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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The metabolic fate of the Alzheimer beta/A4 amyloid precursor protein (APP) includes intraamyloid proteolysis that leads to the production of secreted N-terminal and cell-associated C-terminal fragments.
Why it matters
This cell study found that chloroquine inhibited intracellular degradation of the amyloid precursor protein but not its secretion in PC12 cells. It is early laboratory work on how amyloid precursor protein is processed and does not show any treatment or prevention for Alzheimer's disease.
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Mouse trisomy 16 has been proposed as an animal model of Down syndrome (DS), since this chromosome contains homologues of several loci from the q22 band of human chromosome 21.
Why it matters
This mapping study found that the mouse chromosome 16 region includes the amyloid precursor protein gene and markers linked to familial Alzheimer disease. It is basic genetic mapping and does not test treatment, cure, or prevention.
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A recent randomized trial demonstrated clear cerebrospinal-fluid DHA target engagement without detectable improvement in cognition or brain volume over 24 months.
Why it matters
A recent randomized trial found clear target engagement of DHA in cerebrospinal fluid but no detectable improvement in cognition or brain volume over 24 months. The authors stress this does not prove DHA lacks biological effects and does not explain why no functional benefit was seen, and they propose mitochondrial reserve as a possible modifier to be tested.
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Spatial analyses localised early hippocampal tau-PET signal predominantly to the anterior CA1.
Why it matters
Measuring tau-PET in the CA1 subfield rather than the whole hippocampus gave more biologically consistent Braak stage II classifications and fewer stage regressions at follow-up. The authors suggest this may help characterize early AD and support participant selection in trials, but it is not itself a treatment or cure.
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The proteinopathy of the RNA-binding protein TDP-43, characterized by nuclear clearance and cytoplasmic inclusion, is a hallmark of multiple neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD).
Why it matters
Using CRISPR interference screening in human neurons, this study identified DCPS as a genetic modifier of TDP-43 loss-of-function neurotoxicity, showing that loss of TDP-43 hyperactivates P-bodies and increases mRNA decay, and that reducing DCPS improves neuronal survival. It identifies DCPS as a potential therapeutic target but these are laboratory findings with no treatment, cure or prevention tested in patients.
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Our findings were compared to other published RNA sequencing data of tauopathies (Alzheimer's dementia, progressive supranuclear palsy and FTLD with MAPT), FTLD-TDP (subtypes A&B) and available proteomics of this cohort.
Why it matters
This study analyzed RNA and protein in the temporal cortex of frontotemporal lobar degeneration with TDP-43 type C pathology, finding upregulation of damage response, cell structure and RNA splicing processes and downregulation of synaptic processes, including eleven synaptic genes affected at both RNA and protein level. It describes disease-related molecular changes and does not test any treatment, cure or prevention.
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Inflammatory responses are characterized by the activation of immune cells, while inflammatory biomarkers intricately interact with the immune system.
Why it matters
This cross-sectional study found associations between circulating immune cell phenotypes and inflammatory biomarkers in dementia-free participants. It provides information about immune and inflammatory relationships but does not test any treatment, cure, or prevention for Alzheimer's disease.
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Cerebral small vessel disease (CSVD) is a chronic, progressive cerebrovascular disorder affecting small arteries, arterioles, venules, and capillaries, and is a leading contributor to stroke, vascular dementia, and cognitive impairment.
Why it matters
This review describes neuroinflammation and blood-brain barrier dysfunction as central processes in cerebral small vessel disease, a contributor to vascular dementia, and discusses potential biomarkers and therapies targeting this axis. No treatment is proven here, and the work is a review of mechanisms and early translational research.
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Individuals with msWMH showed systematic deficits in face-memory processing across encoding, maintenance, and retrieval, accompanied by reduced theta power and synchronization, altered alpha power, and disrupted theta-gamma coupling.
Why it matters
Asymptomatic people with moderate-to-severe white matter hyperintensities showed hidden visual short-term memory deficits along with altered brain oscillations and damage to specific white matter tracts, with theta oscillations mediating the link between tract integrity and global cognition. The authors suggest theta activity may be a preclinical intervention target, but this is a finding about brain function, not a tested treatment.
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We found that ∼25% of donors lived in high deprivation contexts, 52% had at least one incidence of CVD, and the cohort identified as .05).
Why it matters
In a national brain donor cohort, about 25% of donors lived in highly deprived neighborhoods and 52% had at least one incidence of cerebrovascular disease. More disadvantaged neighborhoods predicted cerebrovascular disease neuropathology.
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Iron was 2-fold higher in DSAD. Iron storage proteins and lipid peroxidation were increased in prefrontal cortex, but not in the cerebellum.
Why it matters
Brains of people with Down syndrome and Alzheimer's disease showed higher iron levels and signs of a cell death process called ferroptosis, with greater lipid damage than in Alzheimer's alone. These findings suggest that targeting iron and lipid damage might be a future treatment approach, but this is early brain tissue research.
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Data collection began in March 2024. So far 562 people completed a pre-screening online questionnaire, with 190 passing pre-screening of whom 54% met eligibility criteria.
Why it matters
This is a feasibility study still collecting data, with only 19 participants randomized so far, testing a combination of intranasal insulin and oral semaglutide in older adults with metabolic syndrome at high dementia risk. No cognitive results are reported yet, so it cannot show whether the combination helps thinking or prevents dementia.
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This is primarily a mouse-model study (in amyloid-plaque mouse models such as 5xFAD, with some human tissue validation) identifying a newly recognized, protective state of brain immune cells (microglia) that expresses genes normally associated with the immune system's lymphocytes.
Why it matters
In mouse models, researchers identified a protective state of brain immune cells controlled by the protein PU.1, and lowering PU.1 reduced amyloid-related brain damage. Because the core experiments were in mice, this is early-stage evidence about a possible future drug target, not a human treatment finding.
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Cerebral small vessel disease (SVD) is frequently comorbid with Alzheimer's disease (AD), and brain endothelial cells (BECs) express genes associated with AD genetic risk.
Why it matters
This study mapped gene regulation in human brain vascular cells and found that Alzheimer's heritability is primarily immune related, while small vessel disease heritability involves the neurovascular unit. Computer screening suggested possible drug classes for Alzheimer's, but these are not proven treatments.
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Neuroaxonal damage underlies permanent disability in various neurological conditions, both neuroautoimmune and neurodegenerative.
Why it matters
This review describes neurofilament light chain as a marker of nerve damage that is being studied in Alzheimer's and other neurodegenerative diseases, though its disease specificity is limited. It notes that neurofilaments are increasingly investigated in Alzheimer's but are not yet established as a specific clinical tool for it.
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< 0.1). -ε4 status, and Aβ load, and not mediated by markers of neuroaxonal degradation.
Why it matters
This population-based study found that increasing white matter hyperintensity volume was linked to faster hippocampal atrophy, independent of APOE4 status and amyloid load. The authors say the results need replication in more diverse cohorts, so no treatment or prevention is established.
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SnRNA-seq analysis revealed elevated microglial proportions across all dementia subtypes compared to NCI.
Why it matters
Analysis of brain tissue from several dementia subtypes found increased microglia and a distinct microglial state with higher MSR1-mediated phagocytosis, including in Parkinson's disease dementia and dementia with Lewy bodies. This describes a shared feature across dementias but does not report a treatment or cure.
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Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer’s disease (AD).
Why it matters
This laboratory study using human brain tissue and cells found that a gene network involving SEMA6D and TREM2 is active near amyloid plaques and appears disrupted in later Alzheimer's stages. The findings suggest that loss of SEMA6D signaling may impair microglial activation and Aβ clearance, but this is early mechanistic work and no treatment was tested in patients.
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Progressive cortical thinning in multiple cognition-related regions was significantly associated with cBF atrophy.
Why it matters
This longitudinal study found that cholinergic basal forebrain atrophy was associated with cortical thinning, which accounted for about 44% of the relationship between basal forebrain degeneration and cognitive decline, with stronger effects in people with elevated amyloid-β. The authors suggest basal forebrain and cortical thinning as early biomarkers and highlight targeting cholinergic dysfunction in early intervention strategies, but no treatment or cure was tested.
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Lack of vitamin D is associated with cognitive decline and Alzheimer's disease.
Why it matters
In older adults with memory complaints, the study found no significant cross-sectional associations between plasma vitamin D and either plasma p-tau181 or plasma NfL. This means the data did not show a link between vitamin D levels and these Alzheimer's-related blood markers.
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45/100
White matter hyperintensities (WMH) are associated with cortical thinning in distant brain regions.
Why it matters
In this study of older adults without dementia, global white matter hyperintensity burden, especially periventricular, was cross-sectionally associated with cortical thinning in temporal regions involved in early Alzheimer's disease, with stronger associations in amyloid-positive individuals. The associations were not found longitudinally, and the study does not test any treatment, cure, or prevention.
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Vascular dementia (VaD), the second-leading cause of dementia, is primarily a white matter ischemic disease with no direct therapies.
Why it matters
In a mouse model of vascular dementia, two intercellular signaling systems were disrupted, and an A3AR-specific agonist restored tissue integrity and behavioral function. This study reveals intercellular signaling targets and provides a foundation for developing therapies for vascular dementia, though findings are from animal models.
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Fourteen individuals with DS and five age-matched euploid controls were studied, with all DS cases showing HFOs.
Why it matters
In a small study of 14 people with Down syndrome, high-frequency brain oscillations appeared before Alzheimer's dementia and were seen in all cases. The authors call these oscillations promising biomarkers that may predict dementia in adults with Down syndrome, but say the trend with age needs further confirmation.
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Neuronal dysfunction has been extensively studied as a central feature of neurodegenerative tauopathies.
Why it matters
In a stem cell model, microglia carrying a MAPT mutation showed abnormalities including stalled phagocytosis and disrupted TREM2/TYROBP networks, and factors they released reduced synaptic density in neurons. The authors say this has implications for developing therapeutics for tauopathies, but this is laboratory work, not a treatment.
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Extracellular vesicles (EVs) are membrane-enclosed nanoparticles released by most cell types, and from multiple sub-cellular compartments.
Why it matters
This review examines evidence that TDP-43 is associated with extracellular vesicles, which may either help clear aggregated protein or spread it between cells. It discusses potential use of extracellular vesicles as biomarkers, but reports no treatment, cure or prevention.
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.
- Hypoperfusion in frontotemporal dementia and Alzheimer disease by arterial spin labeling MRI
- Primary antiphospholipid syndrome: functional outcome after 10 years
- Meta-analysis of glucose metabolism across Alzheimer's, Parkinson's and ALS reveals distinct patterns of cortical hypometabolism versus subcortical hypermetabolism with disease-specific spatial signatures
- Disease-Associated Mutations of TREM2 Alter the Processing of N-Linked Oligosaccharides in the Golgi Apparatus
- Single-Cell RNA-Seq Reveals the Transcriptional Landscape and Heterogeneity of Aortic Macrophages in Murine Atherosclerosis
- Copper inhibits beta-amyloid production and stimulates the non-amyloidogenic pathway of amyloid-precursor-protein secretion
- Potential Neuroregenerative and Neuroprotective Effects of Uridine/Choline-Enriched Multinutrient Dietary Intervention for Mild Cognitive Impairment: A Narrative Review
- Mechanisms of Cell-to-Cell Transmission of Pathological Tau: A Review
- Abundant non-inclusion α-synuclein pathology in Lewy body-negative LRRK2-mutant cases
- Microglia as a key player in Aβ‐related astrocyte reactivity