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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& aims The combination of atezolizumab and bevacizumab (atezo+bev) is the current standard of care for advanced hepatocellular carcinoma (HCC), providing a median overall survival (OS) of 19.2 months.
Why it matters
This study used single-cell RNA sequencing to define response patterns to atezolizumab plus bevacizumab in advanced liver cancer. It does not study Alzheimer's disease and provides no information on treating, curing or preventing it.
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Microglia are central players in Alzheimer's disease pathology but analyzing microglial states in human brain samples is challenging due to genetic diversity, postmortem delay and admixture of pathologies.
Why it matters
Human stem cell-derived microglia grown inside the brains of amyloid-model mice (138,577 single cells profiled) took on a disease-associated profile like mouse microglia, but with a stronger HLA state the authors call "likely related to antigen presentation in response to amyloid plaques", plus a pro-inflammatory cytokine/chemokine response to Aβ oligomers. Deleting TREM2 or APOE, or using APOE variants or TREM2 R47H in the transplanted cells, changed these responses in different ways. This is a cell-in-mouse study with no patients and no treatment tested, so it describes how human immune cells react, not a way to prevent or treat Alzheimer's.
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Triggering receptor expressed on myeloid cells 2 (TREM2) plays a critical role in microglial activation, survival, and apoptosis, as well as in Alzheimer's disease (AD) pathogenesis.
Why it matters
This genome-wide association study in 3,350 individuals identified four loci for cerebrospinal fluid sTREM2, including two independent missense variants in the MS4A locus. This is a genetic association study, so it does not show whether modifying these variants would treat, cure or prevent Alzheimer's disease.
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59/100
Amyloid-related imaging abnormalities (ARIA) were the most common adverse events reported in the phase 3 ENGAGE and EMERGE trials of aducanumab, an anti-amyloid monoclonal antibody.
Why it matters
This study performed genome-wide association studies of amyloid-related imaging abnormalities (ARIA) in participants in the aducanumab phase 3 ENGAGE and EMERGE trials, since APOE ε4 carrier status was already known to increase ARIA risk. It looks at genetic risk factors for a side effect of treatment, not at whether the drug cures or prevents Alzheimer's disease.
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Identifying therapeutics to delay, and potentially reverse, age-related cognitive decline is critical in light of the increased incidence of dementia-related disorders forecasted in the growing older population 1 .
Why it matters
In aged male mice, platelet factors from young blood plasma reduced hippocampal neuroinflammation and improved hippocampal-dependent cognitive impairments. This is an animal study, so it does not yet show that the same approach treats or prevents Alzheimer's disease in people.
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Plasma β-synuclein demonstrated discriminative properties for Aβ PET positive and negative subjects.
Why it matters
Blood β-synuclein levels were higher in people with amyloid PET positivity and could predict amyloid status in those with mild cognitive impairment. The authors state β-synuclein is not a direct marker of amyloid pathology, so it reflects synaptic degeneration rather than the amyloid deposits themselves.
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These findings suggest an association of sHHV infection with white matter volume loss, attentional decline, and astrogliosis.
Why it matters
In 1,009 mostly cognitively normal older adults, having a symptomatic herpes virus diagnosis was linked to greater loss of white matter volume over time and to faster cognitive decline. This is an observational cohort study and does not show that treating or preventing herpes viruses would treat, cure or prevent Alzheimer's disease.
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To test whether cerebrospinal fluid (CSF) growth-associated protein 43 (GAP-43) concentration is elevated in Alzheimer's disease (AD) dementia and its associations with other hallmarks of AD, we examined the CSF GAP-43 measurements of 787 participants (245 cognitively normal (CN), 415 individuals with mild cognitive impairment (MCI) and 127 individuals with AD dementia) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study.
Why it matters
This study found that a protein called GAP-43 in spinal fluid was higher in people with Alzheimer's dementia and was linked to tau pathology. It is about a potential biomarker for diagnosis and monitoring, not a treatment, cure, or prevention.
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There is an urgent need to improve the understanding of neuroinflammation in Alzheimer's disease (AD).
Why it matters
This study found that certain cerebrospinal fluid inflammatory proteins, including sAXL and sTyro3, were linked to better brain structure and cognitive outcomes in people with Alzheimer's disease. It is an observational study and does not show that targeting these proteins would treat or prevent the disease.
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Traumatic brain injury (TBI) constitutes one of the strongest environmental risk factors for several progressive neurodegenerative disorders of cognitive impairment and dementia that are characterized by the pathological accumulation of hyperphosphorylated tau (p-Tau).
Why it matters
Mice given a closed head injury once daily for 5 consecutive days developed tau build-up that progressed over 1 to 24 weeks, including around blood vessels, a feature considered defining of chronic traumatic encephalopathy in people. A linked literature review found that less than 1% of mouse head-injury studies (25/3756) reported tau using immunostaining, and only 3 reported tau around blood vessels. The authors say the model replicates key human features, making it a useful tool for studying how head injury leads to tau disease, although these are mouse results.
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59/100
Clear cell renal carcinoma (ccRCC) is a heterogeneous disease with a variable post-surgical course.
Why it matters
This study analyzed macrophages in kidney cancer, not Alzheimer's disease. It provides no information about treating, curing, or preventing Alzheimer's disease.
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Plasma NfL level is a valuable noninvasive biomarker that supplements magnetic resonance imaging scans and possibly reflects the severity of CSVD burden.
Why it matters
In this longitudinal study of 496 nondemented participants, higher plasma neurofilament light levels were associated with a greater burden of cerebral small vessel disease. It does not report any treatment, cure, or prevention of Alzheimer's disease.
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59/100
We identified individuals with an incident diagnosis of PD (n=1276) and controls (n=500 406) in UK Biobank.
Why it matters
This study investigated environmental and prodromal risk factors for Parkinson's disease and whether genetic risk scores improve prediction. It concerns Parkinson's disease, not Alzheimer's disease, and does not test any treatment, cure, or prevention for Alzheimer's.
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Immune-regulatory mechanisms of drug-free remission in rheumatoid arthritis (RA) are unknown.
Why it matters
This study used single-cell transcriptomics to profile synovial tissue macrophages in rheumatoid arthritis. It concerns rheumatoid arthritis and does not test any treatment, cure or prevention for Alzheimer's disease.
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Cerebrospinal fluid (CSF) biomarkers are useful in the diagnosis and the prediction of progression of several neurodegenerative diseases.
Why it matters
In this cohort, all neurodegenerative diseases studied showed increased CSF neurofilament light chain, with the highest levels in ALS, frontotemporal dementia, corticobasal syndrome, and progressive supranuclear palsy, and levels were associated with cognitive impairment in the AD and FTD spectrum. These are marker findings and do not test any treatment, cure, or prevention.
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Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease and affects 1% of the population above 60 years old.
Why it matters
In this cross-sectional study, soluble TREM2 was elevated in Parkinson's disease subgroups that also had increased tau in cerebrospinal fluid. This links TREM2 to tau-related changes in Parkinson's, but it is an observational finding and not a treatment or prevention result for Alzheimer's.
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Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repeated subconcussive and concussive head injury.
Why it matters
Chronic traumatic encephalopathy (CTE), a tau disease tied to repeated head blows, can currently only be confirmed after death, so this review examined seven brain-imaging studies, mostly of professional athletes. Several scan measures differed between suspected CTE and controls, and tau-binding PET was the most promising because it separated CTE from both controls and Alzheimer's disease. The authors say combining imaging methods should improve accuracy, which may eventually allow diagnosis in living people.
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The innate immune system is implicated in Parkinson's disease (PD), but peripheral in-vivo clinical evidence of the components and driving mechanisms involved and their relationship with clinical heterogeneity and progression to dementia remain poorly explored.
Why it matters
In 41 people with Parkinson's disease grouped by dementia risk, researchers measured monocyte subsets, surface markers and serum markers including alpha-synuclein and caspase-1. This is a small observational study about immune signals in Parkinson's disease and does not directly inform Alzheimer's treatment, cure or prevention.
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Recently, increasing evidence has suggested the association between gut dysbiosis and Alzheimer's disease (AD) progression, yet the role of gut microbiota in AD pathogenesis remains obscure.
Why it matters
In mouse models, GV-971 (sodium oligomannate) suppressed gut dysbiosis and neuroinflammation and reversed cognition impairment, and elevated phenylalanine and isoleucine and increased Th1 cells were also seen in two small cohorts of patients with mild cognitive impairment due to Alzheimer's disease. Much of this work is in animals and small human cohorts, and it reports no cure or prevention.
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Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been associated with increased risk for sporadic, late-onset Alzheimer's disease.
Why it matters
In mice, removing Trem2 or carrying the R47H variant reduced microglia around amyloid plaques and allowed neuritic plaque tau aggregates to seed and spread more easily. This shows TREM2 and microglia help limit tau pathology near plaques, but it is animal work.
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Delirium following surgery is common and associated with adverse outcomes.
Why it matters
In this cohort of older adults having elective hip or knee surgery, low cerebrospinal fluid beta-amyloid 1-42 was independently associated with postoperative delirium. The authors suggest delirium after surgery may be an early sign of Alzheimer disease, but this does not show any way to treat or prevent it.
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Our search resulted in the inclusion and full-text review of 137 articles.
Why it matters
This review of 137 articles found wide variation in how white matter hyperintensities were segmented and that only a minority of studies gave a clear definition of them. It calls for standardization of definitions and methods and reports no treatment, cure, or prevention findings.
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Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy that is associated with repetitive head impacts or exposure to blast waves.
Why it matters
This laboratory study used cryo-electron microscopy to determine the structure of tau filaments from the brains of three people with chronic traumatic encephalopathy, finding they differ from those in Alzheimer's disease. It describes filament structure and notes that no disease-modifying therapies currently exist, so it reports no treatment, cure or prevention.
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Forty-one women who underwent BSO and 49 control participants were recruited.
Why it matters
In this study of 41 women who had bilateral salpingo-oophorectomy before menopause and 49 control participants, amygdala volume was smaller in the surgery group, suggesting that abrupt hormonal changes may lead to medial temporal lobe structural abnormalities later in life. It is an observational finding and does not show that any treatment, cure or prevention for Alzheimer's disease works.
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The 751 study participants were older (median age [interquartile range], 87 years [51-105 years]), 395 (54%) were women, and 324 (44%) were APOE ε4 carriers.
Why it matters
In 738 autopsied people from Mayo Clinic research programmes who had Alzheimer-type brain changes, carrying the APOE ε4 gene variant was linked to TDP-43, a protein associated with hippocampal shrinkage and cognitive decline. The link was statistically significant in people whose brains had intermediate-to-high Alzheimer's likelihood (604 people), but not in the smaller low-likelihood group (134 people, P = .10). This is an association from brain tissue after death, not proof that ε4 causes TDP-43 build-up, and it reports no treatment 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.
- Neighborhood environmental deprivation predicts the generalized neurocognitive deficit in schizophrenia
- Amyloid β causes excitation/inhibition imbalance through dopamine receptor 1-dependent disruption of fast-spiking GABAergic input in anterior cingulate cortex
- Distinct Sensitivity of MRI Versus [ 18 F]FDG‐PET To Detect Cerebral Changes Across the Alzheimer's Continuum in Down Syndrome: A Multimodal Imaging Study
- The association between neighborhood deprivation and DNA methylation in an autopsy cohort
- Microglial Reactivity Correlates with Presynaptic Loss Independent of β-Amyloid and Tau
- The expression of microRNA miR-107 decreases early in Alzheimer's disease and may accelerate disease progression through regulation of beta-site amyloid precursor protein-cleaving enzyme 1
- Alterations in stress granule dynamics driven by TDP-43 and FUS: a link to pathological inclusions in ALS?
- Association Between Life's Simple 7 and Noncardiovascular Disease: The Multi-Ethnic Study of Atherosclerosis
- Cerebrospinal fluid neurofilament concentration reflects disease severity in frontotemporal degeneration
- Inhibiting Glycogen Synthase Kinase 3 Suppresses TDP-43-Mediated Neurotoxicity in a Caspase-Dependent Manner