Calcium in the initiation, progression and as an effector of Alzheimer's disease pathology. [PDF]
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
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
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
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]
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
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Label free visualization of amyloid plaques in Alzheimer's disease with polarization-sensitive photoacoustic Mueller matrix tomography [PDF]
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
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?
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
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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
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Parenchymal and vascular Aβ-deposition and its effects on the degeneration of neurons and cognition in Alzheimer's disease [PDF]
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
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