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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Physical Examination.—Physical examination revealed that the patient was well developed, but poorly nourished, with an appearance of chronic illness.
Why it matters
This is a 1932 case report of a fatal case of systemic blastomycosis, describing the patient's appearance of chronic illness. It has no relevance to treating, curing, or preventing Alzheimer's disease.
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The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders.
Why it matters
In preclinical work using patient-derived organoids and animal models, suppressing KCTD20 with siRNA or antisense oligonucleotide increased lysosomal exocytosis, reduced tau aggregation and increased neuron survival. This is early laboratory research, and the authors describe it as a new preclinical modality rather than a proven treatment.
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Alzheimer disease is one of the causes of dementia that could make the patient lose their memories until they unable to do normal activities.
Why it matters
This laboratory work compared two antibody labelling methods, horseradish peroxidase and biotin, for use in an ELISA test that measures the Alzheimer's-related protein Amyloid-β42. It is a technical methods study about test reagents and does not test any treatment, prevention or cure in patients.
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Down syndrome (DS), caused by trisomy of chromosome 21, exhibits significant phenotypic variability, including intellectual disability, early-onset Alzheimer disease (AD), congenital heart defects (CHDs), haematological malignancies, and immune dysregulation.
Why it matters
This review describes genetic variants, including in APP, BACE2, APOE, and PICALM, that contribute to Alzheimer's disease risk in people with Down syndrome. It highlights the complexity of genotype-phenotype relationships and the potential for precision medicine, but does not report a treatment or cure.
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Here, new phenoxide derivatives of diisopropyl flourophosphate for reaction with Lewis basic sites on acetyl cholinesterase (AChE) were designed.
Why it matters
This work designed and modeled new chemical derivatives intended to inhibit acetylcholinesterase and raise acetylcholine levels. It is computational and docking work only, with no testing in animals or people, so it does not establish any treatment, cure or prevention for Alzheimer's disease.
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Intersectin is an evolutionarily conserved multifunctional adaptor protein with multifunctional domains.
Why it matters
This review describes the structure and roles of the protein intersectin in endocytosis and exocytosis and its possible links to neurodegenerative diseases. It is a summary of existing knowledge and does not test any treatment, cure or prevention for Alzheimer's disease.
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Little is known about the chronic sequelae of isopropanol ingestion.
Why it matters
This single case report describes a patient who consumed isopropyl alcohol for at least 17 years and developed cerebellar dysfunction and dementia among other problems. It is a case report about chronic isopropanol ingestion, not about treating, curing or preventing Alzheimer's disease.
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An extra copy of the amyloid precursor protein gene (APP) is present in Down syndrome (DS) and APP duplication (APPdup), increasing the risk of Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA).
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16/100
Plasma p-tau217 concentrations were positively associated with plasma TNF- (Kendalls {tau} = 0.339; P < .001) and IL-6 (Kendalls {tau} = 0.310; P < .001) concentrations.
Why it matters
Some blood donors had higher levels of a tau protein marker (p-tau217) than expected, and these higher levels were linked to markers of inflammation. The researchers say it is unclear whether these elevations are clinically meaningful, so this is an early finding that needs confirmation and does not show any treatment or prevention.
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16/100
Simulation results were benchmarked against real-world population estimates, over a wide range of demographic and genetic parameters.
Why it matters
This study used simulation to examine how family history can help distinguish inherited from non-inherited forms of ALS, not Alzheimer's disease. It has no direct implications for treating, curing, or preventing Alzheimer's disease.
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IntroductionFrontotemporal lobar degeneration (FTLD) is a devastating disease that commonly results in early onset dementia, yet its rarity and heterogeneity limit large-scale research and clinical trials.
Why it matters
This study found that passive smartphone data, such as step count and battery use, was feasible to collect and reflected disease severity in people with frontotemporal lobar degeneration. It is early work on remote monitoring tools and does not test any treatment.
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder whose genetic architecture and underlying molecular mechanisms remain incompletely understood, particularly in sporadic disease.
Why it matters
This genetic study of ALS, not Alzheimer's disease, found that predicted blood DNA methylation at certain sites was associated with ALS risk. It is basic research into ALS biology and has no direct implications for treating or preventing Alzheimer's disease.
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ObjectiveEffective strategies to prevent Alzheimers disease and related dementias (ADRD) are limited.
Why it matters
In a database study, older adults who took varenicline for smoking cessation had a lower risk of developing Alzheimer's disease and related dementias than those who used nicotine replacement therapy. This is observational evidence only, and the authors call for further research before varenicline could be considered for prevention.
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16/100
We focus on neuroinflammation in disorders associated with frontotemporal lobar degeneration (FTLD).
Why it matters
This study found that a brain chemical marker, myo-inositol, was elevated in a disease-affected brain region in people with frontotemporal lobar degeneration and was linked to inflammation markers and worse cognitive scores. It is research into measuring neuroinflammation, not a treatment or cure.
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Neuroinflammation is a principal driver of brain atrophy and cognitive decline in Alzheimers disease (AD).
Why it matters
In a small study of 49 people with mild Alzheimer's disease, a stem cell therapy called laromestrocel was linked to less brain inflammation, less brain shrinkage, and better cognitive scores compared with placebo. These are early results from a small sample, and larger trials are needed to confirm whether the treatment is safe and effective.
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16/100
--Clinical trajectories after a diagnosis of mild cognitive impairment (MCI) vary widely, so prognostic models must account for both the timing of subsequent diagnoses and unequal follow-up.
Why it matters
This study built a model using age and a blood marker, p-tau217, to predict which people with mild cognitive impairment will develop dementia. The model worked moderately well in one group but its accuracy in a second group was uncertain, with a wide range that included near-chance results, so it is not yet ready for clinical use.
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Alzheimer’s disease (AD) pathology including amyloid beta (Aβ) plaques and tau tangles accumulate with age in Down Syndrome (DS).
Why it matters
This postmortem brain tissue study found reduced binding of a radiotracer to nicotinic acetylcholine receptors in Down syndrome and Alzheimer's disease brains. It describes a cholinergic abnormality but tests no treatment or prevention.
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IntroductionGenetic studies have shown the APOL1 variant p.N264K, also called M1, is associated with markedly lower kidney disease risk when co-inherited with the G2-risk allele.
Why it matters
This laboratory study looked at how two versions of the APOL1 gene affect cell channels when they occur together on the same chromosome. It is basic in-vitro research about kidney disease genetics, not a study of Alzheimer's disease or its treatment.
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Gross brain findings help guide differential diagnosis, but their diagnostic value across major neurodegenerative diseases remains incompletely characterized.
Why it matters
This study found that large language models could extract gross brain findings from autopsy reports to help classify neurodegenerative diseases, with high sensitivity for PSP and MSA but low sensitivity for combined Alzheimer's and Lewy body disease. It is a diagnostic aid, not a treatment, cure, or prevention.
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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.
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.
- Cerebrospinal fluid inflammatory markers in Parkinson's disease--associations with depression, fatigue, and cognitive impairment
- Redox proteomics analysis of HNE-modified proteins in Down syndrome brain: clues for understanding the development of Alzheimer disease
- Existing Pittsburgh Compound-B positron emission tomography thresholds are too high: statistical and pathological evaluation
- Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR
- Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression
- The Status of Neuroimaging with SPECT and PET in Germany: Results from the 1st Survey on Nuclear Neuroimaging in Germany in 2023
- 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