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.
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Inflammatory cerebral amyloid angiopathy (CAA) typically affects older patients who present with acute or subacute cognitive decline, headache, behavioral change, seizures, and focal neurological deficits.
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Dysfunctional variants of the innate immune cell surface receptor TREM2 (triggering receptor expressed on myeloid cells-2) were identified as major genetic risk factors for Alzheimer's disease and other neurodegenerative conditions.
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Several lines of evidence support immune response in brain as a mechanism of injury in Alzheimer disease (AD).
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Alzheimer's disease (AD) is characterized by the accumulation and deposition of amyloid-beta (Aβ) peptides in the brain.
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Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by a progressive loss of memory and cognitive skills.
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Apolipoprotein (apo) E4 is the major genetic risk factor for Alzheimer's disease and is associated with poor clinical outcome following traumatic brain injury and other neuropathological disorders.
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The ε4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and affects clinical outcomes of chronic and acute brain damages.
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38/100
Here we showed that activation of primary astrocytes from TR APOE mice with LPS led to TR APOE-dependent differences in cytokine secretion that were greatest in TR APOE2 and that were associated with differences in NF-kappaB subunit activity.
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Chronically activated glia associated with amyloid plaques might contribute to neuronal dysfunction in Alzheimer's disease (AD) through generation of neuroinflammatory molecules.
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It is now generally accepted that the lesions of Alzheimer disease (AD) are associated with a host of inflammatory molecules, including complement proteins, as well as with many activated microglia.
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36/100
Matrix metalloproteinases are versatile endopeptidases with many different functions in the body in health and disease.
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The blood-brain barrier (BBB) is a vital boundary between neural tissue and circulating blood.
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The cytokine interleukin-6 (IL-6) plays a critical role in the pathogenesis of inflammatory disorders and in the physiological homeostasis of neural tissue.
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Inflammation may play a role in neural damage in preclinical AD.
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Hypertension (HTN) doubles the risk of Alzheimer’s disease (AD), but the mechanisms remain unclear.
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The blood–brain barrier (BBB) limits the entry of neurotoxic blood-derived products and cells into the brain that is required for normal neuronal functioning and information processing.
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Recent genome-wide association studies implicate microglia in Alzheimer's disease (AD) pathogenesis; however, their biological significance remains poorly understood.
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Structural and functional brain connectivity, synaptic activity, and information processing require highly coordinated signal transduction between different cell types within the neurovascular unit and intact blood-brain barrier (BBB) functions.
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Despite decades of intensive research, the biological mechanisms that causally underlie depression are still unclear, and therefore the development of novel effective antidepressant treatments is hindered.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder of the brain, which is characterized by the formation of extracellular amyloid plaques (or senile plaques) and intracellular neurofibrillary tangles.
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Microglia serve key homeostatic roles, and respond to neuronal perturbation and decline with a high spatiotemporal resolution.
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Chronic glial activation and neuroinflammation induced by the amyloid‐β peptide (Aβ) contribute to Alzheimer's disease ( AD ) pathology.
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Androstene derivatives incorporating amino acid methyl esters were prepared, and their anti‐inflammatory effects were evaluated in lipopolysaccharide (LPS)‐activated BV‐2 microglial cells.
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Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD).
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Alzheimer's disease (AD) is the world's most common dementing illness, affecting over 150 million patients.
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.
- APOE-Targeted Therapeutics for Alzheimer's Disease
- Alzheimer's disease and angiogenesis
- Compromised MAPK signaling in human diseases: an update
- Cerebral Amyloid Angiopathy-Related Inflammation: A Case Report and Literature Review
- Interrelation of oxidative stress and inflammation in neurodegenerative disease: role of TNF
- Neuroinflammation is associated with Alzheimer's disease co-pathology in dementia with Lewy bodies
- Ocular Fundus Photography as a Tool to Study Stroke and Dementia
- APOE and immunity: Research highlights
- Genetic Risk Factors for Alzheimer Disease: Emerging Roles of Microglia in Disease Pathomechanisms
- CCL23: A Chemokine Associated with Progression from Mild Cognitive Impairment to Alzheimer's Disease