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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In SPRINT, the overall interaction between age and SBP on WMHv change was not statistically significant ( P =0.18).
Why it matters
In two large trials, intensive blood pressure control reduced the progression of white matter hyperintensities more in younger participants than in older ones. The overall interaction between age and blood pressure was not statistically significant in SPRINT, so the age-related difference is not definitive.
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Both the Keto and ADF groups demonstrated significant weight loss, but cognitive performance improved most notably in the ADF group, in association with reduced inflammation.
Why it matters
In this study, alternate-day fasting improved cognitive performance most notably and was linked to reduced inflammation, and mouse experiments showed the cognitive benefits depended on gut microbiota and enhanced microglial function. The authors state that further studies are required to fully explain the mechanisms, so this is not yet a proven treatment for Alzheimer's.
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• Low ALPS index was significantly associated with high risk of MCI, and the risk of MCI decreased linearly with a higher ALPS index • High ALPS index was dose-dependently associated with a decreased progression from MCI to AD • High ALPS index may delay the MCI onset approximately 3.8 years among CN participants and delay MCI progression to AD by approximately 3.5 years in MCI group • Aβ in choroid plexus, tau in part of the cortex and executive function were partially mediate ALPS-AD association We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors.
Why it matters
In 519 participants, a higher ALPS index was associated with lower risk of mild cognitive impairment and slower progression to Alzheimer's disease, with estimated delays of about 3.8 and 3.5 years. This is an observational association and does not establish a treatment, cure or prevention.
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In linear mixed models, vascular endothelial growth factor was significantly associated with incident DWI-positive lesions over 1 year.
Why it matters
In a longitudinal neuroimaging study, certain blood biomarkers of vascular dysfunction were linked to small vessel disease progression, and platelet-selectin levels were associated with mild cognitive impairment at one year. These findings could help stratify patients at high risk of rapid-progression small vessel disease, but they are not a treatment or cure.
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APOE ε4) was associated with a greater severity of each of Braak NFT stage [odds ratio (OR) = 3.07, P = 2.34 × 10-32], Thal amyloid phase (OR = 3.57, P = 3.28 × 10-29) and LBD subtype (OR = 1.78, P = 9.85 × 10-9), with similar findings observed in the independent replication series (Braak NFT stage, OR = 2.30, P = 2.70 × 10-11; Thal amyloid phase, OR = 3.17, P = 6.39 × 10-18; LBD subtype, OR = 2.68, P = 3.85 × 10-10).
Why it matters
This genome-wide association study found that the APOE ε4 allele was the most prominent genetic determinant of severity of neuropathology in Lewy body disease, while other associations were not confirmed in the replication series. It does not test any treatment or prevention, so it mainly adds to understanding of genetic drivers rather than offering a cure.
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The final model, which included age, systolic blood pressure >140, atrial fibrillation, and tobacco use, achieved an AUC of 0.83 (95% CI 0.75-0.90) in the development cohort (N=143, 62.4±12.6 years, 44% female, 36% non-white race) and 0.85 (95% CI 0.77-0.92) in the validation cohort (N=127, 65.2±16.8 years, 51% female, 34% non-white race), with similar results using WMH measurements derived from cMRI (N=120, p=0.98, AUC=0.86, 95% CI 0.77-0.93).
Why it matters
A risk score using age, high systolic blood pressure, atrial fibrillation and tobacco use predicted significant white matter hyperintensity burden with good accuracy, and portable MRI measurements agreed with conventional MRI. This could support screening to manage vascular risk factors, but it does not show that screening prevents dementia.
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53/100
Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women).
Why it matters
A higher baseline DTI-ALPS index was linked to better processing speed and cognitive index over time, but perivascular space burden, DTI-ALPS index and PSMD were not linked to risk of all-cause dementia. These markers may help track cognitive decline but showed limited link to dementia risk, and no treatment was tested.
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We studied the promising Alzheimer biomarker plasma tau phosphorylated at threonine 231 (p-tau231) in a cohort of cardiac arrest patients who survived to intensive care to predict long-term neurological outcomes.
Why it matters
This study examined plasma p-tau231 and total tau as predictors of long-term neurological outcome in patients who survived cardiac arrest. It is about prognosis after cardiac arrest, not about treating, curing, or preventing Alzheimer's disease.
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These findings suggest significant binding of lecanemab to cerebral amyloid angiopathy in DS.
Why it matters
In postmortem brain tissue from 15 people with Down syndrome, the Alzheimer's drug lecanemab bound to amyloid plaques but also bound extensively to brain blood vessels, which raises safety concerns. The authors say clinical trials are needed to evaluate whether lecanemab is safe in people with Down syndrome.
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Higher levels of neuroinflammation, neurodegeneration, and synaptic dysfunction in older adults were attenuated in KL-VS HET .
Why it matters
In 454 cognitively unimpaired older adults, carrying the KLOTHO KL-VS variant was linked to less age-related change in cerebrospinal fluid markers of neuroinflammation, neurodegeneration, and synaptic dysfunction. This is an observational finding about a possible resilience factor, not a treatment or prevention.
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Single-cell RNA sequencing data generated with SmartSeq2 (≈8000 genes/cell) in 16 588 single cells isolated during atherosclerosis progression in Ldlr -/- Apob 100/100 mice with human-like plasma lipoproteins and from humans with asymptomatic and symptomatic carotid plaques was clustered into multiple subtypes.
Why it matters
This study is about atherosclerosis, not Alzheimer's disease, and used single-cell RNA sequencing to map gene-regulatory networks in mice and human plaques. It reports no Alzheimer's treatment, cure or prevention.
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The results of this proof-of-principle study will be used to assess the potential of target engagement of minocycline for CAA.
Why it matters
This paper describes the plan for the BATMAN trial, which will give minocycline, an antibiotic known to affect inflammation, or a placebo for 3 months to 60 people with hereditary or sporadic cerebral amyloid angiopathy, where amyloid builds up in brain blood vessels. The main goal is to see whether the drug lowers inflammation markers in spinal fluid. It is a design paper, so no results are reported in this record.
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TREM2 is an innate immune receptor expressed by microglia in the adult brain.
Why it matters
Microglia made from patient cells carrying a TREM2 loss-of-function mutation showed defects in lysosomal function and lipid metabolism. This is laboratory cell work on a rare genetic disease and does not show that any treatment prevents or cures Alzheimer's disease.
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Macrophages are central orchestrators of the tissue response to injury, with distinct macrophage activation states playing key roles in fibrosis progression and resolution.
Why it matters
This study identified a macrophage subset in human liver and lung fibrosis, not Alzheimer's disease. It does not test any Alzheimer's treatment, cure, or prevention.
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Obesity-induced chronic liver inflammation is a hallmark of nonalcoholic steatohepatitis (NASH)-an aggressive form of nonalcoholic fatty liver disease.
Why it matters
This study is about nonalcoholic steatohepatitis, showing that prolonged overnutrition caused TREM2 shedding and impaired clearance of dying liver cells, sustaining liver inflammation. It does not concern Alzheimer's disease and reports no treatment for it.
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53/100
In addition to tau and Aβ pathologies, inflammation plays an important role in Alzheimer's disease (AD).
Why it matters
In P301S tau mice, this study found that TREM2-independent microgliosis promotes tau-mediated neurodegeneration in the presence of ApoE4. It is an animal study and does not establish any treatment, cure or prevention for Alzheimer's disease.
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Cribriform prostate cancer, found in both invasive cribriform carcinoma (ICC) and intraductal carcinoma (IDC), is an aggressive histological subtype that is associated with progression to lethal disease.
Why it matters
This study is about cribriform prostate cancer and its tumor microenvironment, not Alzheimer's disease. It has no implications for treating, curing or preventing Alzheimer's disease.
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53/100
TREM2 is exclusively expressed by microglia in the brain and is strongly linked to the risk for Alzheimer's disease (AD).
Why it matters
In mice engineered to overexpress TREM2, the normal form reduced amyloid deposition and nerve damage only during the early stage of amyloid seeding, while the R47H risk variant did not. This suggests that boosting TREM2 may only help if given very early, and these are animal findings not yet shown in people.
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Acne affects 1 in 10 people globally, often resulting in disfigurement.
Why it matters
This study found TREM2 macrophages with lipid metabolism and proinflammatory gene programs in acne lesions, a skin disease unrelated to Alzheimer's. It provides no information about treating, curing or preventing Alzheimer's disease.
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These findings suggest that the loss of perivascular AQP4 localization may contribute to the development of AD pathology in human populations.
Why it matters
In human post mortem tissue and in mice, loss of perivascular aquaporin-4 localization was associated with impaired glymphatic exchange and promoted amyloid beta plaque formation. These findings suggest a possible contributor to Alzheimer's disease development, but they are from animal and post mortem studies and do not establish a treatment, cure, or prevention.
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In humans, aging, triggers increased plasma concentrations of triglycerides, cholesterol, low-density lipoproteins and lower capacity of high-density lipoproteins to remove cellular cholesterol.
Why it matters
This study describes how aging alters cholesterol metabolism in the liver and nervous system, drawing on rodent studies and suggesting a link between late-onset Alzheimer's disease and metabolic syndrome. Much of the evidence comes from animals, so it is preliminary and cannot show that changing cholesterol metabolism would treat or prevent Alzheimer's disease in people.
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In neurodegenerative diseases, extracellular vesicles (EVs) transfer pathogenic molecules and are consequently involved in disease progression.
Why it matters
This study identified cell type-specific extracellular vesicle protein markers and found that a protein module enriched in astrocyte-specific markers was most significantly associated with Alzheimer's disease pathology and cognitive impairment. The hub protein integrin-β1 was elevated in astrocyte-specific vesicles and associated with brain β-amyloid and tau load, suggesting a role in disease progression rather than a treatment.
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53/100
The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 ( TREM2 ), a microglia-specific gene in the brain, increases risk for late-onset Alzheimer’s disease (AD).
Why it matters
In brain tissue from people with Alzheimer's and in mice, the R47H TREM2 variant was linked to more inflammatory microglia and, in female mice, worse tau-related memory problems. This is early research combining human tissue analysis and animal models, not a treatment.
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Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood.
Why it matters
This study analyzed brain tissue from deceased donors and found that complement pathway genes C4A and C4B were among the most differently expressed genes in people with the protective APOE ε2 variant. It is early, laboratory-based work and does not show that targeting these genes would treat or prevent Alzheimer's disease.
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GRN mutations cause frontotemporal dementia (GRN-FTD) due to deficiency in progranulin (PGRN), a lysosomal and secreted protein with unclear function.
Why it matters
In Grn -/- mice, loss of progranulin caused a deficiency in BMP and storage of glucosylsphingosine, and a protein replacement strategy was investigated. This is animal research on frontotemporal dementia, not a treatment or cure for 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.
- Combination of Intranasal insulin and oral semaglutide for cognition in older adults with metabolic syndrome at high dementia risk
- Human carbonyl reductase (CBR) localized to band 21q22.1 by high-resolution fluorescence in situ hybridization displays gene dosage effects in trisomy 21 cells
- Reducing Neuroinflammation and Risk of Mild Cognitive Impairment and Alzheimer’s Disease by Reducing Dietary Lipopolysaccharides, Arachidonic Acid, and Advanced Glycation End Products
- Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration
- The Neutrophil to Lymphocyte Ratio Is Associated With the Risk of Subsequent Dementia in the Framingham Heart Study
- Identification of pure subcortical vascular dementia using 11C-Pittsburgh compound B
- Multipotent Mesenchymal Stem Cell Therapy for Vascular Dementia
- Gut Microbiome–Sphingolipid Metabolism–Brain Axis Interactions: Neuroprotective Effects of Amitriptyline as Functional Inhibitor of Acid Sphingomyelinase in a Mouse Model of Tauopathy
- Microglia in neurodegenerative disease
- Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases