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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47/100
Using spatial cell-type-enriched transcriptomics, we compare plaque-induced gene (PIG) expression in microglia-touching plaques, neighboring plaques, and far from plaques in an aged Alzheimer's mouse model with late plaque development.
Why it matters
In aged Alzheimer's mouse models, this study found that plaque-induced gene upregulation in microglia, including for TREM2, is prevented by the Trem2 R47H/R47H risk mutation, and that TREM2-dependent genes relate to phagocytic and degradative processes. These are animal findings about microglial response to amyloid plaques and do not demonstrate a treatment or cure.
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Sodium glucose cotransporter 2 (SGLT2) inhibitors originally developed for the treatment of type 2 diabetes are clinically very effective drugs halting chronic kidney disease progression.
Why it matters
This study is about kidney disease, not Alzheimer's disease, and found that empagliflozin reduced kidney fibrosis and improved kidney function in rats after 5/6 nephrectomy. It reports no Alzheimer's treatment, cure or prevention.
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Cholesteryl ester transfer protein inhibition (CETP) has been shown to increase levels of high-density lipoprotein cholesterol (HDL-C) and reduce levels of low-density lipoprotein cholesterol (LDL-C).
Why it matters
This study examined whether lowering CETP and PCSK9 together is linked to coronary artery disease risk and other outcomes. It is about heart disease, not Alzheimer's disease, so it provides no information on treating, curing, or preventing dementia.
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The tumor-adipose microenvironment (TAME) is a universal microecosystem, that is characterized by the dysfunction of lipid metabolism, such as excessive free fatty acids (FFAs).
Why it matters
This study concerns the tumor-adipose microenvironment in breast cancer, reporting that M2-like macrophage infiltration is associated with poor survival. It concerns cancer, not Alzheimer's disease, and provides no information about treating, curing or preventing Alzheimer's disease.
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The mechanistic target of rapamycin (mTOR) signaling pathway plays a major role in key cellular processes including metabolism and differentiation; however, the role of mTOR in microglia and its importance in Alzheimer's disease (AD) have remained largely uncharacterized.
Why it matters
In the 5XFAD mouse model, activating mTOR in microglia upregulated Trem2 and enhanced amyloid-β clearance, reduced spine loss and improved cognitive function, with Trem2 acting downstream of mTOR. This is mouse work identifying a pathway and does not demonstrate a treatment for people.
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Foam cells play a vital role in the initiation and development of atherosclerosis.
Why it matters
This review is about foam cells in atherosclerosis, not Alzheimer's disease, so it offers no direct information about treating, curing or preventing Alzheimer's. It describes how foam cells arise from monocytes, vascular smooth muscle cells, stem/progenitor cells and endothelium cells, based on technologies such as lineage tracing and single-cell RNA sequencing.
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They also suggest that FW elevation occurs in the locus coeruleus to transentorhinal cortex tract, nucleus basalis of Meynert, and hippocampus in the transition from CN to EMCI, while other basal forebrain regions and the entorhinal cortex are not affected until a later stage of AD.
Why it matters
Higher free water on diffusion MRI in the locus coeruleus to transentorhinal cortex tract, nucleus basalis of Meynert and hippocampus was associated with greater clinical diagnosis severity, cognitive impairment and plasma neurofilament light. This identifies an imaging marker of early Alzheimer disease changes but does not test any treatment.
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Galectin-3 (Gal-3) is an evolutionarily conserved and multifunctional protein that drives inflammation in disease.
Why it matters
This review describes Galectin-3 as a protein that drives inflammation and notes that loss of Gal-3 function can diminish symptoms of neurodegenerative diseases such as Alzheimer's in recent studies. It is a review of molecular pathways and does not report a tested treatment, cure, or prevention for Alzheimer's disease in people.
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While macrophages are among the most abundant immune cell type found within primary and metastatic mammary tumors, how their complexity and heterogeneity change with metastatic progression remains unknown.
Why it matters
This study is about macrophages in lungs bearing metastatic breast tumors in mice, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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47/100
Heterozygous genetic variants within the TREM2 gene show a strong association with increased Alzheimer's disease (AD) risk.
Why it matters
In mice, acutely reducing Trem2 with antisense oligonucleotides increased microglial phagocytosis and slowed amyloid deposition. This is an early animal study and does not yet show a treatment, cure, or prevention for Alzheimer's disease in people.
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47/100
We explored the potential link between chronic inflammatory arthritis and COVID-19 pathogenic and resolving macrophage pathways and their role in COVID-19 pathogenesis.
Why it matters
This study compared macrophage pathways in COVID-19 and rheumatoid arthritis and found shared myeloid pathways. It is about COVID-19 and rheumatoid arthritis, not Alzheimer's disease, so it does not inform Alzheimer's treatment, cure or prevention.
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47/100
Tauopathies consist of over 25 different neurodegenerative diseases that include argyrophilic grain disease (AGD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Pick's disease (PiD).
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47/100
Pancreatic ductal adenocarcinoma (PDA) is accompanied by reprogramming of the local microenvironment, but changes at distal sites are poorly understood.
Why it matters
This study is about pancreatic cancer and found high C1qa, C1qb, and Trem2 expression in macrophage populations in mice and human tumor samples. It provides no information about treating, curing, or preventing Alzheimer's disease.
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Tau and Aβ assemblies of Alzheimer's disease (AD) can be visualized in living subjects using positron emission tomography (PET).
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47/100
Proregenerative responses are required for the restoration of nervous-system functionality in demyelinating diseases such as multiple sclerosis (MS).
Why it matters
In a mouse model of demyelinating injury, a Western diet impaired microglial clearance of myelin debris and lesion recovery. This is early animal work on multiple sclerosis-like injury and does not show that any treatment prevents or cures Alzheimer's disease.
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These results indicate that in Alzheimer's disease, tau pathology is closely associated with reduced synaptic density and synaptic dysfunction.
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By engaging membrane-bound TREM2, the selected antibody was shown to promote their cellular proliferation, uptake of oligomeric beta amyloid/apoptotic neurons, and activation in a Syk and Akt dependent manner.
Why it matters
A monoclonal antibody that binds TREM2 was shown to activate microglia and improve cognitive function in Alzheimer's disease models. This is laboratory and animal work, so it does not yet show a treatment for people.
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Elevated microglial activation in the right amygdala-entorhinal-hippocampal complex of App NL-G-F mice is associated with better spatial learning.
Why it matters
In a mouse model, higher microglial activation in certain right-brain regions was linked to better spatial learning, while amyloid PET showed no such link. This is animal research and does not show any treatment, cure, or prevention for people.
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Herein, we demonstrate that endogenous Tyrobp transcription is specifically increased in recruited microglia.
Why it matters
In transgenic mice, overexpressing TYROBP in microglia decreased amyloid burden but increased tau phosphorylation, revealing a TREM2-independent TYROBP-APOE link. This is animal research and does not establish a treatment for Alzheimer's disease.
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Mechanisms underlying the protective effect of apolipoprotein E ( APOE ) ε2 against Alzheimer’s disease (AD) are not well understood.
Why it matters
By analyzing brain gene expression from 982 autopsied donors, including 135 APOE ε2/ε3 carriers, this study linked complement pathway genes C4A and C4B and the gene HSPA2 to the protective effect of APOE ε2 against Alzheimer's disease. These findings point to possible biological pathways behind protection, but they come from donated brain tissue and do not establish a treatment or prevention.
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47/100
Alzheimer's disease (AD) is a progressive, late-onset dementia with no effective treatment available.
Why it matters
This study tested whether β-hydroxybutyrate reduces Alzheimer's pathology in a mouse model by inhibiting the NLRP3 inflammasome. It is animal research, so it does not show that a ketogenic diet or this compound helps people with Alzheimer's disease.
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Microglia-specific genetic variants are enriched in several neurodegenerative diseases, including Alzheimer's disease (AD), implicating a central role for alterations of the innate immune system in the disease etiology.
Why it matters
In mice carrying a protective PLCG2 variant linked to lower Alzheimer's risk, the variant strengthened some immune cell functions. This is early animal work on immune function and does not show that any treatment prevents or cures Alzheimer's disease in people.
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To study the mechanisms by which the p.R47H variant of the microglia gene and Alzheimer's disease (AD) risk factor TREM2 increases dementia risk, we created Trem2 R47H KI rats.
Why it matters
In rats with the TREM2 R47H variant, increased TNF-α, enhanced excitatory transmission and reduced LTP occurred even with normal Aβ levels, and blocking TNF-α prevented some of these effects. This is animal research and does not yet provide a treatment for Alzheimer's disease.
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Microglia, once viewed as static bystanders with limited homeostatic functions, are now considered key players in the development of neuroinflammatory and neurodegenerative diseases.
Why it matters
This review discusses lipid and lipoprotein metabolism in microglia and notes that single-cell RNA-sequencing studies have found changes in genes involved in these processes. It does not report testing any treatment or prevention for Alzheimer's disease in people.
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The present study explores the associations of soluble TREM2, an important regulator of microglial activity linked to Alzheimer's disease (AD), with other known inflammatory proteins in cerebrospinal fluid (CSF).
Why it matters
In 303 participants including controls, mild cognitive impairment and Alzheimer's dementia patients, several inflammatory proteins in cerebrospinal fluid differed significantly between ATN groups. This is an observational study and does not show whether these proteins cause Alzheimer's disease or whether targeting them would treat it.
From across this topic
10 of the 4,748 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.
- The alpha secretase ADAM10: A metalloprotease with multiple functions in the brain
- Detection of biomarkers with a multiplex quantitative proteomic platform in cerebrospinal fluid of patients with neurodegenerative disorders
- Alpha-synuclein pathology does not predict extrapyramidal symptoms or dementia
- Hippocampal overexpression of TREM2 ameliorates high fat diet induced cognitive impairment and modulates phenotypic polarization of the microglia
- Systemic infection and delirium: when cytokines and acetylcholine collide
- RIPK1 expression and inhibition in tauopathies: implications for neuroinflammation and neuroprotection
- The role of plasma inflammatory markers in late-life depression and conversion to dementia: a 3-year follow-up study
- Frontotemporal dementia and corticobasal degeneration in a family with a P301S mutation in tau
- Comparative binding properties of the tau PET tracers THK5117, THK5351, PBB3, and T807 in postmortem Alzheimer brains
- Notch signaling regulates platelet-derived growth factor receptor-beta expression in vascular smooth muscle cells