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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Neuropsychiatric symptoms (NPS), commonly concomitant with Alzheimer's disease (AD), substantially impair the quality of life and accelerate disease progression, yet reliable biomarkers for early identification of individuals at high NPS risk remain elusive.
Why it matters
Adding selected cerebrospinal fluid proteins improved prediction of neuropsychiatric symptom risk in people with mild cognitive impairment or mild Alzheimer's disease over two years. This is a biomarker prediction study and does not test any treatment, cure or prevention.
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Among the 92 participants in the ITT population (mean age 71.9 years; mean education 16.5 years; 61/92, 66%, women; 88/92, 96%, White), 82 (89%) completed all study activities.
Why it matters
In this randomized trial of healthy older adults, speed-based cognitive training increased a marker of acetylcholine transporter binding in brain regions supporting attention, memory, and executive function. It was conducted in healthy older adults and does not show that this training prevents or treats Alzheimer's disease.
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SES and LA were associated with better cognitive performance at baseline, but were not associated with cognitive decline over time.
Why it matters
This longitudinal study found that higher socioeconomic status and lifestyle activity were linked to better baseline cognition and reduced some harmful effects of amyloid and white matter hyperintensity burden on cognitive decline. The authors suggest interventions targeting socioeconomic risk factors may be most effective early, before neurodegenerative changes begin.
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To develop a simplified smell test for identifying patients with Parkinson's disease (PD), we reevaluated the Sniffin'-Sticks-Identification-Test (SST-ID) and University-of-Pennsylvania-Smell-Identification-Test (UPSIT), using three case-control studies.
Why it matters
This study developed a simplified 7-odorant smell test that performed similarly to longer tests in distinguishing Parkinson's disease and dementia with Lewy bodies from healthy controls. It is a diagnostic aid for these conditions, not a treatment, cure or prevention for Alzheimer's disease.
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Population-based evidence directly linking liver diseases to brain disorders is limited, and its genetic and biochemical associations remain unclear.
Why it matters
This cohort study found that people with alcoholic liver disease, non-alcoholic fatty liver disease, and viral hepatitis had poorer cognition and higher risks of dementia and other brain disorders. It suggests that liver diseases are risk factors for brain disorders, with genetic and biochemical factors contributing, but it does not show that treating liver disease prevents dementia.
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In older adults, trazodone is frequently prescribed for anxiety and insomnia owing to its perceived greater tolerability in comparison with benzodiazepines.
Why it matters
In this small longitudinal study of older hypertensive outpatients, trazodone use was linked to a greater drop in blood pressure on standing and a higher rate of syncope and falls. It is an observational study of a medication's risks, not a treatment or cure for Alzheimer's disease.
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54/100
Lung macrophages play a pivotal role in pulmonary fibrosis, with monocyte-derived alveolar macrophages driving disease progression.
Why it matters
This study found TREM2 is elevated on lung macrophages in fibrosis and that deleting or knocking down the receptor disrupted their survival signaling. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Of 1441 plasma proteins surveyed, a 12-protein signature significantly predicted cognitive decline (q-value < .05).
Why it matters
A 12-protein plasma signature significantly predicted cognitive decline, and ten proteins independently predicted incident dementia, with a combined model improving prediction. Four markers were replicated in an independent cohort's cerebrospinal fluid, but further studies are needed to explore therapeutic implications.
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54/100
While macrophage heterogeneity during metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood.
Why it matters
This study concerns metabolic dysfunction-associated steatohepatitis, showing that TREM2+ macrophages are important for fibrosis resolution in the liver. It provides no information about treating, curing or preventing Alzheimer's disease.
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Alzheimer's disease (AD) and dementia in general are age-related diseases with multiple contributing factors, including brain inflammation.
Why it matters
Using high-throughput mass cytometry in mice, this study identified senescent microglia (the brain's immune cells) that carry high levels of the Alzheimer's risk gene TREM2 but are distinct from the better-known "disease-associated microglia." The same protein signature appeared in old mice and in mouse models of amyloid and tau build-up that show cognitive decline, and mice lacking TREM2 had fewer of these cells. This is mouse-only research that links TREM2 to an aging-like microglial state; it does not show cause in people or test any treatment.
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Tauopathies are age-associated neurodegenerative diseases whose mechanistic underpinnings remain elusive, partially due to a lack of appropriate human models.
Why it matters
Using human induced pluripotent stem cell-derived neurons expressing 4R Tau and 4R-P301S Tau, this study identified over 500 genetic modifiers of seeding-induced tau propagation, including retromer VPS29 and genes in the UFMylation cascade, and found the UFMylation cascade altered in tangle-bearing neurons in progressive supranuclear palsy and Alzheimer's disease brains. Inhibiting the UFMylation cascade suppressed tau propagation in vitro and in vivo, but this is a laboratory model providing a platform for identifying strategies rather than a proven treatment.
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The defining feature of Parkinson disease (PD) and Lewy body dementia (LBD) is the accumulation of alpha-synuclein (Asyn) fibrils in Lewy bodies and Lewy neurites.
Why it matters
This laboratory study determined the atomic structure of alpha-synuclein fibrils from Lewy body dementia tissue, which may aid study of disease mechanisms, imaging agents and therapeutics. It is early structural research and does not test any treatment, cure or prevention in patients.
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Triggering receptor expressed on myeloid cells 2 (Trem2) is a myeloid cell-specific gene expressed in brain microglia, with variants that are associated with neurodegenerative diseases, including Alzheimer's disease.
Why it matters
In developing mice, lacking Trem2 left neurons in one part of the hippocampus with compromised energy metabolism and abnormal mitochondria. This is early animal work on brain development and does not show that any treatment prevents or cures Alzheimer's disease.
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In the field of neurodegeneration, speech and language assessments are useful for diagnosing aphasic syndromes and for characterizing other disorders.
Why it matters
This paper calls for cross-linguistic research to address inequity in speech and language markers for neurodegenerative diseases, noting that most studies focus on English-speaking cohorts. It is a call for global equity in research and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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Developing a single-domain assay to identify individuals at high risk of future events is a priority for multi-disease and mortality prevention.
Why it matters
Using 1,461 blood proteins measured in 52,006 UK Biobank participants, researchers trained a neural network risk score (ProRS) that separated people by future risk for 45 conditions. Dementia was one of 10 endpoints where accuracy was high (C-index above 0.80), and the score matched or beat established clinical indicators for almost all endpoints. The authors say it was validated only inside UK Biobank and needs independent testing before clinical use; it predicts risk and does not treat or prevent Alzheimer's disease.
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Neurodegenerative disorders, including Alzheimer's disease, are associated with microgliosis.
Why it matters
This review discusses the idea that stimulating TREM2 with agonistic antibodies could be a therapeutic option, based on evidence that some microglial genes have protective functions. It is a review of a proposed approach, not a tested treatment, and reports no cure or prevention.
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Neurofilament light chain (NfL) is a promising biomarker for risk stratification and disease monitoring of dementia, but its utility in the preclinical disease stage remains uncertain.
Why it matters
In 4,705 dementia-free people, higher plasma neurofilament light was linked to worse baseline cognition, faster decline on one task, and poorer white matter integrity, but not to gray matter volumes or thickness. This concerns a marker of brain injury and risk, not a treatment, cure or prevention.
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LBD/A+T+ and AD cases showed significantly increased CSF levels of synaptic and neuroaxonal biomarkers compared with LBD/A-T- and control subjects.
Why it matters
In patients with Lewy body disease, several CSF synaptic and neuroaxonal markers did not differ from controls but were increased in Alzheimer's disease, and one marker was decreased only in a specific subgroup. This is about using CSF markers to detect co-occurring Alzheimer's pathology in Lewy body disease, not about treating, curing or preventing it.
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The apolipoprotein E4 (APOE4) allele is associated with an increased risk of Alzheimer disease and a decreased risk of glaucoma, but the underlying mechanisms remain poorly understood.
Why it matters
In two mouse glaucoma models, microglia shifted to a neurodegenerative state, and mice lacking Apoe in microglia or carrying the human APOE4 allele were protected from retinal ganglion cell loss. Targeting the APOE-Galectin-3 pathway reduced retinal degeneration, suggesting it could be a treatment target for glaucoma.
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Heart failure (HF) is a frequent consequence of myocardial infarction (MI).
Why it matters
This study looked at immune cells in mouse hearts after a heart attack, not in Alzheimer's disease. It provides no information about treating, curing or preventing Alzheimer's.
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54/100
Significant progress has been made in understanding the pre-symptomatic phase of amyotrophic lateral sclerosis.
Why it matters
This paper reviews lessons from the pre-symptomatic phase of amyotrophic lateral sclerosis, not Alzheimer's disease, and notes challenges with using non-genetic biomarkers such as counselling and consent. It offers no findings on treating, curing or preventing Alzheimer's disease.
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Amyotrophic lateral sclerosis overlapping with frontotemporal dementia (ALS/FTD) is a fatal and currently untreatable disease characterized by rapid cognitive decline and paralysis.
Why it matters
This study developed a human brain organoid slice model that shows early molecular pathology of C9ORF72 ALS/FTD and reveals early astrocyte and neuronal changes. It is a laboratory model of ALS/FTD, not Alzheimer's disease, and is early research that does not yet provide a treatment or cure.
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Upon demyelinating injury, microglia orchestrate a regenerative response that promotes myelin repair, thereby restoring rapid signal propagation and protecting axons from further damage.
Why it matters
In male mice, this study showed that cholesterol esterification and lipid droplet formation in microglia and macrophages are needed to clear myelin debris and support remyelination. It concerns myelin repair in mice and provides no information about treating, curing or preventing Alzheimer's.
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Overall visual ratings showed complete concordance between radiotracers for both the medial temporal lobe and the neocortex.
Why it matters
This study compared two tau PET tracers and found they performed equally well in visual interpretation, with one showing a greater dynamic range in signal estimates. It is about imaging tools and does not test any treatment, cure, or prevention.
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Neurodegeneration occurring in multiple sclerosis (MS) contributes to the progression of disability.
Why it matters
This study found that oxidized phosphatidylcholines in multiple sclerosis lesions drive neurodegeneration, which was ameliorated by microglia in cultured cells and after injection into mouse spinal cords. It concerns multiple sclerosis, not Alzheimer's disease, and reports no Alzheimer's 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.
- Genetic modification of the phenotypes produced by amyloid precursor protein overexpression in transgenic mice
- Effect of chronic high-dose exogenous cortisol on hippocampal neuronal number in aged nonhuman primates
- TREM2 shedding by cleavage at the H157-S158 bond is accelerated for the Alzheimer's disease-associated H157Y variant
- The spectrum of hippocampal sclerosis: a quantitative magnetic resonance imaging study
- Peripheral GFAP and NfL as early biomarkers for dementia: longitudinal insights from the UK Biobank
- Small-molecule PET Tracers for Imaging Proteinopathies
- Brain network efficiency is influenced by the pathologic source of corticobasal syndrome
- Truncated stathmin-2 is a marker of TDP-43 pathology in frontotemporal dementia
- Experimental evidence for temporal uncoupling of brain Aβ deposition and neurodegenerative sequelae
- Association of Plasma Neurofilament Light With Small Vessel Disease Burden in Nondemented Elderly: A Longitudinal Study