Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Lewy body dementia (LBD), which includes Parkinson's disease dementia and dementia with Lewy bodies, is characterized by progressive cognitive decline, α-synuclein (α-Syn) aggregation, and concurrent microglial activation and neuroinflammation.
Why it matters
In a mouse model of Lewy body dementia, exosomes from activated microglia worsened alpha-synuclein buildup and cognitive deficits, while removing microglia reduced these changes. This is early animal and laboratory work on Lewy body dementia, not a treatment for Alzheimer's disease.
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Dementia is a growing global health concern in aging societies, leading to a progressive decline in cognitive function that severely impairs daily life.
Why it matters
This review examines whether the cGAS-STING pathway could be a target for diagnosing and treating dementia by reducing chronic neuroinflammation. It does not report testing any treatment in people, so any therapy based on this idea remains unproven.
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The pathological loss of nuclear TDP-43 is a hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to extensive alterations in RNA metabolism and a broad number of neuronal transcripts.
Why it matters
Using Drosophila and human iPSC-derived motoneurons, this study identified Rab4 as a target of TDP-43 whose expression recovered synaptic vesicle recycling and locomotor function in TDP-43-deficient motoneurons. These findings define a regulatory axis and offer a framework to identify compensatory targets, but they are from model systems and not yet treatments.
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Tau hyperphosphorylation has been considered a major contributor to neurodegeneration in Alzheimer's disease (AD) and frontotemporal dementia, and related tauopathies have gained prominence in the development of therapies for these conditions.
Why it matters
In rTg4510 tau mice, impaired nest-building, learning and exploratory behavior were associated with specific glial gene expression changes. This is animal research that examines links between glial reactivity and behavior and does not test a treatment for people.
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Exercise injuries present a significant challenge in medicine and public health, impacting exercise performance, career longevity, and overall quality of life.
Why it matters
This article is about using OMICS and artificial intelligence to assess exercise injury 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 immune system plays a dynamic role in neurodegenerative diseases, and purinergic receptors allow immune cells to recognize neuronal signaling, cell injury, or stress.
Why it matters
In human microglia-like cells, blocking P2RX7 reduced inflammatory cytokine expression and restored amyloid beta uptake, and P2RX7 expression mediated the link between IL18 and several Alzheimer's traits in postmortem brain. This is laboratory and tissue research, so it does not yet show that P2RX7-targeting drugs treat Alzheimer's disease in patients.
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A bidirectional relationship has been identified between dementia and epilepsy.
Why it matters
This retrospective study of 50 patients found an association between severe dementia grades and drug-resistant epilepsy, and describes a bidirectional relationship between dementia and epilepsy. It does not test any treatment, cure or prevention for Alzheimer's disease.
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These findings provide preliminary evidence that tPBM may effectively improve neuropsychological, physiological, and psychological outcomes in individuals with MCI.
Why it matters
In 36 older adults with mild cognitive impairment, those receiving transcranial photobiomodulation showed improved cognitive efficiency, eye movement measures and depressive symptoms compared with controls. The authors describe this as preliminary evidence that the approach may improve these outcomes.
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Cytoplasmic mislocalisation and nuclear depletion of TDP-43 are pathological hallmarks of amyotrophic lateral sclerosis (ALS), including mutations in the C9ORF72 gene that characterise the most common genetic form of ALS (C9ALS).
Why it matters
This study reports karyopherin-α4 pathology in the spinal cord of TDP-43-positive sporadic ALS and C9ALS patients, and shows in human cells and fruit flies that cytoplasmic accumulation of TDP-43 causes this karyopherin pathology. It identifies KPNA4 as a potential therapeutic target but does not test any treatment, cure or prevention in patients.
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The primary analysis demonstrated significant improvements in multiple episodic memory measures across both intervention groups, with no significant differences observed between groups.
Why it matters
In this trial, adding prefrontal theta-gamma tACS to cognitive training did not produce robust improvements in episodic memory compared with sham stimulation plus cognitive training. Both groups improved on several memory measures, but the brain stimulation gave no clear added benefit.
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The fMRI entropy classifier matched the tau PET model in accuracy and outperformed it in F1 score (0.64 vs. 0.61) and area under the curve (AUC; 0.73 vs. 0.67).
Why it matters
This study found that an fMRI-based measure of brain complexity classified mild cognitive impairment about as accurately as tau PET imaging. This suggests fMRI entropy could serve as a non-invasive alternative to tau PET for detecting cognitive impairment related to Alzheimer's disease.
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JOURNAL/nrgr/04.03/01300535-202606000-00056/figure1/v/2026-02-11T151048Z/r/image-tiff Cerebral small vessel disease is a major vascular contributor to cognitive impairment and dementia.
Why it matters
In spontaneously hypertensive rats, the NLRP3 inhibitor MCC950 suppressed inflammasome activation and inflammation and improved cognitive function along with brain pathology. This is animal research, so it does not yet show that MCC950 treats cerebral small vessel disease or dementia in people.
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High Resolution Image Download MS PowerPoint Slide Pathological aggregates of TDP-43 are implicated in Alzheimer’s disease, frontotemporal dementia, and amyotrophic lateral sclerosis.
Why it matters
This study developed cell-based biosensors to monitor TDP-43 multimerization and used them to screen an FDA-approved compound library, identifying ketoconazole as a molecule that stabilizes functional nuclear TDP-43 in an NTD-dependent manner and partially restores motor function in a TDP-43 worm model. These are early laboratory and animal findings, so they do not yet show any treatment or prevention benefit in people.
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TAR DNA-binding protein 43 (TDP-43) pathology is linked to the neurodegenerative disorders amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Huntington disease (HD).
Why it matters
In mice, overexpressing TDP-43 in the hypothalamus caused hypothalamic atrophy, loss of specific neuropeptide-producing neurons, TDP-43 inclusions, high blood sugar independent of food intake, and apathy-like behavior. The authors conclude TDP-43 can have direct pathological effects in the hypothalamus that may contribute to non-motor symptoms in TDP-43 proteinopathies.
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M07-TFN showed higher binding affinities and stronger activation of hTREM2 signaling than all previously described anti-hTREM2 antibodies. p-Syk activation was increased 30-fold in hTREM2-overexpressing HEK293 cells and fourfold in human microglia cells compared to baseline.
Why it matters
This study tested a fully human anti-TREM2 antibody called M07-TFN, which showed strong TREM2 signaling activation, improved human microglia viability, crossed a human blood-brain barrier model, and improved memory and reduced plaque load in 5xFAD mice. These are animal and laboratory results, so it is too early to say whether this antibody treats or prevents Alzheimer's disease in people.
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Tau protein plays a pivotal role in maintaining neuronal structure and function through its regulation of microtubule stability and neuronal polarity.
Why it matters
This review describes how tau normally supports neuronal structure and how its hyperphosphorylation, misfolding, and aggregation contribute to Alzheimer's disease and other tauopathies. It is a summary of biology and does not report any treatment, cure, or prevention.
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The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β.
Why it matters
This review describes how the NLRP3 inflammasome pathway destroys neuronal cells through IL-18, IL-1β and the N-terminal fragment of GSDMD in vascular dementia, and proposes that blocking this pathway is a new therapeutic strategy. The proposed treatment target is for vascular dementia, not Alzheimer's disease, and no clinical trial results are reported.
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Vascular dementia (VD), characterized by cognitive decline and behavioral disorders, has seen a rapid increase in prevalence in recent years.
Why it matters
In a mouse model of vascular dementia, treatment with human embryonic stem cell-derived multipotent mesenchymal stem cells improved working and long-term memory and was linked to enhanced angiogenesis, preserved blood-brain barrier integrity and improved hippocampal organisation. These findings are from an animal model of vascular dementia and do not establish a treatment, cure or prevention for Alzheimer's disease.
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Clinical data, animal and cell studies show that some antidiabetic drugs, including glucagon-like peptide 1 receptor agonists (GLP-1RAs), exert therapeutic effects in Alzheimer's disease (AD) via modulation of amyloid-β peptide (Aβ) metabolism.
Why it matters
This laboratory study examined the direct interactions of GLP-1(7-37) and its analogues semaglutide, liraglutide and exenatide with monomeric Aβ40/Aβ42 and their effects on Aβ fibrillation and cytotoxicity. It notes that these direct interactions and their functional consequences had remained unexplored.
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BackgroundTo date, cholinomimetics remain central in the pharmacotherapy of Alzheimer's disease (AD) dementia.
Why it matters
In 32 patients with amnestic mild cognitive impairment or mild dementia due to Alzheimer's disease, temporo-parietal gray matter and perfusion were more closely associated with cholinergic deficit than basal forebrain measures. The authors note that the amnestic syndrome can also result from non-Alzheimer's neuropathology such as TDP-43 proteinopathy and argyrophilic grain disease.
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Patients with Alzheimer's disease (AD) have two types of abnormal protein buildups: amyloid plaques and neurofibrillary tangles, in addition to the early synaptic dysfunction associated with the enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE).
Why it matters
In cell experiments, an extract of the plant Caliphruria subedentata protected SH-SY5Y cells against damage caused by Aβ (1-42) peptide and Okadaic acid, and computational work suggested it interacts with AChE, BuChE, NMDA and GSK3. These are in vitro and in silico findings only, so no conclusion can be drawn about treating or preventing Alzheimer's disease in people.
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The CU- group had lower baseline GAP-43 than all Aβ+ groups, but not the other Aβ- groups.
Why it matters
Among people who were amyloid-positive, higher baseline levels of the protein GAP-43 in cerebrospinal fluid were linked to faster functional decline in those with objectively defined subtle cognitive decline or mild cognitive impairment. This is a biomarker finding about predicting decline, not a treatment or cure.
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Viral genomes encode viral transcriptional regulators (vTRs) that manipulate host gene expression to facilitate replication and evade immune detection.
Why it matters
Viral transcriptional regulators were mapped and their human targets enriched in neurodegenerative disorders, including Alzheimer's disease. Drug repurposing analysis identified candidate drugs for Alzheimer's disease, but these are potential therapeutic targets for future investigation.
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Transgenic iPSC lines provide a unique tool to study the molecular and genetic mechanisms of FTDP-17 caused by the presence of the c.2013T > G (p.N279K) mutation, as well as to test potential drugs in vitro.
Why it matters
This describes transgenic induced pluripotent stem cell lines created to study the molecular and genetic mechanisms of FTDP-17 caused by a specific mutation. The lines are a tool for in vitro study and drug testing, not a treatment or cure.
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Based on the fusion of the topological features of the multimodal FBN and SBN, the accuracy for the diagnosis of MCI in patients with unilateral MCA steno-occlusive disease reached 90.00%.
Why it matters
A multimodal fusion model diagnosed mild cognitive impairment in patients with unilateral middle cerebral artery steno-occlusive disease with 90% accuracy and an AUC of 0.9149. The authors say efficient automated diagnosis could facilitate early detection and timely intervention to delay or prevent disease progression, but this is a diagnostic tool.
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.
- Regional cerebral perfusion in patients with Alzheimer's disease and mild cognitive impairment: effect of APOE epsilon4 allele
- Kisunla (donanemab) — EU Marketing Authorization (EPAR), following CHMP re-examination
- Decreased synaptic proteins in neuronal exosomes of frontotemporal dementia and Alzheimer's disease
- Endothelium-Macrophage Crosstalk Mediates Blood-Brain Barrier Dysfunction in Hypertension
- Tau is associated with atrophy in MCI independently of beta‐amyloid and APOE e4 genotype
- Aquaporin-4 deficiency induced white matter injury via upregulated complement component 3 in cerebral small vessel disease
- Short telomeres in patients with vascular dementia: an indicator of low antioxidative capacity and a possible risk factor?
- The dorsal raphe nucleus shows phospho-tau neurofibrillary changes before the transentorhinal region in Alzheimer's disease. A precocious onset?
- Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans
- Risk Factors for Phenoconversion in Rapid Eye Movement Sleep Behavior Disorder