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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Alzheimer's Disease (AD) is a progressive neurodegenerative disorder and the leading cause of cognitive decline in older adults.
Why it matters
In laboratory experiments, silodosin inhibited butyrylcholinesterase at low micromolar levels but inhibited acetylcholinesterase only at high micromolar levels, and cell viability assays showed concentrations under 10 micromolar were safe. This is an in vitro and in silico study, so it does not show that silodosin treats Alzheimer's disease in people.
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Neurodegenerative diseases (NDs) are common chronic diseases with unknown etiology, and the association between virus and its pathogenesis is not clear.
Why it matters
Using genetic analysis, this study found evidence that infectious mononucleosis, mainly caused by Epstein-Barr virus, may have a causal effect on Alzheimer's disease risk. This suggests a possible viral link to Alzheimer's disease, but the finding comes from statistical genetic methods and does not prove that preventing mononucleosis would prevent Alzheimer's disease.
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Tau aggregation driven by microtubule-associated protein tau (MAPT) mutations is central to frontotemporal dementia pathology, yet no disease-modifying therapies effectively target mutant tau.
Why it matters
In laboratory peptide and cell assays, purpurin and oleocanthal inhibited aggregation of mutant tau more effectively than wild-type tau and suppressed intracellular tau propagation. These are early in-vitro findings and do not yet show a treatment, cure or prevention in people.
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GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation.
Why it matters
In rats with vascular dementia, ginsenoside Rc improved cognitive deficits and reduced synaptic disruption and neuronal apoptosis in the hippocampal CA1 region. This is an animal study, so it does not yet show that ginsenoside Rc treats dementia in humans.
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In plasma, most complement analytes were not significantly different between spFTD and HC; the exceptions were C4 and FB, significantly decreased in spFTD vs HC ( p = 0.0192 and p = 0.0181, respectively), suggesting complement consumption in classical and alternative pathways.
Why it matters
This study measured complement proteins in blood, exosomes, and cerebrospinal fluid and found signs of complement dysregulation in people with symptomatic frontotemporal dementia. It is a biomarker study only and does not test any treatment, so it does not show whether targeting complement would help patients.
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Vascular dementia (VaD) is a neurodegenerative disorder characterized by chronic oxygen insufficiency, leading to the generation of oxygen-free radicals, inflammatory responses, disturbances in iron metabolism, lipid peroxidation, and other pathological changes that disrupt intracellular homeostasis.
Why it matters
This paper describes how iron imbalance and ferroptosis contribute to neuronal death in vascular dementia, and how heme oxygenase-1 may protect neurons by reducing oxidative stress and inflammation. It provides a theoretical framework for potentially treating vascular dementia-related neuronal injury but does not report a tested treatment.
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The apolipoprotein ε4 allele (APOE4) is associated with decreased longevity and increased vulnerability to age-related declines and disorders across multiple systems.
Why it matters
In early middle-aged mice with human APOE alleles, 17α-estradiol improved several health-related measures, often with a bigger effect in APOE4 mice. These results suggest that longevity-promoting interventions may be especially helpful for people with APOE4, but this is animal research.
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This study shows that WMHs do not significantly alter gray matter nicotinic signaling in directly connected regions.
Why it matters
In 39 participants, white matter hyperintensity volumes correlated with age and cognitive scores, but nicotinic acetylcholine receptor binding in WMH-connected gray matter did not differ from unaffected regions. The study found no significant effect of WMH on this receptor system, though it did find decreased binding in the medial cholinergic pathway of Alzheimer's patients.
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Tauopathies, including Alzheimer's disease and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), are characterized by the aberrant aggregation of tau protein into neurofibrillary tangles.
Why it matters
In mice engineered to carry human tau with two FTDP-17 mutations, the extracted tau aggregates could force normal human and mouse tau to clump and these clumps could be passed on in lab studies. This is early animal and cell work, so it does not yet show a way to treat or prevent Alzheimer's in people.
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: Integrating clinical bioinformatics with computational drug design, this study establishes a translational paradigm for nanomaterial development.
Why it matters
This study describes a nanomaterial, M2exo@HMPB, designed to target the AIM2 inflammasome as a possible therapy for vascular dementia, combining clinical bioinformatics with computational drug design. It is early development work and does not report testing in patients, so no treatment, cure or prevention is established.
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The obtained data is noteworthy.
Why it matters
This case-control study examined an APP gene polymorphism and found that the GG genotype was associated with significantly higher odds of being an Alzheimer's case, while the C allele was less frequent in cases. It is a genetic association study and does not test or demonstrate any treatment, cure or prevention.
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Tauopathies, including Alzheimer's disease (AD) and Frontotemporal Dementia (FTD), are histopathologically defined by the aggregation of hyperphosphorylated pathological tau (pTau) as neurofibrillary tangles in the brain.
Why it matters
In the rTg4510 mouse model of frontotemporal dementia, only the Qβ-PHF1 tau vaccine, not the Qβ-AT8 vaccine, rescued cognitive deficits and reduced pathological tau and microgliosis. This is animal vaccine research, and sera from vaccinated mice reacted to tau pathology in human Alzheimer's brain sections.
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The advent of disease-modifying therapies for neurodegenerative diseases may result in a growing demand for nuclear neuroimaging procedures presenting opportunities but also challenges to the nuclear medicine community.
Why it matters
This survey of nuclear neuroimaging in Germany found that availability of amyloid PET with well-certified quality can be taken for granted, so access to amyloid PET will not be a major bottleneck for new Alzheimer's treatments. It does not test any treatment, cure, or prevention.
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Both V3 width and plasma Hcy concentration were negatively correlated with MoCA scores in PD (r=-0.358, P<0.001; r=-0.187, P=0.013, respectively).
Why it matters
In Parkinson's disease patients, wider third ventricle width and higher plasma homocysteine were linked to worse cognition, and a wider third ventricle predicted conversion from mild cognitive impairment to dementia. Baseline homocysteine levels were not suitable for predicting cognitive change over time.
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IBC effectively ameliorates AD pathology through autophagy-mediated clearance of Aβ and suppressing neuroinflammation in 5x-FAD mice.
Why it matters
In astrocyte cultures and 5x-FAD mice, isobavachalcone promoted clearance of amyloid beta and inhibited the NLRP3 inflammasome, and treated mice showed improved memory and motor performance. These are laboratory and animal results, so the compound has not been shown to treat Alzheimer's disease in people.
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Mild Cognitive Impairment (MCI) represents a critical stage between normal aging and dementia, with limited effective interventions currently available.
Why it matters
In SAMP8 mice, Kai-Xin-San improved memory and reduced amyloid beta deposition, neuroinflammation, and pyroptosis via the NLRP3/Caspase-1 pathway. This is animal research, so it does not yet show that this herbal formula treats mild cognitive impairment or prevents dementia in people.
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In particular, the severity of HIV-associated neurocognitive disorders (HAND) has been greatly reduced, significantly decreasing the prevalence of HIV-associated dementia [1].
Why it matters
In a mouse model of HIV infection, the viral protein Nef contributed to neuroinflammation and myelin impairment, with effects appearing additive to other HIV factors. This is animal and laboratory research on HIV-related cognitive problems, not a treatment or prevention for Alzheimer's disease.
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Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits.
Why it matters
This review describes a rat model that carries two human gene mutations and develops Alzheimer's-like pathology with age, which researchers can use to study the disease. It does not report a treatment or cure, but says the model may help identify biomarkers for early detection and test potential therapies.
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According to the World Health Organization (WHO), peripheral and central neurological disorders affect approximately one billion people worldwide.
Why it matters
This project developed deep learning models to detect and classify small white matter hyperintensity lesions on MRI, with the best model reaching high accuracy. It is a technical imaging study and does not test any treatment, cure or prevention for Alzheimer's disease.
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Misfolding and aggregation of microtubule-associated tau protein is implicated in a variety of neurodegenerative disorders (named tauopathies), including Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE).
Why it matters
Computer simulations found that acetylation at residue K353 reduced tau aggregation by weakening peptide interactions and disrupting salt bridges. This is a molecular modeling study and does not test any treatment in animals or people.
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• To clarify the key role of Muscone delayed the development of vascular dementia (VD). • To reveal synaptic function in VD associated with neuronal pentraxin receptor (NP2). • To reveal that Muscone alleviates VD through the BDNF-TrkB-NP2 signaling pathway initially.
Why it matters
In a rat model of vascular dementia and in HT22 cells, Muscone improved cognitive performance and synaptic measures via the BDNF-TrkB-NP2 pathway. These are animal and cell findings and do not yet show a treatment, cure or prevention in people.
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In this review, we outline the significant roles of necroptosis and its molecular mechanisms in the pathological process of VaD, with a particular focus on the role of necroptosis in modulating neuroinflammation and exacerbating the disruption of BBB permeability in VaD, and elaborate on the molecular regulatory mechanisms and the centrally involved cells of necroptosis mediated by tumor necrosis factor-α in neuroinflammation in VaD.
Why it matters
This review outlines the roles of necroptosis in vascular dementia, focusing on neuroinflammation and blood-brain barrier disruption, and analyzes the possibility of targeting necroptosis as a treatment strategy. It provides new treatment ideas but no confirmed therapy or cure.
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We aimed to investigate the potential therapeutic effects of the active substance of green tea, epigallocatechin-3-gallate (EGCG), on behavioral phenotypes and markers of neurogenesis in an Alzheimer disease (AD) rat model.
Why it matters
In a rat model of streptozotocin-induced Alzheimer-like disease, a 25 mg/kg dose of EGCG improved spatial memory deficits and returned APP and BDNF expression toward control levels. These findings are from an animal model only and do not show that EGCG treats or prevents Alzheimer's disease in people.
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Since 2007, the Medicare Severity Diagnosis Related Groups classification system has favored billing codes for acute encephalopathy over delirium codes in determining hospital reimbursement and several quality-of-care value metrics, despite broad overlap between these sets of diagnostic codes.
Why it matters
This is a policy proposal asking Medicare to reclassify delirium codes to match acute encephalopathy codes for reimbursement purposes. It concerns hospital payment and quality metrics, not the treatment, cure, or prevention of Alzheimer's disease.
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This study aimed to analyze whether taurine has a nootropic effect on short-term and long-term memory in a model of sporadic dementia of the Alzheimer's type (SDAT).
Why it matters
In rats with a sporadic Alzheimer-like condition, taurine improved memory, protected neurons and reduced astrogliosis in the hippocampus. This is animal research, so it does not yet show that taurine helps people with 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.
- beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease
- Phenotypes and ontogeny of senescent hepatic stellate cells in metabolic dysfunction-associated steatohepatitis
- Cerebral microinfarcts: a systematic review of neuropathological studies
- Co-occurrence of multiple pathologies in a case of frontotemporal dementia with TBK1 mutation: first in vivo detection of alpha-synuclein and tau co-pathology
- Memantine is a clinically well tolerated N-methyl-D-aspartate (NMDA) receptor antagonist--a review of preclinical data
- Baseline Performance Predicts tDCS-Mediated Improvements in Language Symptoms in Primary Progressive Aphasia
- Synchronous hyperactivity and intercellular calcium waves in astrocytes in Alzheimer mice
- A G-rich element forms a G-quadruplex and regulates BACE1 mRNA alternative splicing
- Suppressed proliferation and apoptotic changes in the rat dentate gyrus after acute and chronic stress are reversible
- AD-linked R47H-TREM2 mutation induces disease-enhancing microglial states via AKT hyperactivation