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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Symptomatic GRN carriers showed elevated WMHs, primarily in the frontal lobe, while no significant increase was observed in symptomatic C9orf72 or MAPT carriers.
Why it matters
This study found that white matter hyperintensities are elevated in symptomatic GRN frontotemporal dementia carriers, primarily in the frontal lobe, and precede other biomarkers like NfL elevation and atrophy. It suggests WMHs as early markers for progression models but no treatment or cure.
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The primary outcome of this clinical trial is the change in the Vascular Dementia Assessment Scale-cognitive subscale from baseline to 12 months.
Why it matters
This is a protocol for a randomized, double-blind, placebo-controlled trial testing Tongxinluo capsule in cerebral small vessel disease, with the primary outcome being change in a vascular dementia cognitive scale at 12 months. No results are available yet, so it cannot yet show whether this traditional Chinese medicine affects cognitive decline.
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48/100
Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are subtypes of Lewy body dementia, and are considered two ends of a disease spectrum.
Why it matters
Using quantitative susceptibility mapping, this study found higher values in widespread brain regions in people with Lewy body dementia compared with cognitively normal people with Parkinson's disease, and higher values in Parkinson's disease dementia than in dementia with Lewy bodies. The authors suggest understanding these differences could enable targeted subtype-specific treatments, but no treatment, cure or prevention is tested.
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Plasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations.
Why it matters
Measuring plasma pTau217 in people with Parkinson's disease, Lewy body dementia, and 4-repeat tauopathies, levels were lower in cognitively normal Parkinson's and control individuals than in those with greater cognitive impairment. The study examines a blood biomarker for detecting amyloid and tau pathology, not a treatment.
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Cerebral small vessel disease (cSVD) is characterised by white matter hyperintensities (WMH) and contributes to stroke and dementia.
Why it matters
In this cross-sectional study of 60 participants, retinal arteriole/venule ratio was inversely related to white matter hyperintensity severity and directly related to cerebrovascular reactivity, suggesting loss of normal arteriovenous coordination in small vessel disease. This is an observational imaging finding and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Polygenic risk scores (PRSs) predict an individual's genetic risk for complex diseases, yet their utility in elucidating disease biology remains limited.
Why it matters
The paper introduces scPRS, a graph neural network framework that computes single-cell-resolved polygenic risk scores and outperformed traditional PRS approaches, including for Alzheimer's disease. It is a methodological tool for genetic risk prediction and mechanistic study, not a treatment, cure, or prevention.
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Parkinson's disease (PD), a complex neurodegenerative disorder characterized by selective loss of substantia nigra (SN) dopaminergic neurons, pathological aggregation of α-synuclein (α-syn), and chronic neuroinflammation, is fundamentally driven by redox imbalance and oxidative stress.
Why it matters
This review discusses cell death pathways, oxidative stress and therapeutic innovations in Parkinson's disease. It is about Parkinson's disease, not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Alzheimer’s disease (AD), the leading cause of senile dementia, lacks effective therapies.
Why it matters
In a mouse model of amyloidosis, blocking microglial connexin43 hemichannels, either by genetic knockout or with a nanoparticle-delivered peptide, shifted microglia to a neuroprotective state and reduced amyloid-related pathology and cognitive impairment. These are animal results, and the authors call for advancing this approach into clinical trials rather than claiming it works in patients.
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Hippocampal and serum irisin levels were progressively reduced in CCH mice.
Why it matters
In mice with chronic reduced brain blood flow, exercise-induced irisin reduced neuroinflammation and hippocampal neuron death and improved memory and behavior through the integrin αVβ5/AMPK/mTOR pathway. These findings are in animals and do not yet show that irisin or exercise treats cognitive impairment in people.
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Increased phosphorylation of TDP-43 is a pathological hallmark of several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
This review examines the conflicting evidence on whether TDP-43 phosphorylation drives disease progression or serves a neuroprotective role in conditions including frontotemporal dementia. It highlights unresolved questions about the regulation of TDP-43 phosphorylation and does not report a treatment or cure.
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White matter hyperintensities (WMH) are neuroimaging markers linked to an elevated risk of cognitive decline.
Why it matters
This study describes a deep learning model that automatically measures white matter hyperintensity severity from brain scans using visual ratings as the only supervisory signal. The authors say this approach has the potential to advance preventive and precision medicine by improving assessment of vascular cognitive impairment, but it is a tool for measurement rather than a treatment or cure.
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UNC13A (rs12608932-CC) is associated with both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), and shortens survival in ALS.
Why it matters
In 626 patients with frontotemporal dementia, homozygosity for rs12608932-C in UNC13A was associated with shorter survival. This has implications for patient counselling and trial design, but does not provide a treatment, cure or prevention.
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This innovative study aims to test the feasibility of iTBS as a cognitive enhancement strategy in MCI.
Why it matters
This is a study protocol testing whether intermittent theta burst stimulation is feasible as a cognitive enhancement strategy in mild cognitive impairment. If feasible, it could lead to a larger trial testing whether it can remediate cognitive decline or delay progression to dementia.
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Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) are overwhelmingly linked to TDP-43 dysfunction.
Why it matters
In animal work, blocking TDP-43 SUMOylation led to age-dependent TDP-43 pathology and sex-specific behavioral deficits, and SUMOylation was correlated with human aging and disease states. This presents SUMOylation as an early physiological stress response whose disruption may raise risk, but no treatment is tested in patients.
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Our findings indicate that liver fat mediates associations between cardiometabolic factors and WMHs and that WMHs mediate the association between liver fat and cognitive performance.
Why it matters
In this UK Biobank analysis, liver fat was linked to white matter hyperintensities and to cognitive performance, and it mediated the link between cardiometabolic factors and these brain measures. This points to cardiometabolic and liver health as possible targets for reducing small vessel disease that can contribute to dementia, though the study shows associations, not cause and effect.
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cBF volume declined at comparable rates in iRBD-to-PD and iRBD-to-DLB converters, but atrophy was more severe at DLB phenoconversion. cBF atrophy correlated with attention, executive, and memory deficits.
Why it matters
Basal forebrain degeneration evolves from the prodromal stage of Lewy body diseases and predicts dementia, highlighting a window for cholinergic-targeted intervention. In iRBD, baseline cBF z-score below -1.0 predicted dementia with a hazard ratio of 9.57.
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-heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens.
Why it matters
In a human brain tissue model, repeated mild controlled blows reactivated latent HSV-1 and led to amyloid and phosphorylated tau accumulation and activated gliosis, effects that were absent in mock-infected tissue. This is a laboratory model, so it suggests a possible contributing mechanism but does not prove that preventing such injuries or infections prevents Alzheimer's disease.
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Sex differences for clinicopathological correlations in LBD also occur at the regional pathology level.
Why it matters
In 357 brain donors with a high likelihood of Lewy body dementia pathology, females were less likely to receive a clinical diagnosis and had more Lewy bodies, neurofibrillary tangles and senile plaques in various regions than males. This suggests females face a higher risk of clinical underdiagnosis, which matters for getting the right diagnosis but does not address treating, curing or preventing the disease.
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48/100
Lewy body patients showed a significantly higher degree of WMSA in the external capsule cholinergic pathway despite no significant differences in global WMSA compared to controls.
Why it matters
In Lewy body patients, white matter hyperintensities were greater in the external capsule cholinergic pathway than in controls even though global white matter hyperintensities did not differ, and these measures were linked to more frontal atrophy. This suggests cerebrovascular disruption of cholinergic pathways may relate to frontal atrophy but does not test any treatment, cure or prevention.
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Early increases in plasma NfL may reflect early white matter microstructural changes prior to dementia in DS.
Why it matters
In 30 adults with Down syndrome without dementia, higher plasma neurofilament light chain was associated with altered diffusion measures in selected white matter tracts. The authors suggest plasma NfL may reflect early white matter changes before dementia, but this cross-sectional study does not test treatment or prevention.
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Glioblastomas (GBM) are incurable central nervous system (CNS) cancers characterized by substantial myeloid cell infiltration.
Why it matters
This study found that TREM2 is immunoprotective in glioblastoma, with genetic or pharmacological TREM2 deficiency promoting tumour progression in vivo. It concerns central nervous system cancers, not Alzheimer's disease, and reports no treatment, cure, or prevention for Alzheimer's disease.
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The gut microbiota and tumor-associated macrophages (TAMs) affect tumor responses to anti-programmed cell death protein 1 (PD-1) immune checkpoint blockade.
Why it matters
This study is about cancer immunotherapy in mice, not Alzheimer's disease. It found that TREM2 deficiency combined with anti-PD-1 treatment enhanced tumor elimination, which does not inform Alzheimer's treatment.
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M1/M2 paradigm of macrophage plasticity has existed for decades.
Why it matters
This review is about macrophage diversity in human cancers and does not study Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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Treatments for neurodegenerative disorders remain rare, but recent FDA approvals, such as lecanemab and aducanumab for Alzheimer disease (MIM: 607822), highlight the importance of the underlying biological mechanisms in driving discovery and creating disease modifying therapies.
Why it matters
This study created an open multi-omic resource using summary-data-based Mendelian randomization to identify genetic targets for drug discovery and repurposing for neurodegenerative diseases. It provides a framework for identifying targets rather than reporting a treatment that cures or prevents Alzheimer's disease.
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A total of 1,156 Mexican American and 587 non-Hispanic White participants were included (mean age = 68 years, standard deviation = 10; 65% female).
Why it matters
In 1,156 Mexican American and 587 non-Hispanic White older adults, serum GFAP levels were associated with demographic and clinical factors, and the study examined its diagnostic accuracy. This is about understanding a biomarker across diverse groups, not about 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.
- The many faces of α-synuclein: from structure and toxicity to therapeutic target
- A pathologic cascade leading to synaptic dysfunction in alpha-synuclein-induced neurodegeneration
- Physical exercise and epigenetic modifications in skeletal muscle, brain, and heart
- Acute transient cognitive dysfunction and acute brain injury induced by systemic inflammation occur by dissociable IL-1-dependent mechanisms
- Preventive Effect of Quercetin in a Triple Transgenic Alzheimer's Disease Mice Model
- Synergistic Interactions between Abeta, tau, and alpha-synuclein: acceleration of neuropathology and cognitive decline
- Apolipoprotein E epsilon4 associated with chronic traumatic brain injury in boxing
- Role of Endogenous Lipopolysaccharides in Neurological Disorders
- A new aspartyl protease on 21q22.3, BACE2, is highly similar to Alzheimer's amyloid precursor protein beta-secretase
- TREM2+ macrophages suppress CD8+ T-cell infiltration after transarterial chemoembolisation in hepatocellular carcinoma