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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Among 455,306 UK Biobank participants, 37 carried one copy of the APOE Christchurch variant (allele frequency 0.004%).
Why it matters
Among 455,306 UK Biobank participants, 37 carried one copy of the APOE Christchurch variant and none had developed Alzheimer's or mild cognitive impairment by the data freeze. The sample was too small to directly test dementia risk, so this cannot establish that the variant protects against Alzheimer's.
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Across 3 study samples, combining the functional connectome and molecular properties substantially enhanced the explanatory power compared to single modalities, providing a valuable tool to explain regional susceptibility to tau deposition in AD.
Why it matters
Across three studies, combining brain connectivity, MAPT gene expression, and amyloid PET explained more of the regional pattern of tau deposition in Alzheimer's disease than connectivity alone. This improves understanding of how tau spreads in the brain but does not test treatment, cure, or prevention.
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51/100
Alzheimer's disease (AD) remains one of the grand challenges facing human society.
Why it matters
This paper describes a cell therapy approach to restore microglial Trem2 function in a mouse model of Alzheimer's disease, based on genetic evidence that microglia help prevent neuron degeneration. It is animal work and does not show a treatment or cure for people.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is strongly linked to Alzheimer's disease (AD) risk, but its functions are not fully understood.
Why it matters
This study found that TREM2 binds complement C1q and attenuates classical complement activation, and that in mice with mutant human tau, reduced Trem2 increased complement-mediated microglial engulfment of synapses and accelerated synaptic loss. This is largely animal and human brain tissue work and does not establish a treatment, cure or prevention for Alzheimer's disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) plays important roles in brain microglial function in neurodegenerative diseases, but the role of TREM2 in the GBM TME has not been examined.
Why it matters
This study is about glioblastoma, not Alzheimer's disease, and found that blocking TREM2 increased antitumor activity of myeloid cells and reduced tumors in mice. It provides no evidence about treating, curing, or preventing Alzheimer's disease.
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Sleep loss is associated with cognitive decline in the aging population and is a risk factor for Alzheimer's disease (AD).
Why it matters
In mice, chronic sleep deprivation worsened microglial reactivity and amyloid-beta deposition in a TREM2-dependent manner. It is an animal study, so it does not show that improving sleep prevents or treats Alzheimer's disease in people.
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Huge efforts in developing specific and stable tracers for PET/SPECT imaging have been made.
Why it matters
Covering 28 articles, this review tracks the development of imaging tracers for PET and SPECT scans that bind TSPO, a protein that marks brain inflammation in dementia. The authors note a key limitation: inflammation affects the whole brain, making small changes hard to detect, partly addressed by using the cerebellum as a reference and developing tracers that bind TSPO more strongly. It is about imaging tools, not treatment.
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Tumor cells promote the recruitment of immunosuppressive neutrophils, a subset of myeloid cells driving immune suppression, tumor proliferation, and treatment resistance.
Why it matters
This study identified senescent-like neutrophils expressing TREM2 that promote tumors and suppress immunity in prostate cancer. It is about cancer, not Alzheimer's, and provides no information about treating, curing or preventing Alzheimer's.
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There is growing evidence that cognitive decline can be affected by both nutritional aspects and inflammation.
Why it matters
Among community-dwelling older adults, plasma NfL was associated with markers of inflammation and cellular stress, while amyloid ratio was not associated with nutritional or inflammatory markers. This is about understanding relationships between blood markers, not about treating, curing, or preventing Alzheimer's disease.
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There is increasing appreciation that non-neuronal cells contribute to the initiation, progression and pathology of diverse neurodegenerative disorders.
Why it matters
This review examines how astrocytes contribute to the initiation, progression and pathology of neurodegenerative disorders including Alzheimer's disease, and how their normal supporting functions change. It reports no treatment or prevention outcome, only a research direction.
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The apolipoprotein E (APOE)ε4 allele is the strongest genetic risk factor for late-onset AD and is associated with aberrant cerebrospinal fluid levels (CSF) of total tau (t-tau), phosphorylated tau (p-tau), and amyloid-β (Aβ).
Why it matters
In 1599 mid-to-late life people without dementia, this study examined how sex, APOE ε4 status and CSF amyloid interact to affect CSF tau levels. It explores risk biology but does not test any treatment or prevention.
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& aims Previous single-cell RNA-sequencing analyses have shown that Trem2-expressing macrophages are present in the liver during obesity, non-alcoholic steatohepatitis (NASH) and cirrhosis.
Why it matters
This study is about TREM2-expressing macrophages in the liver during obesity, non-alcoholic steatohepatitis and cirrhosis, not Alzheimer's disease, so it provides no direct information about treating, curing or preventing Alzheimer's. Its findings come from mouse dietary models, bone marrow transplantation and single-cell sequencing.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery.
Why it matters
This review gathers earlier research suggesting that TREM2, an immune receptor found mainly on the brain's microglia and on macrophages in the body, is a risk factor for Alzheimer's and helps control how fats are handled. In the brain, it is described as affecting cholesterol, myelin and phospholipid metabolism and pushing microglia into a "disease-associated" state; in the body, as influencing obesity and related conditions such as high cholesterol, atherosclerosis and fatty liver disease. It presents TREM2 as a *potential* metabolic drug target and reports no new data or treatment results.
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Participants with higher total-tau and NfL at baseline had a higher risk of stroke and several stroke subtypes.
Why it matters
In 4,661 stroke-free participants followed for a mean of 10.8 years, higher baseline total-tau and NfL levels were associated with increased risk of stroke, while Aβ40, Aβ42, and Aβ42/40 were not. This study examines stroke risk, not Alzheimer's treatment, cure, or prevention.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor expressed by macrophages and microglia in the central nervous system (CNS).
Why it matters
This review discusses whether soluble TREM2 is an innocent bystander or an active player in neurological diseases, noting that TREM2 variation can cause Nasu-Hakola disease and increase risk for Alzheimer's disease and frontotemporal dementia. It raises questions about TREM2 as a target but reports no treatment or cure.
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Haploinsufficiency of the progranulin (PGRN)-encoding gene (GRN) causes frontotemporal lobar degeneration (GRN-FTLD) and results in microglial hyperactivation, TREM2 activation, lysosomal dysfunction, and TDP-43 deposition.
Why it matters
In mice lacking progranulin, removing TREM2 reduced microglial hyperactivation but did not fix lysosomal problems or neurotoxicity, and antagonistic TREM2 antibodies were tested on patient-derived macrophages. This indicates that blocking TREM2 alone is not enough to correct the broader damage in this frontotemporal dementia model.
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The association of testosterone concentrations with dementia risk remains uncertain.
Why it matters
This UK Biobank prospective cohort study examined whether lower serum testosterone and sex hormone-binding globulin levels are associated with higher incidence of dementia and Alzheimer's disease in men. It is observational, so it cannot show that raising testosterone would prevent dementia.
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51/100
White matter hyperintensities (WMH) are among the most common radiological abnormalities in the ageing population and an established risk factor for stroke and dementia.
Why it matters
This genetic study found a rare variant in the GBE1 gene linked to lower amounts of white matter hyperintensities in the brain, which are a risk factor for stroke and dementia. It is about understanding genetic influences on brain changes and does not test any treatment, cure, or prevention.
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Microglial-mediated neuroinflammation plays an important role in vascular dementia, and modulating neuroinflammation has emerged as a promising treatment target.
Why it matters
In rats with chronic cerebral hypoperfusion, daily NAD+ injection improved cognitive function and reduced neuroinflammation and mitochondrial damage through the Sirt1/PGC-1α pathway. This is animal research on vascular dementia, so it does not establish benefit for people with Alzheimer's disease.
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While insulin-like growth factor-1 (IGF-1) is a well-established modulator of aging and longevity in model organisms, its role in humans has been controversial.
Why it matters
Using UK Biobank data from 440,185 people, this study found that high insulin-like growth factor 1 was linked to lower disease risk in younger people but higher risk of disease or death, including dementia, in older people. It describes risk patterns only and does not test any treatment, cure, or prevention.
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Ovarian carcinomas (OCs) are poorly immunogenic and immune checkpoint inhibitors (ICIs) have offered a modest benefit.
Why it matters
This study in ovarian cancer found that high T-cell and macrophage densities identified a subgroup with better outcomes, while in clear cell carcinomas high macrophage density was linked to low T-cell frequency. It is about ovarian cancer, not Alzheimer's disease, and does not show a treatment or cure for Alzheimer's.
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APOE and Trem2 are major genetic risk factors for Alzheimer's disease (AD), but how they affect microglia response to Aβ remains unclear.
Why it matters
In preclinical mouse models, APOE3 lipoproteins helped microglia migrate toward and take up amyloid-beta and improved cognition, unlike APOE4. This is animal research and does not establish a treatment for people.
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51/100
Loss-of-function TREM2 mutations strongly increase Alzheimer's disease (AD) risk.
Why it matters
This study examined Trem2 deficiency in mice with tau alone or with both amyloid and tau pathology to see how TREM2 affects later Alzheimer's stages. It is animal work and does not establish a treatment, cure or prevention for people.
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Susceptibility-weighted imaging (SWI) evolved from simple two-dimensional T2*-weighted sequences to three-dimensional sequences with improved spatial resolution and enhanced susceptibility contrast.
Why it matters
This technical review describes an MRI method that is sensitive to substances such as calcium and iron and can show findings like microbleeds and iron deposition in dementia and other brain conditions. It is a description of an imaging technique, not a study of treating, curing, or preventing Alzheimer's disease.
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TREM2 is a pattern recognition receptor, expressed on microglia and myeloid cells, detecting lipids and Aβ and inducing an innate immune response.
Why it matters
Wild-type soluble TREM2 blocked Aβ aggregation and broke up preformed Aβ oligomers, while the Alzheimer's-linked R47H mutant increased Aβ aggregation. This is laboratory work on mechanisms and does not yet show a treatment, cure, or prevention for Alzheimer's disease in people.
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.
- Hepatic encephalopathy: An update of pathophysiologic mechanisms
- An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model
- Neurotransmitter-related enzymes and indices of hypoxia in senile dementia and other abiotrophies
- Obesity, diabetes, and leptin resistance promote tau pathology in a mouse model of disease
- Higher CSF sTREM2 attenuates ApoE4-related risk for cognitive decline and neurodegeneration
- Profile of MIF in Developing Hippocampus: Association With Cell Proliferation and Neurite Outgrowth
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders
- Induction of cytokines in glial cells surrounding cortical beta-amyloid plaques in transgenic Tg2576 mice with Alzheimer pathology
- Cellular Models of Aggregation-dependent Template-directed Proteolysis to Characterize Tau Aggregation Inhibitors for Treatment of Alzheimer Disease
- Reduction of brain beta-amyloid (Abeta) by fluvastatin, a hydroxymethylglutaryl-CoA reductase inhibitor, through increase in degradation of amyloid precursor protein C-terminal fragments (APP-CTFs) and Abeta clearance