[HTML][HTML] Dysfunction of the blood-brain barrier in cerebral microbleeds: from bedside to bench

H Wang, C Zhang, Y Qiu, A Chen, Y Li, B Hu - Aging and disease, 2021 - ncbi.nlm.nih.gov
Cerebral microbleeds (CMBs) are a disorder of cerebral microvessels that are characterized
as small (< 10 mm), hypointense, round or ovoid lesions seen on T2*-weighted gradient …

[HTML][HTML] Stochastic non-enzymatic modification of long-lived macromolecules-A missing hallmark of aging

A Fedintsev, A Moskalev - Ageing research reviews, 2020 - Elsevier
Damage accumulation in long-living macromolecules (especially extracellular matrix (ECM)
proteins, nuclear pore complex (NPC) proteins, and histones) is a missing hallmark of aging …

The role of extracellular matrix in human neurodegenerative diseases

P Pintér, A Alpár - International journal of molecular sciences, 2022 - mdpi.com
The dense neuropil of the central nervous system leaves only limited space for extracellular
substances free. The advent of immunohistochemistry, soon followed by advanced …

Advanced glycation end-products disrupt the blood–brain barrier by stimulating the release of transforming growth factor–β by pericytes and vascular endothelial …

F Shimizu, Y Sano, O Tominaga, T Maeda, M Abe… - Neurobiology of …, 2013 - Elsevier
Diabetic encephalopathy is now accepted as an important complication of diabetes. The
breakdown of the blood–brain barrier (BBB) is associated with dementia in patients with type …

Do astrocytes collaborate with neurons in spreading the “infectious” Aβ and Tau drivers of Alzheimer's disease?

I Dal Prà, A Chiarini, L Gui, B Chakravarthy… - The …, 2015 - journals.sagepub.com
Evidence has begun emerging for the “contagious” and destructive Aβ42 (amyloid-beta42)
oligomers and phosphorylated Tau oligomers as drivers of sporadic Alzheimer's disease …

Vascular oxidative stress and mitochondrial failure in the pathobiology of Alzheimer's disease: a new approach to therapy

M Sochocka, ES Koutsouraki… - CNS & Neurological …, 2013 - ingentaconnect.com
Vascular and metabolic dysfunctions and mitochondrial failure are now believed to be
contributors to Alzheimer's disease (AD) pathogenesis. Vascular dysfunction includes …

The potential mechanisms of Aβ-receptor for advanced glycation end-products interaction disrupting tight junctions of the blood-brain barrier in Alzheimer's disease

W Wan, H Chen, Y Li - International Journal of Neuroscience, 2014 - Taylor & Francis
The receptor for advanced glycation end-products (RAGE) is a multiligand membrane
receptor that has been implicated in the cytotoxicity effects of β-amyloid protein (Aβ) in AD …

Adiponectin controls the apoptosis and the expression of tight junction proteins in brain endothelial cells through AdipoR1 under beta amyloid toxicity

J Song, SM Choi, DJ Whitcomb, BC Kim - Cell death & disease, 2017 - nature.com
Alzheimer's disease (AD) is the most common neurodegenerative disease, characterized by
excessive beta amyloid (Aβ) deposition in brain, leading to blood–brain barrier (BBB) …

Aβ-induced senescent retinal pigment epithelial cells create a proinflammatory microenvironment in AMD

L Cao, H Wang, F Wang, D Xu, F Liu… - … ophthalmology & visual …, 2013 - iovs.arvojournals.org
Purpose.: Chronic inflammation is implicated in the pathogenesis of AMD. The source of
chronic inflammation is often attributed to the progressive activation of immune cells over …

[HTML][HTML] Calcium-sensing receptor antagonist (calcilytic) NPS 2143 specifically blocks the increased secretion of endogenous Aβ42 prompted by exogenous fibrillary …

U Armato, A Chiarini, B Chakravarthy, F Chioffi… - … et Biophysica Acta (BBA …, 2013 - Elsevier
The “amyloid-β (Aβ) hypothesis” posits that accumulating Aβ peptides (Aβs) produced by
neurons cause Alzheimer's disease (AD). However, the Aβs contribution by the more …