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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Triggering receptor expressed on myeloid cells-2 (TREM2) is a transmembrane receptor of the immunoglobulin superfamily and a crucial signaling hub for multiple pathological pathways that mediate immunity.
Why it matters
This is a pan-cancer analysis of TREM2 across 33 cancer types, not a study of Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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Microglia are key in the homeostatic well-being of the brain and microglial dysfunction has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD).
Why it matters
This study describes the generation of microglia-like cells from human induced pluripotent stem cells with distinct phenotypes for mechanistic studies in Alzheimer's disease. It is a cell model development study and reports no treatment or clinical outcome.
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Overactivated microglia and neuroinflammation are considered to play a crucial role in the progression of Alzheimer's disease (AD).
Why it matters
In APP/PS1 transgenic mice, TREM2 overexpression rescued cognitive deficits by reducing neuroinflammation via the JAK/STAT/SOCS pathway. It is an animal study, so it does not yet show any treatment or prevention for Alzheimer's disease in people.
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Transcriptome-wide association studies (TWASs) have been widely used to integrate gene expression and genetic data for studying complex traits.
Why it matters
This paper describes a new statistical method for finding genes linked to traits and applies it to identify associations between expression of ZC3H12B and KCTD12 and Alzheimer-related measures. It is a methods and genetics study and does not test any treatment or prevention.
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A major challenge in neurobiology is the identification of the mechanisms by which protein misfolding leads to cellular toxicity.
Why it matters
In Down syndrome brain tissue and mice, a stress pathway called PERK was chronically activated and blocking it in mice helped some cell functions. This is early laboratory and animal work and does not establish a treatment for people.
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44/100
Alzheimer's Disease (AD) is a neurodegenerative disorder influenced by aging and genetic risk factors.
Why it matters
This study used mice bred to carry human APOE3 or APOE4 together with a Trem2 knockout to look at whether APOE and TREM2 interact in ways that affect Alzheimer's pathology. It is animal research only and reports no treatment, cure or prevention for people.
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In vitro binding assays demonstrated a high binding affinity of 18 F-SMBT-1 to MAO-B (dissociation constant, 3.7 nM).
Why it matters
This laboratory study describes a new PET tracer, 18F-SMBT-1, that binds selectively to MAO-B and may be useful for monitoring astrogliosis in the brain. It is early, mainly in-vitro and animal work, and does not test any treatment, cure or prevention for Alzheimer's disease.
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Delirium is a complex and multifactorial condition associated with long-term cognitive decline.
Why it matters
Comparing cerebrospinal fluid from 15 patients with infection-related delirium, 29 with Alzheimer's disease and other comparison groups, researchers found 8 inflammatory proteins raised and 23 proteins lowered in both delirium and Alzheimer's. These included CX3CL1 and CD200R1, markers of communication between neurons and microglia (the brain's immune cells), and proteins involved in synapses. The authors suggest synapse damage and loss of microglial control may be shared by both conditions, possibly linking infections, delirium and long-term cognitive decline.
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The present study examines functional contributions of microglia in host defense, demyelination, and remyelination following infection of susceptible mice with a neurotropic coronavirus.
Why it matters
In mice, depleting microglia before a brain infection increased death and weakened control of the virus. This is an animal study of viral brain infection, not Alzheimer's disease, so it does not show how to treat, cure or prevent Alzheimer's.
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Individuals with Down syndrome (DS) develop Alzheimer's disease (AD)-related neuropathology, characterized by amyloid plaques with amyloid β (Aβ) and neurofibrillary tangles with tau accumulation.
Why it matters
In this exploratory study, young adults with Down syndrome who did not yet have dementia (n = 15) had higher blood sTREM2 and inflammatory markers than age-matched controls (n = 16). In the Down syndrome group, sTREM2 correlated positively with 24 of the measured cytokines, while there were no significant correlations in controls. The authors present it as a preliminary basis for studying immune changes before dementia in Down syndrome.
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Differently from other myeloid cells, microglia derive exclusively from precursors originating within the yolk sac and migrate to the CNS under development, without any contribution from fetal liver or postnatal hematopoiesis.
Why it matters
This study compared microglia and peripheral macrophage profiles across lifespan and in neuroinflammation. It is a basic biology study and does not test any treatment, cure or prevention for Alzheimer's disease.
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44/100
Insulin resistance associates with increased risk for cognitive decline and dementia; however, the underpinning mechanisms for this increased risk remain to be fully defined.
Why it matters
In mice with high-fat diet-induced brain insulin resistance, mitochondrial ATP production and oxidative enzyme activities decreased, while oxidative stress increased. Improving insulin sensitivity with aerobic exercise and metformin restored brain mitochondrial function in these insulin-resistant states.
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44/100
Variants in the microglial receptor TREM2 confer risk for multiple neurodegenerative diseases.
Why it matters
Mice lacking TREM2 had fewer synapses across the cortex and hippocampus at one month of age, and the loss was not due to direct microglia-synapse interactions. This shows TREM2 is needed for normal brain development in mice, which is early biology rather than a treatment finding for Alzheimer's disease.
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44/100
It is not associated with the presence of the APOE -ε4 allele whereas possibly linked to aging, female sex, Hispanic ethnicity and some genetic variants of the chitinase-3-like 1 locus.
Why it matters
This review discusses a biomarker called YKL-40 that may reflect inflammation in neurodegenerative diseases including Alzheimer's disease. It suggests that patients with high levels might benefit from future trials of anti-inflammatory compounds, but no treatment is tested here.
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44/100
Imbalance in production and clearance of amyloid beta (Aβ) is the primary reason for its deposition in Alzheimer disease.
Why it matters
In microglia and neuronal cells, alborixin induced autophagy that cleared amyloid beta and reduced its toxicity, acting through the PI3K-AKT pathway and PTEN. This is laboratory cell work, and the authors describe alborixin only as a potential therapeutic lead, not a proven treatment, cure, or prevention.
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Tau filaments with distinct morphologies and/or isoform compositions underlie a large number of human neurodegenerative diseases.
Why it matters
This work describes the ordered assembly of tau protein and reports that tau filaments adopt one fold in Alzheimer's disease and a different fold in Pick's disease, establishing distinct conformers. It is basic structural research and does not report a treatment, cure, or prevention for Alzheimer's disease.
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Triggering receptor expressed on myeloid cells-2 (TREM2) is an innate immune receptor that promotes phagocytosis by myeloid cells such as microglia and macrophages.
Why it matters
This study used bone marrow chimeric mice to test whether TREM2 on brain microglia or on circulating macrophages is responsible for its helpful role after experimental stroke. It is animal research about stroke, not Alzheimer's disease, and reports no Alzheimer's treatment, cure or prevention.
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Alzheimer's disease (AD) is the leading cause of age-related dementia among the elderly population.
Why it matters
This review discusses how TREM2 in microglia relates to amyloid plaques and tau tangles in Alzheimer's disease. As a review, it summarizes existing research and does not itself show that any treatment prevents or cures Alzheimer's disease.
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44/100
The plasma reference graphical analysis appeared to be the optimal method of quantification for 18 F-RO-948, yielding strictly time-consistent values of distribution volume and distribution volume ratio at 90 min against the analyses at 120 and 200 min. The reference tissue graphical analysis and SUV ratio were cross-validated against plasma reference graphical analysis.
Why it matters
This study evaluated a PET radioligand, 18F-RO-948, for measuring tau in the brain, finding it reproducible and able to separate Alzheimer disease subjects from controls. It is about a brain imaging method for measuring tau, not about treating, curing or preventing Alzheimer's disease.
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Early-onset Alzheimer disease (AD)-like pathology in Down syndrome is commonly attributed to an increased dosage of the amyloid precursor protein (APP) gene.
Why it matters
In Down syndrome induced pluripotent stem cell-derived neurons, deleting the extra copy of the APP gene reduced beta-amyloid production and amyloid aggregates but did not affect several tau-related Alzheimer's disease phenotypes or increased apoptosis. This is a cell-based study showing APP's role in amyloid aspects but challenging the idea that APP levels alone cause tau changes or neuronal death.
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Glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2), a major modulator of glutamate homeostasis in astrocytes, is assessed in post-mortem human brain samples of frontal cortex area 8 in advanced stages of Alzheimer disease (AD) and terminal stages of dementia with Lewy bodies (DLB) in order to gain understanding of astrogliopathy in diseases manifested by dementia.
Why it matters
In postmortem frontal cortex, GLT1 protein levels were not altered in Alzheimer disease or dementia with Lewy bodies, while GFAP was increased in both and ALDH1L1 in Alzheimer disease. The study found only a non-significant decrease in GLT1-to-GFAP and GLT1-to-ALDH1L1 ratios and reports no treatment or prevention effect.
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Neuroinflammation and overactivated microglia underlies the pathogenesis of Parkinson's disease (PD).
Why it matters
This study discusses TREM2 as a way microglia may shift between inflammatory and protective states in Parkinson's disease. It concerns Parkinson's disease, not Alzheimer's disease treatment or prevention.
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Diabetic insulin resistance and pro-diabetic diet are reported to increase dementia risk through unknown mechanisms.
Why it matters
In mice fed a pro-diabetic diet, blood-brain barrier dysfunction and inflammation appeared before any cognitive decline or neurodegeneration. This is an animal study, so it cannot show that the same sequence happens in people or that any treatment prevents Alzheimer's disease.
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44/100
DNAX-activating protein of 12 kDa (DAP12) is a signaling adapter protein expressed in cells that participate in innate immune responses.
Why it matters
This work describes how the TREM2/DAP12 complex influences microglial inflammatory responses through the JNK signaling pathway, noting that TREM2 acts as a negative regulator while TREM1 amplifies immune responses. Loss-of-function mutations in either DAP12 or TREM2 cause Nasu-Hakola disease, linking these molecules to brain disorders, but the study does not test any treatment or prevention approach for Alzheimer's disease.
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With the publication in 2015 of the consensus statement by the perfusion study group of the International Society for Magnetic Resonance in Medicine (ISMRM) and the EU-COST action 'ASL in dementia' on the implementation of arterial spin labelling MRI (ASL) in a clinical setting, the development of ASL can be considered to have become mature and ready for clinical prime-time.
Why it matters
This review discusses technical developments in arterial spin labelling MRI for measuring perfusion and mapping flow territories, noting remaining challenges such as uncertainty in labelling efficiency and arterial transit time artefacts. It concerns imaging methods, not treating, curing, or preventing Alzheimer's disease.
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.
- Multi-View Separable Pyramid Network for AD Prediction at MCI Stage by 18F-FDG Brain PET Imaging
- Plasma long-chain omega-3 fatty acids and atrophy of the medial temporal lobe
- Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration
- Molecular Insights into α-Synuclein Fibrillation: A Raman Spectroscopy and Machine Learning Approach
- Structure of alpha-synuclein fibrils derived from human Lewy body dementia tissue
- Microglia in human immunodeficiency virus-associated neurodegeneration
- Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain
- Hereditary frontotemporal dementia is linked to chromosome 17q21-q22: a genetic and clinicopathological study of three Dutch families
- The potential for beta-structure in the repeat domain of tau protein determines aggregation, synaptic decay, neuronal loss, and coassembly with endogenous Tau in inducible mouse models of tauopathy
- Association of Chronic Kidney Disease With Plasma NfL and Other Biomarkers of Neurodegeneration: The H70 Birth Cohort Study in Gothenburg