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 4,948 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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16/100
White matter hyperintensities (WMH), a key MRI-marker of cerebral small vessel disease (cSVD), are common in older adults and associated with an increased risk of stroke and dementia.
Why it matters
This study found that a polygenic risk score for white matter hyperintensities was associated with incident stroke and dementia, and identified pathway-specific risk scores involved in lipid metabolism and other processes. It may inform precision prevention and drug development for cerebral small vessel disease, but no treatment, cure, or prevention was tested.
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BackgroundBone marrow megakaryocytes, the primary source of brain-derived neurotrophic factor (BDNF) in the blood, secrete BDNF-packed platelets into the bloodstream.
Why it matters
This meta-analysis found that blood levels of BDNF decline with age in people over 60, but not in younger adults. It does not test any treatment, so it cannot show whether changing BDNF levels would prevent or treat dementia.
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Greater baseline WMH burden was associated with differential longitudinal progression in converters across eleven clinical outcomes, including cognition, gait, and functional independence (all q<0.05).
Why it matters
In people with newly diagnosed Parkinson's disease, greater baseline white matter hyperintensity burden was linked to different progression in cognition, gait, and functional independence. It is about prognosis in Parkinson's disease, not about treating, curing, or preventing Alzheimer's disease.
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BackgroundTuberous sclerosis complex (TSC) is a rare autosomal dominant neurodevelopmental disorder caused by loss-of-function mutations in TSC1 or TSC2, resulting in chronic hyperactivation of the mechanistic target of rapamycin (mTOR) pathway.
Why it matters
This study found elevated plasma phosphorylated tau-217 in people with tuberous sclerosis complex, with levels similar to those in Alzheimer's disease and higher than in cognitively unimpaired people. It suggests a biological overlap between the two conditions and implications for mTOR-targeted intervention, but no treatment, cure, or prevention was tested.
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Monoamine oxidase B (MAO-B) is a high-density protein located mainly in astrocytes that influences mitochondrial function and transition to astrogliosis.
Why it matters
This study found higher levels of the protein MAO-B in the brain in females and in people with treatment-resistant depression, and that some antidepressants occupied MAO-B. It suggests MAO-B may help explain sex differences in diseases like Alzheimer's, but it did not test any Alzheimer's treatment, cure, or prevention.
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ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels.
Why it matters
This genetic study found some associations between endocannabinoid system gene variants and dementia risk, brain volume, and protein levels, but colocalization analyses did not support shared causal variants. It highlights candidate pathways for further research, not a treatment, cure, or prevention.
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Spatial omics enables the integration of high-dimensional molecular organization with clinical outcomes, yet incorporating spatial single-cell information into predictive models at the population scale remains challenging.
Why it matters
This study introduced a tool called SPIN that uses spatial omics data to predict dementia status and find related gene networks. It is a technical method for research and prediction, not a treatment, cure, or prevention for Alzheimer's disease.
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Sex differences in Alzheimers disease (AD) genetic effects and regulatory contexts remain incompletely resolved.
Why it matters
This study identified sex-specific genetic signals and cellular pathways related to Alzheimer's disease risk. It suggests that sex-specific genetic architectures should be considered for future targeted treatment strategies, but no treatment, cure, or prevention was tested.
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Multi-trait QTL (xQTL) colocalization has shown great promises in identifying causal variants with shared genetic etiology across multiple molecular modalities, contexts, and complex diseases.
Why it matters
This study introduced a statistical method for integrating multi-omics data and applied it to aging brain tissue, identifying more colocalized loci and explaining more Alzheimer's disease heritability than fine-mapping alone. It is a genetics methodology study and does not test any treatment, cure or prevention.
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Dopamine replacement therapy (DRT) alleviates motor symptoms in Parkinsons disease (PD) but can trigger hallucinations in a subset of patients, yet the neural basis of this selective vulnerability is unknown.
Why it matters
This study found that dopamine replacement therapy increased sensitivity to induced hallucinations only in Parkinson's patients who already had hallucinations, linked to cortico-striatal hyperconnectivity. It concerns Parkinson's disease hallucinations and does not test any treatment, cure or prevention for Alzheimer's disease.
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BackgroundUnderstanding the mechanisms underlying brain aging and age-related pathological changes is essential for advancing brain health research.
Why it matters
This study calibrated and externally validated a mathematical model of brain aging that includes amyloid beta, tau, neuroinflammation and neuronal death, and found it predicted these features with reduced error. It is a modeling framework for studying brain aging and does not test any treatment, cure or prevention.
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Service members with traumatic brain injury are at approximately two- to four-fold higher risk of Alzheimers disease or related dementias than those without such an injury, with risk increasing with injury severity.
Why it matters
This study found that a marker called neoGFAP showed a trend-level advantage over total GFAP for distinguishing mild cognitive impairment plus Alzheimer's from non-Alzheimer subjects, with a significant advantage only in a small subset of 23 subjects. It is a biomarker study and does not test any treatment, cure or prevention.
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ImportancePatients are increasingly learning Alzheimers disease (AD) genetic and biomarker results through electronic health portals.
Why it matters
This trial found that a patient-centered digital platform was comparable to clinician-led telehealth sessions for returning APOE and pTau-217 results, with no significant between-group differences after pTau-217 disclosure. It addresses how risk information is delivered, not how Alzheimer's disease is treated, cured or prevented.
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The purpose of this meta-analysis was to determine the common signature of dysregulated brain glucose metabolism in late-onset age-associated neurodegenerative diseases (A2NDs), including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis.
Why it matters
This meta-analysis found that altered brain glucose metabolism is a shared feature across Alzheimer's, Parkinson's and ALS, but each disease shows its own distinct spatial pattern of metabolic change. It does not test any treatment, cure or prevention, so it offers no direct implications for those goals.
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INTRODUCTIONBiomarkers for monitoring disease activity and treatment response in peripheral neuropathies remain limited.
Why it matters
This study measured blood levels of big tau, brain-derived tau and neurofilament light chain in people with nerve disorders, multiple sclerosis, Alzheimer's disease and healthy controls. It is about biomarkers for peripheral neuropathies and does not test any treatment, cure or prevention for Alzheimer's disease.
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Individuals with Down syndrome (DS) display developmental delay, intellectual disability, premature brain ageing, and an increased risk of Alzheimer-like neurodegeneration.
Why it matters
This laboratory study using brain organoids from trisomic and euploid cells found early growth delay, reduced oligodendroglial specification, and impaired maturation in Down syndrome. It is early in-vitro work with no treatment or prevention findings.
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Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease.
Why it matters
This study found that polygenic and proteomic risk scores for neurodegenerative diseases overlap no more often than chance except where APOE dominates, and that genetic signal concentrates in specific plasma co-expression modules. It concerns risk score methodology, not treating, curing or preventing Alzheimer's disease.
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ObjectivesNon-invasive brain stimulation (NIBS) holds significant promise for treating neurological and neuropsychiatric conditions, yet translation into routine clinical practice remains limited.
Why it matters
This focus group study explored stakeholder views on non-invasive brain stimulation and found cautious optimism alongside barriers such as limited awareness, cost-effectiveness challenges and regulatory uncertainty. It concerns barriers to clinical adoption of a potential treatment, not evidence that it treats or prevents Alzheimer's disease.
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Self-repairs - in-utterance revisions in which a speaker abandons and reformulates their speech - are a promising interpretable marker for speech-based cognitive screening.
Why it matters
This study compared methods for automatically detecting self-repairs in speech on the DementiaBank ADReSS corpus, finding a locally deployable encoder was a more plausible route than larger models or complex prompts. It concerns a potential speech-based screening marker, not treatment, cure or prevention.
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We examined whether their metabolomic profiles also differed and whether subtype-related metabolic patterns were associated with dementia, stroke, and all-cause mortality.
Why it matters
This study found that metabolomic signatures differed across data-driven type 2 diabetes subtypes, with lipid and lipoprotein patterns associated with dementia, stroke and all-cause mortality, and no significant stroke results. These are observational associations that may inform risk understanding, not a treatment or cure.
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Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex.
Why it matters
This computational method identified subpopulations of microglia associated with Alzheimer's disease, characterized by depletion of homeostatic programs and localization to specific brain regions. It is a research framework for fine-mapping disease-relevant cell types from genetic and single-cell data, not a treatment or cure.
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Cognitive and behavioural impairment frequently accompanies motor decline in amyotrophic lateral sclerosis (ALS), with 15% of cases meeting the diagnostic criteria for frontotemporal dementia (FTD).
Why it matters
This genetic analysis mapped shared and distinct architecture linking ALS, sporadic frontotemporal dementia and cognitive traits, highlighting genes such as MEF2C and UNC13A. It is a gene-finding study and does not test any treatment, cure or prevention.
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Structural variants (SVs) are a major source of genetic variation yet remain underexplored in healthy aging and neurodegenerative diseases.
Why it matters
Long-read genome sequencing found many structural variants missed by short-read methods and implicated variants at loci including TMEM106B, BIN3 and NBEAL1 in Alzheimer's and Parkinson's disease. This is a genetic architecture study, not a treatment or prevention trial.
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Isolated REM sleep behaviour disorder (RBD) is the strongest prodromal marker of Parkinsons disease (PD) and dementia with Lewy bodies, yet diagnosis requires video-polysomnography with assisted montage and expert scoring and does not scale to screening or trial enrichment.
Why it matters
A self-applied system using electrodes behind the ears detected REM sleep behaviour disorder, a prodromal marker of Parkinson's disease and dementia with Lewy bodies, with high accuracy in home recordings. The authors present it as a scalable detection tool for screening and longitudinal studies, not as a treatment or cure.
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Hexanucleotide repeat expansions in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet the predictive information contained within associated inflammatory and proteinopathy markers remains incompletely characterised.
Why it matters
Machine-learning models using post-mortem inflammatory and proteinopathy markers in C9orf72-ALS performed worse when validation kept observations from the same person together. This is a methods finding about neuropathology studies of ALS and frontotemporal dementia, not a treatment or cure.
From across this topic
10 of the 4,930 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.
- Patient‐derived forebrain cortical organoids reveal biphasic tau–MAP6–microtubule axis dysfunction in tauopathy
- Hippocampal CA1 apical neuropil atrophy in mild Alzheimer disease visualized with 7-T MRI
- TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy
- Neurotoxic reactive astrocytes are induced by activated microglia
- Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders
- Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease
- Animal models of Parkinson's disease: an empirical comparison with the phenomenology of the disease in man
- A Perspective on Nrf2 Signaling Pathway for Neuroinflammation: A Potential Therapeutic Target in Alzheimer's and Parkinson's Diseases
- Upregulation of neuronal PGC-1α ameliorates cognitive impairment induced by chronic cerebral hypoperfusion
- The new mutation, E46K, of alpha-synuclein causes Parkinson and Lewy body dementia