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
Exercise-induced oxidative stress results from the overproduction of reactive oxygen and nitrogen species (ROS/RNS) during intense physical activity, potentially impairing muscle function and recovery.
Why it matters
This review discusses how phenolic compounds may protect against exercise-induced oxidative stress but also warns that excessive antioxidant supplementation may interfere with beneficial exercise adaptations. It does not study Alzheimer's disease.
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Plasma phosphorylated Tau217 (pTau217) demonstrated the highest diagnostic accuracy for AD, DLB, and FTD (area under the curve [AUCs]: 0.9, 0.84, and 0.79, respectively).
Why it matters
This study found that plasma phosphorylated Tau217 demonstrated the highest diagnostic accuracy for Alzheimer's disease, dementia with Lewy bodies, and frontotemporal dementia. It also identified new plasma biomarkers that are expressed differently in these dementias, providing a noninvasive method for differential diagnosis.
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Thirty-two patients met the inclusion criteria (n=11 moderate-to-severe SVD, mean age 72 ± 10 years, 6 women; n = 21 none-to-minimal SVD, mean age 70 ± 10 years, 12 women).
Why it matters
This study found that a new blood flow measurement on MRI was strongly linked to markers of small vessel disease in the brain in a small group of 32 patients. It is an imaging study in a small sample and does not test any treatment, cure, or prevention for Alzheimer's disease.
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The glymphatic system, a vital brain perivascular network for waste clearance, hinges on the functionality of the aquaporin 4 (AQP4) water channel.
Why it matters
This narrative review discusses how glymphatic dysfunction and sleep disorders may contribute to cerebral small vessel disease by hindering waste removal and compromising blood-brain barrier integrity, and it suggests lifestyle modifications and personalized medicine as possible treatment avenues. These are proposed directions requiring further study, not established treatments, cures, or prevention for Alzheimer's disease.
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Our results elucidate the characteristics and genetic associations of p‐tau217 in a population‐based setting.
Why it matters
In this population-based twin sample of people without a clinical Alzheimer's diagnosis, higher plasma p-tau217 and likely Alzheimer's neuropathologic change were associated with older age and having an APOE ε4 allele, and heritability was estimated at 0.56. This describes a blood biomarker and its genetic associations in people without symptoms, not a treatment or cure.
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(cobalamin)-dependent pathways. Supplementation of B vitamins has been shown to effectively reduce plasma homocysteine levels.
Why it matters
This review is about B vitamin supplementation, homocysteine and thrombotic risk and contains no information on Alzheimer's disease. It reports no findings relevant to treating, curing or preventing dementia.
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The median PPA and NPA were 83.4% and 88.9%, respectively, with lower bounds of 2-sided 95% CIs being 50% or greater for all readers.
Why it matters
This study validated a method where readers visually assess 18F-Flortaucipir PET scans to stratify Alzheimer's disease, finding almost perfect agreement between and within readers. The authors say the method may support staging and prognosis, and that future work could examine treatment response among visually stratified participants in disease-modifying therapy trials.
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47/100
Total serum TDP-43 levels increased by 16.5% (95% CI: 5.9%-27.9%, p = 0.0021) on postoperative day one compared to baseline levels.
Why it matters
In patients having major cardiac surgery, total serum TDP-43 levels rose after the operation, and the rise was larger in those who developed postoperative delirium. The authors suggest TDP-43 may serve as a prognostic biomarker for acute neurological injury and blood-brain barrier integrity after cardiac surgery.
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In bvFTD patients, longer interoceptive-ACWs than controls were observed in the bilateral fronto-temporal and parietal regions.
Why it matters
Findings suggest a core allostatic-interoceptive deficit occurs in people with behavioral-variant frontotemporal dementia, with altered interoceptive intrinsic neural timescales potentially underpinning complex behaviors. Structural neural correlates involved the anterior cingulate, insula, orbitofrontal cortex, hippocampus, and angular gyrus.
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This raises the suggestion that a decreased neurovascular coupling in the disease process of AD is related to comorbid small vessel disease.
Why it matters
In 119 people with cognitive complaints or dementia, weaker neurovascular coupling was linked to more white matter hyperintensities and lobar brain bleeds. This supports the idea that small vessel disease may be involved in Alzheimer's disease, but it is an observational study and does not show that treating this coupling changes outcomes.
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There are many reports about the comorbidity of NPH and other neurodegenerative diseases1–3; the primary findings in neuropathological studies of patients with NPH include amyloid plaques and hyperphosphorylated tau protein inclusions.2,4 This suggests that proteinopathy may be one of the potential causes of NPH.
Why it matters
This is a single autopsy case report of one person who had normal pressure hydrocephalus along with several misfolded proteins found in the brain. It cannot show that protein buildup causes normal pressure hydrocephalus or change how the condition is treated.
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Plasma from individuals with a higher WMH burden was associated with increased BBB disruption in hBMEC.
Why it matters
This study found that plasma from people with more white matter hyperintensities caused more blood-brain barrier disruption in cells, and that higher blood pressure, body mass index, blood glucose and lipid levels were linked to greater disruption. It suggests chronic vascular risk factors may impair the blood-brain barrier and contribute to white matter damage and cognitive decline in small vessel disease.
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Synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, are characterized by the aggregation of α-synuclein.
Why it matters
This review summarizes progress on PET tracers for alpha-synuclein, noting that most are still in pre-clinical stages and that distinguishing synucleinopathies from tauopathies remains difficult. It concerns imaging tools for diagnosis and drug development, not a treatment, cure, or prevention.
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Postoperative delirium (POD) is often under-recognized in clinical practice.
Why it matters
This multicohort study found that preoperative blood NfL and GFAP levels were higher in older hip fracture surgery patients who developed postoperative delirium, and higher levels independently predicted it after adjustment. CSF NfL was also elevated in delirium, but no significant difference was seen for CSF GFAP, and the authors note further research is needed.
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Hyperhomocysteinemia (HHcy) is an established risk factor for cognitive impairment.
Why it matters
In this cross-sectional study of 507 patients, plasma homocysteine levels showed no significant association with cerebrospinal fluid biomarkers of Alzheimer's disease. Higher homocysteine was instead linked to more severe white matter lesions, which the authors say challenges the link between homocysteine and Alzheimer's disease pathophysiology while highlighting a connection to microvascular cognitive impairment.
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Plasma p-tau-181 and GFAP are closely associated with synaptic density measured using 18 F-SynVesT-1 PET/MRI, with the relationship primarily influenced by tau accumulation rather than Aβ deposition or cortical thickness. © RSNA, 2024 Supplemental material is available for this article.
Why it matters
Among 120 participants, higher plasma p-tau-181 and GFAP were associated with lower synaptic density on PET imaging, with the relationship mainly influenced by tau accumulation rather than amyloid deposition or cortical thickness. This is about biomarkers and brain imaging, not a treatment or cure.
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The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor that affects cellular phenotypes by modulating phagocytosis and metabolism, promoting cell survival, and counteracting inflammation.
Why it matters
This study is about kidney injury, not Alzheimer's disease, and found that TREM2 deficiency worsened renal injury in mice by promoting macrophage apoptosis and polarization. It reports no Alzheimer's treatment, cure or prevention.
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47/100
Trem2 (triggering receptor on myeloid cells 2), a surface lipid receptor, is expressed on foamy macrophages within atherosclerotic lesions and regulates cell survival, proliferation, and anti-inflammatory responses.
Why it matters
This mouse study tested a Trem2 agonist antibody (AL002a) in atherosclerosis-prone mice to see whether it would improve plaque stability. It concerns atherosclerosis in mice and does not report any treatment, cure, or prevention for Alzheimer's disease.
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Parkinson's disease (PD) is a complex syndrome for which there is no disease-modifying treatment on the market.
Why it matters
GLP-1 class drugs such as exendin-4, liraglutide and lixisenatide, already on the market for diabetes, showed clear effects in improving motor activity in Parkinson's patients in phase II trials. Liraglutide also showed improvement in cognition and brain shrinkage in a phase II trial in patients with Alzheimer's disease.
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Metabolic dysfunction-associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (NASH), is an advanced stage of metabolic fatty liver disease.
Why it matters
This study identifies MS4A7 as a driver by which TREM2+ macrophages contribute to metabolic dysfunction-associated steatohepatitis. It is about liver disease and not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Recent genetic studies on Alzheimer's disease (AD) have brought microglia under the spotlight, as loci associated with AD risk are enriched in genes expressed in microglia.
Why it matters
This review discusses SHIP1, encoded by the Alzheimer's disease-associated gene INPP5D, as a regulator of microglial phagocytosis and immune response, and its connection to the NLRP3 inflammasome in human iPSC-derived microglial cells. It is a review of microglial signalling and does not report a tested treatment, cure, or prevention for Alzheimer's disease.
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Vascular mechanisms of Alzheimer's disease (AD) may constitute a therapeutically addressable biological pathway underlying dementia.
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Lecanemab cleared amyloid-β in two-thirds and reduced the rate of cognitive and functional worsening in people with mild cognitive impairment and mild dementia due to Alzheimer disease in an 18-month double-blinded randomized placebo-controlled trial reported by van Dyck et al.
Why it matters
In an 18-month double-blinded randomized placebo-controlled trial, lecanemab cleared amyloid-β in two-thirds of people with mild cognitive impairment and mild dementia due to Alzheimer disease and reduced the rate of cognitive and functional worsening. This indicates the drug can affect both a brain marker of the disease and the pace of symptom decline in these patients.
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47/100
Nearly a dozen monoclonal antibodies (mAbs) directed against beta-amyloid (Aβ) have been developed for the treatment of Alzheimer disease (AD), and most of these mAbs are undergoing clinical trials.
Why it matters
This review describes lecanemab, an anti-beta-amyloid monoclonal antibody with high affinity for large soluble Aβ protofibrils, and notes that phase 2 data suggested a possible efficacy signal with manageable risk of amyloid-related imaging abnormalities. At the time of writing it was still being studied in phase 3 trials, so no cure or confirmed clinical benefit is established.
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Age-associated microglial dysfunction contributes to the accumulation of amyloid-β (Aβ) plaques in Alzheimer's disease.
Why it matters
Naturally aged microglia in mice phagocytosed less Aβ over time, with gene expression changes resembling those seen in neurologic disease. This describes an age-related change in microglial function but does not test any treatment, cure, or prevention 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.
- CRISPR/Cas13a-Powered Electrochemical Microfluidic Biosensor for Nucleic Acid Amplification-Free miRNA Diagnostics
- Patients with amyotrophic lateral sclerosis and other neurodegenerative diseases have increased levels of neurofilament protein in CSF
- Bezafibrate treatment rescues neurodevelopmental and neurodegenerative defects in 3D cortical organoid model of MAPT frontotemporal dementia
- Neuropathology of variants of progressive supranuclear palsy
- FUS Phase Separation Is Modulated by a Molecular Chaperone and Methylation of Arginine Cation-π Interactions
- Microglial activation states drive glucose uptake and FDG-PET alterations in neurodegenerative diseases
- In vivo imaging of microglial activation with [11C](R)-PK11195 PET in idiopathic Parkinson's disease
- Progranulin AAV gene therapy for frontotemporal dementia: translational studies and phase 1/2 trial interim results
- Association of white matter hyperintensity volume with decreased cognitive functioning: the Framingham Heart Study
- Effects of aspirin plus extended-release dipyridamole versus clopidogrel and telmisartan on disability and cognitive function after recurrent stroke in patients with ischaemic stroke in the Prevention Regimen for Effectively Avoiding Second Strokes (PRoFESS) trial: a double-blind, active and placebo-controlled study