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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Chimeric antigen receptor (CAR) -T cell therapy is an efficient therapeutic strategy for specific hematologic malignancies.
Why it matters
This study is about CAR-T cell therapy for colorectal cancer, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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The mechanisms underlying how urban air pollution affects Alzheimer's disease (AD) are largely unknown.
Why it matters
In this study, ozone exposure impaired microglia's ability to form a protective barrier around Aβ plaques, leading to more damaged neurites and increased plaque load. This suggests that air pollution may worsen Alzheimer's pathology through effects on the immune system, but it does not show a treatment or cure.
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48/100
Sepsis-induced cardiomyopathy (SICM) is common in septic patients with a high mortality and is characterized by an abnormal immune response.
Why it matters
This study is about sepsis-induced cardiomyopathy and identifies a cardiac-resident macrophage subpopulation in a mouse model of sepsis, not Alzheimer's disease, so it provides no direct information about treating, curing or preventing Alzheimer's. Its findings come from single-cell RNA sequencing and fate mapping in mice.
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Neuroinflammation is one of the most important processes in secondary injury after traumatic brain injury (TBI).
Why it matters
In a mouse model of traumatic brain injury, the TREM2 agonist COG1410 alleviated neural damage via Akt/CREB/BDNF signalling. This is animal work in brain injury and does not show a treatment for Alzheimer's disease.
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The p-tau181/Aβ 1-42 ratio showed the best prediction of Aβ-PET across all participants (area under the curve [AUC] = 0.905, 95% confidence interval [CI]: 0.86-0.95) and in CN (AUC = 0.873; 0.80-0.94), and symptomatic (AUC = 0.908; 0.82-1.00) adults.
Why it matters
The plasma p-tau181/Aβ1-42 ratio predicted amyloid PET status and correlated with the same ratio in cerebrospinal fluid and with future cognitive decline. This is a biomarker study and does not show that any treatment based on this ratio can prevent or cure Alzheimer's disease.
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Variants in the microglial immune receptor TREM2 are associated with enhanced risk of onset in sporadic Alzheimer's disease (AD).
Why it matters
In mice, deleting Trem2 increased the spread of tau and tau pathology through microglia exosomes. This is animal work identifying a mechanism, not a proven treatment for people.
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The pathological hallmark of neurodegenerative diseases is the formation of toxic oligomers by proteins such as alpha-synuclein (aSyn) or microtubule-associated protein tau (Tau).
Why it matters
Using digital single particle counting, this study found that alpha-synuclein aggregate concentration discriminated Parkinson's disease and dementia with Lewy bodies patients from normal controls, while tau aggregates were significantly elevated in progressive supranuclear palsy patients compared to all other groups. The findings suggest this method can differentiate neurodegenerative disease diagnostic groups and may improve pre-clinical and clinical applications.
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Cholesterol loaded macrophage foam cells are a prominent feature of atherosclerotic plaques.
Why it matters
This study describes how cholesterol-loaded macrophage foam cells resemble TREM2-positive microglia seen in neurodegenerative diseases, and tests whether liver X receptors mediate anti-inflammatory effects in these cells. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Spatial transcriptomics enables the simultaneous measurement of morphological features and transcriptional profiles of the same cells or regions in tissues.
Why it matters
This paper presents MUSE, a computational method for integrating spatial transcriptomics and imaging data. It is a tool for studying tissues and does not test any treatment, cure or prevention for Alzheimer's disease.
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Recently, attention has been focused on the central role of TREM2 in diverse pathologies.
Why it matters
This analysis of human hepatocellular carcinoma tissues found TREM2 expressed mainly by a macrophage subpopulation resembling lipid-associated macrophages. It is about liver cancer and not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Our trial showed that olfactory-stimulated oxygenation differences in the orbitofrontal cortex detected by fNIRS were associated with cognitive impairment and cognitive-related objectives.
Why it matters
In this single-group trial of 97 people, a measure of brain oxygenation during smelling was linked to cognitive impairment and cognitive test scores. The study was small and open-label, and it only tests a possible diagnostic tool, not any treatment, cure, or prevention.
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Clinical symptoms correlate with underlying neurodegenerative changes in the vast majority of people.
Why it matters
Using spatial protein profiling in hippocampal tissue from 14 individuals, 11 proteins differed in tangle-bearing neurons between resilient and demented people. This is a small tissue study of protein expression patterns and does not test a treatment, cure or prevention.
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18 F-SMBT-1 showed robust entry into the brain and reversible binding kinetics, with high tracer retention in basal ganglia, intermediate retention in cortical regions, and the lowest retention in cerebellum and white matter, which tightly follows the known regional brain distribution of MAO-B ( R 2 = 0.84).
Why it matters
This first-in-humans study found that the PET tracer 18F-SMBT-1 binds selectively to MAO-B in the brain and may serve as a marker of reactive astrogliosis. The authors state that further validation in a much larger series is needed, and it does not test any treatment, cure or prevention.
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48/100
This study failed to find associations of circulating NfL and PGRN levels with frailty among community-dwelling older adults in adjusted analyses.
Why it matters
High plasma NfL was linked to pre-frailty or frailty at baseline, but this association did not remain significant in further analysis. This is about physical frailty in older adults and does not show any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is the most common cause of dementia, yet there is no cure or diagnostics available prior to the onset of clinical symptoms.
Why it matters
This work analyzes extracellular vesicles from human Alzheimer's brain tissue and notes that microglial vesicles may help spread proteins such as tau and amyloid-beta. It is exploratory and does not demonstrate a treatment, cure, or prevention.
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Skin allo- and xenotransplantation are the standard treatment for major burns when donor sites for autografts are not available.
Why it matters
This study examined collagen deposition and activated Trem2-positive macrophages after xenogeneic skin transplantation. It concerns skin grafting and wound healing, not Alzheimer's disease, and provides no information on treating, curing or preventing Alzheimer's disease.
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Perivascular spaces (PVS) are fluid-filled compartments that are part of the cerebral blood vessel wall and represent the conduit for fluid transport in and out of the brain.
Why it matters
This review describes enlarged perivascular spaces as a marker of small vessel disease that is more common in Alzheimer's disease and may relate to cognition. Understanding these spaces could matter for developing prevention and treatment strategies, but the review itself reports no tested treatment.
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Primary dysfunction of autophagy due to Mendelian defects affecting core components of the autophagy machinery or closely related proteins have recently emerged as an important cause of genetic disease.
Why it matters
This review describes disorders caused by defective autophagy, which can include early-onset neurodevelopmental and adult-onset neurodegenerative conditions. It does not report any treatment, cure, or prevention for Alzheimer's disease.
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Emerging evidence indicates that impaired mitophagy-mediated clearance of defective mitochondria is a critical event in Alzheimer's disease (AD) pathogenesis.
Why it matters
This work examined how cholesterol changes affect the removal of damaged mitochondria by autophagy in Alzheimer's disease. It describes a mechanism and does not report a treatment, cure or prevention for the disease.
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Autophagy induction by crocetin significantly increased Aβ clearance in N9 cells.
Why it matters
In cells and in a mouse model of Alzheimer disease, crocetin reduced amyloid-beta levels, reduced neuroinflammation and improved memory by inducing autophagy. These are early laboratory and animal findings, and the authors say further development of crocetin is supported, not that it is a proven treatment for people.
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Loss of physiological microglial function may increase the propagation of neurodegenerative diseases.
Why it matters
An age-associated increase in dystrophic microglia was found in the hippocampus and frontal cortex, but the increase was proportional to the age-related increase in total microglia. This is a human brain tissue study of microglial morphology and does not report a treatment, cure, or prevention.
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Parkinson's disease dementia is neuropathologically characterized by aggregates of α-synuclein (Lewy bodies) in limbic and neocortical areas of the brain with additional involvement of Alzheimer's disease-type pathology.
Why it matters
This post-mortem study found increased α-synuclein pathology and activated microglia in Parkinson's disease dementia compared with Parkinson's disease without dementia. It is about neuroinflammation and protein pathology in Parkinson's disease dementia, not about treating or curing Alzheimer's disease.
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Amyloid-β (Aβ) deposits are a relatively late consequence of Aβ aggregation in Alzheimer's disease.
Why it matters
In transgenic mice, at least one antibody (aducanumab) given acutely before amyloid deposits were detectable reduced Alzheimer-like pathology later in life. This is animal research, so it does not yet show whether targeting pre-amyloid seeds early works in people.
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Triggering receptor expressed on myeloid cells 2 (TREM2) has been shown with a neuroprotective function against inflammation and neuronal injury in Alzheimer's disease (AD).
Why it matters
In Alzheimer's disease mice, removing TREM2 increased pro-inflammatory cytokines and worsened cognitive defects, while TREM2 appears to act through the PI3K/AKT/FoxO3a pathway. This is animal research only and does not show that targeting TREM2 would treat or prevent Alzheimer's disease in people.
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The intramembrane protease γ-secretase is a hetero-tetrameric protein complex with presenilin as the catalytic subunit and cleaves its membrane protein substrates within their single transmembrane domains. γ-Secretase is well known for its role in Notch signalling and in Alzheimer's disease, where it catalyzes the formation of the pathogenic amyloid β (Aβ) peptide.
Why it matters
This review lists the many proteins that the enzyme gamma-secretase cuts, including the one that produces amyloid-beta, and notes that long-term blocking of this enzyme may cause side effects. It does not report a treatment, cure or prevention for Alzheimer's.
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.
- Restoration neurite growth by removing the blockage of endosome trafficking in Alzheimer-like mice
- A light and electron microscopic study of experimental portal-systemic (ammonia) encephalopathy. Progression and reversal of the disorder
- Inhibition of calcineurin-mediated endocytosis and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors prevents amyloid beta oligomer-induced synaptic disruption
- Association of DISC1/TRAX haplotypes with schizophrenia, reduced prefrontal gray matter, and impaired short- and long-term memory
- Integrative Brain Transcriptome Analysis Links Complement Component 4 andHSPA2to theAPOEε2 Protective Effect in Alzheimer Disease
- APOE, MAPT, and SNCA genes and cognitive performance in Parkinson disease
- Microglial TREM2/DAP12 Signaling: A Double-Edged Sword in Neural Diseases
- Cinnamon Bud Extract Is a Source of Biomolecules Active against the Aggregation and Condensation of Alzheimer′s-Associated Tau Protein
- Obesity is linked with lower brain volume in 700 AD and MCI patients
- Regulated intramembrane proteolysis of the interleukin-1 receptor II by alpha-, beta-, and gamma-secretase