular Aβ-deposition and its effects on the degeneration of neurons and cognition in Alzheimer's disease [PDF]

open access: yes, 2008
The deposition of the amyloid β-protein (Aβ) is one of the pathological hallmarks of Alzheimer's disease (AD). Aβ-deposits show the morphology of senile plaques and cerebral amyloid angiopathy (CAA). Senile plaques and vascular Aβ-deposits occur first in
Braak, Heiko   +2 more
core   +1 more source

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