Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
-
Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) accumulation, neuroinflammation, synaptic dysfunction, and cognitive decline.
-
The high metabolic demand of retinal neurons requires tightly regulated mechanisms to maintain homeostasis and ensure the efficient clearance of metabolic waste and excess water.
-
Genetic variations in MS4A4A and MS4A6A Triggering receptor expressed on myeloid cells 2 (TREM2) are linked to the regulation of cerebrospinal-fluid-soluble TREM2 levels and are associated with Alzheimer's disease (AD) risk and progression.
-
Triggering receptor expressed on myeloid cells 2 (TREM2) is cell surface transmembrane receptor of the TREM family, predominantly expressed on microglia within the central nervous system (CNS).
-
This review considers the use of these mouse models in understanding the mechanisms of Aβ clearance, cerebral amyloid angiopathy (CAA), blood brain barrier breakdown, neuroinflammation, and neuronal dysfunction in response to Aβ immunotherapy.
-
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease characterized by vascular amyloid-β (Aβ) deposition.
-
Our study has established a significant link between CAA-Aβ antibody immune complex formation, immune activation and vascular damage leading to smooth muscle cell loss.
-
The targeting of amyloid-beta (Aβ) plaques therapeutically as one of the primary causes of Alzheimer's disease (AD) dementia has been an ongoing effort spanning decades.
-
Microglia and neuroinflammation play an important role in the development and progression of Alzheimer's disease (AD).
-
Neuroinflammation is a key pathological feature in neurological diseases, including Alzheimer's disease (AD).
-
Due to commonalities in pathophysiology, age-related macular degeneration (AMD) represents a uniquely accessible model to investigate therapies for neurodegenerative diseases, leading us to examine whether pathways of disease progression are shared across neurodegenerative conditions.
-
During the 4-day meeting, presenters illuminated aspects of the cross-talk between APOE and immunity, with a focus on the roles of microglia, triggering receptor expressed on myeloid cells 2 (TREM2), and components of inflammation (e.g., tumor necrosis factor α [TNFα]).
-
Extracellular deposition of amyloid-β as neuritic plaques and intracellular accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles are two of the characteristic hallmarks of Alzheimer's disease 1,2 .
-
Translocase of outer mitochondrial membrane 40 (TOMM40) is located in the outer membrane of mitochondria.
-
The major neuropathological hallmarks of Alzheimer's disease (AD) are amyloid β (Aβ) plaques and neurofibrillary tangles (NFT), accompanied by neuroinflammation and neuronal loss.
-
Macrophages are important players in the maintenance of tissue homeostasis 1 .
-
Physical exercise is generally beneficial to all aspects of human and animal health, slowing cognitive ageing and neurodegeneration 1 .
-
Neuroinflammation contributes to Alzheimer's disease (AD) progression.
-
The complement system is part of the innate immune system that comprises several small proteins activated by sequential cleavages.
-
Variants in the triggering receptor expressed on myeloid cells 2 gene are linked with an increased risk of dementia, in particular the R47Hhet triggering receptor expressed on myeloid cells 2 variant is linked to late-onset Alzheimer's disease.
-
45/100
The extent of microglial heterogeneity in humans remains a central yet poorly explored question in light of the development of therapies targeting this cell type.
-
45/100
Neuroinflammation and microglial activation are significant processes in Alzheimer's disease pathology.
-
Many risk genes for the development of Alzheimer's disease (AD) are exclusively or highly expressed in myeloid cells.
-
With a rapidly aging global human population, finding a cure for late onset neurodegenerative diseases has become an urgent enterprise.
-
The adult quiescent blood-brain barrier (BBB), a structure organised by endothelial cells through interactions with pericytes, astrocytes, neurons and microglia in the neurovascular unit, is highly regulated but fragile at the same time.
From across this topic
10 of the 730 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Molecular physiology and pathophysiology of tight junctions in the blood-brain barrier
- The NLRP3 and NLRP1 inflammasomes are activated in Alzheimer's disease
- Glycogen Synthase Kinase-3β, NLRP3 Inflammasome, and Alzheimer's Disease
- Semaglutide Attenuates Neuroinflammation in Mice
- Drug repurposing on Alzheimer's disease through modulation of NRF2 neighborhood
- BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology
- Neuroinflammation in Alzheimer's Disease: Focus on NLRP1 and NLRP3 Inflammasomes
- Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes
- Interaction between autophagy and the NLRP3 inflammasome in Alzheimer's and Parkinson's disease
- Review: activation patterns of microglia and their identification in the human brain