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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Plasma p‐tau217 has clinical, neuroimaging, and neuropathological correlates in sporadic FTD and may identify FTD cases with AD co‐pathology.
Why it matters
In a sporadic frontotemporal dementia cohort, plasma Aβ42/Aβ40 showed no clinicopathological associations, while high p-tau217 was present in amnestic dementia, logopenic primary progressive aphasia and APOEε4 carriers and correlated with worse clinical scores and more severe AD co-pathology. The authors suggest plasma p-tau217 may identify frontotemporal dementia cases with AD co-pathology, which is a diagnostic finding and not a treatment, cure or prevention.
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Participants were 60 (range 44-74) years old with 38 (30-51) years' T1D duration.
Why it matters
Among 373 adults with type 1 diabetes, brain injury biomarkers did not show an Alzheimer's-like pattern, though higher NfL was linked to older predicted brain age and cognitive problems. The findings suggest early neurodegeneration in type 1 diabetes may involve non-amyloid mechanisms, and they do not address treating or preventing Alzheimer's disease.
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Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05).
Why it matters
In this cross-sectional study, adults with Down syndrome were more likely to have cerebral microbleeds than controls, and microbleed severity was associated with imaging and fluid Alzheimer disease biomarkers. The authors note that cerebral hemorrhages are an exclusion criterion and potential adverse effect of antiamyloid agents, so characterizing microbleeds matters for that context.
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Down syndrome (DS) is the most common condition with intellectual disability and is caused by trisomy of Homo sapiens chromosome 21 (HSA21).
Why it matters
This longitudinal study in Ts66Yah mice found behavioral changes at older age and altered hippocampal molecular pathways related to aging. It is an animal study that provides insights into how trisomy may contribute to brain pathology with aging, but it does not test any treatment or cure in people.
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55/100
Although heterogeneity of FAP+ Cancer-Associated Fibroblasts (CAF) has been described in breast cancer, their plasticity and spatial distribution remain poorly understood.
Why it matters
This study is about fibroblasts in breast cancer and their spatial organization in tumors, not Alzheimer's disease. It has no implications for treating, curing or preventing Alzheimer's disease.
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Atherosclerotic plaques are complex tissues composed of a heterogeneous mixture of cells.
Why it matters
This study maps the cell types in human carotid atherosclerosis, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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Deciphering the cell-state transitions underlying immune adaptation across time is fundamental for advancing biology.
Why it matters
This paper presents Zman-seq, a single-cell technology that time-stamps circulating immune cells and tracks them in tissues, and applies it to the immune microenvironment in glioblastoma. It concerns a brain tumour, not Alzheimer's disease, and provides no direct information about treating, curing or preventing Alzheimer's.
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Neuronal hyperactivity is a key feature of early stages of Alzheimer's disease (AD).
Why it matters
In cell and animal models, amyloid-beta oligomers made spines hyperactive and exposed phosphatidylserine, which microglia then recognized through TREM2. This is early laboratory work and does not establish a treatment, cure, or prevention for Alzheimer's disease in people.
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Natural killer (NK) cells are commonly reduced in human tumors, enabling many to evade surveillance.
Why it matters
This study is about lung cancer, where TREM2 in monocyte-derived macrophages suppressed NK cells and deleting Trem2 in mice allowed NK cell-mediated tumor regression. It does not concern Alzheimer's disease and reports no treatment for it.
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Loss-of-function variants of TREM2 are associated with increased risk of Alzheimer's disease (AD), suggesting that activation of this innate immune receptor may be a useful therapeutic strategy.
Why it matters
Researchers built a TREM2-activating antibody designed to cross the blood-brain barrier and tested it in mice and in human cells grown in the lab. This is early experimental work and does not show any benefit for treating Alzheimer's disease in people.
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CSF p-tau181 was increased in patients with NIID without amyloid accumulation.
Why it matters
CSF p-tau181 was elevated in patients with neuronal intranuclear inclusion disease, comparable to levels in Alzheimer disease, often with normal amyloid-beta42. This shows p-tau181 is not specific to Alzheimer disease and could complicate its use as a biomarker, but no treatment was tested.
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Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene are associated with increased risk for late-onset AD.
Why it matters
In mice, chronically increasing TREM2 signaling worsened amyloid-associated tau seeding and spreading, contrary to the researchers' hypothesis. This is animal research showing a harmful effect of one approach, not a treatment.
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In addition, hippocampal sclerosis was a common neuropathological comorbidity ( n = 5) and associated with limbic-predominant TDP-43 proteinopathy ( n = 4) or FTLD-TDP ( n = 1).
Why it matters
In this clinicopathological case series of people with repetitive head impacts and traumatic encephalopathy syndrome, hippocampal sclerosis was a common finding and was associated with TDP-43 proteinopathy. This concerns traumatic encephalopathy syndrome, not Alzheimer's disease, so it does not directly inform Alzheimer's treatment or prevention.
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The advent of PET ligands that bind tau pathology has enabled the quantification and visualization of tau pathology in aging and in Alzheimer disease (AD).
Why it matters
This review describes tau PET imaging, noting that the main tracers bind tau aggregates in more advanced Braak stages of Alzheimer's and that preliminary data suggest an elevated tau PET signal predicts cognitive decline over time. It is moving toward use as a diagnostic and possibly prognostic marker, but it is an imaging method and not a treatment or cure.
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Aβ(+) patients with TES (N = 10), but not Aβ(-) TES, had significantly higher plasma P-tau levels than HC (P-tau181: p d = 1.34; P-tau217: p d = 1.59).
Why it matters
In people with traumatic encephalopathy syndrome, plasma P-tau217 fairly distinguished those who were amyloid-positive from those who were amyloid-negative, while P-tau181 did not reach statistical significance. These blood markers may help identify Alzheimer disease pathology in this group, but the study was small and did not test any treatment.
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Inflammation and immune mechanisms are crucially involved in the pathophysiology of the development, acute damage cascades, and chronic course after ischemic stroke.
Why it matters
This review covers immune mechanisms in ischemic stroke and notes that anti-inflammatory drugs are being considered to prevent vascular events. It is about stroke, not Alzheimer's disease, and does not show any Alzheimer's treatment or prevention.
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Astrocytes are abundant glial cells in the central nervous system (CNS) that perform diverse functions in health and disease.
Why it matters
This review describes astrocyte dysfunction in Alzheimer disease and other conditions, and notes that astrocytes regulate glutamate, ion, cholesterol and sphingolipid balance. It is a review of astrocyte biology and reports no treatment, cure or prevention.
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Of 102 607 individuals in the study, 56 559 (55%) were women (median age, 58 years [IQR, 47-67 years]).
Why it matters
This study examined genetic cholesteryl ester transfer protein deficiency and its balance of long-term benefits and harms, including a genetically lower level of non-HDL cholesterol associated with lower cardiovascular mortality. It is about cholesterol genetics and cardiovascular outcomes, not about treating, curing, or preventing Alzheimer's disease.
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Triggering receptor expressed on myeloid cell 2 (TREM2) is linked to risk of neurodegenerative disease.
Why it matters
In mice, losing TREM2 reduced microglia's ability to clear abnormal TDP-43 protein and worsened nerve cell damage and movement problems. This is early animal work on TDP-43-related neurodegeneration, not a treatment or cure for Alzheimer's disease.
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Neurofilament light chain (NfL) and α-synuclein oligomeric seeds (α-syn-s) are promising biomarkers for patients with parkinsonism.
Why it matters
This study measured two biomarkers in spinal fluid and blood to see if they can tell Parkinson's disease apart from atypical parkinsonisms. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Patients with isolated rapid-eye-movement sleep behaviour disorder (RBD) are commonly regarded as being in the early stages of a progressive neurodegenerative disease involving α-synuclein pathology, such as Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy.
Why it matters
This review argues that reliable biomarkers are needed to predict which patients with isolated REM sleep behaviour disorder will develop an α-synucleinopathy such as Parkinson's disease or dementia with Lewy bodies. It also states that biomarkers of progression and subtype will be needed to monitor treatment response once disease-modifying therapies exist.
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55/100
No large-scale characterizations of neurofilament light chain (NfL) have been conducted in diverse populations.
Why it matters
Plasma neurofilament light chain levels were significantly associated with age and with medical co-morbidities common among older adults, which the authors say complicates its utility as a diagnostic biomarker. This is about a biomarker's limitations, not about treating, curing, or preventing Alzheimer's disease.
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In Alzheimer's disease (AD) models, AD risk variants in the microglial-expressed TREM2 gene decrease Aβ plaque-associated microgliosis and increase neuritic dystrophy as well as plaque-associated seeding and spreading of tau aggregates.
Why it matters
In mouse models, depleting microglia in animals with established brain amyloid did not affect amyloid but resulted in less spine and neuronal loss, and microglial repopulation in aged mice improved cognitive and neuronal deficits. This is animal work and does not yet show a treatment, cure or prevention for Alzheimer's disease in people.
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Stress granules are dynamic, reversible condensates composed of RNA and protein that assemble in eukaryotic cells in response to a variety of stressors and are normally disassembled after stress is removed.
Why it matters
In cultured human cells, disassembly of stress granules after heat shock required ubiquitination of G3BP1, which then interacted with FAF2 and p97/VCP. Impaired disassembly has been implicated in ALS, frontotemporal dementia and multisystem proteinopathy, but this cell study tests no treatment or prevention.
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'Covert' cerebral small vessel disease (ccSVD) is common on neuroimaging in persons without overt neurological manifestations, and increases the risk of future stroke, cognitive impairment, dependency, and death.
Why it matters
These guidelines found little direct evidence, mostly of low quality, about managing covert cerebral small vessel disease to prevent outcomes like cognitive decline or dementia. They recommend good blood pressure control in patients with this condition and hypertension, do not recommend antiplatelet drugs such as aspirin, and found no evidence for glucose control without diabetes or for conventional Alzheimer dementia treatments.
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.
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?
- Unaltered expression of Fas (CD95/APO-1), caspase-3, Bcl-2 and annexins in brains of fetal Down syndrome: evidence against increased apoptosis
- Neuregulin-1 and erbB4 immunoreactivity is associated with neuritic plaques in Alzheimer disease brain and in a transgenic model of Alzheimer disease
- Chitinase-3-like-1: a multifaceted player in neuroinflammation and degenerative pathologies with therapeutic implications
- COVID-19 and RA share an SPP1 myeloid pathway that drives PD-L1+ neutrophils and CD14+ monocytes
- Down syndrome fibroblast model of Alzheimer-related endosome pathology: accelerated endocytosis promotes late endocytic defects
- Chronic antidepressant treatment selectively increases expression of plasticity-related proteins in the hippocampus and medial prefrontal cortex of the rat
- Redox proteomics analysis to decipher the neurobiology of Alzheimer-like neurodegeneration: overlaps in Down's syndrome and Alzheimer's disease brain
- The low density lipoprotein receptor regulates the level of central nervous system human and murine apolipoprotein E but does not modify amyloid plaque pathology in PDAPP mice
- A single-nuclei RNA sequencing study of Mendelian and sporadic AD in the human brain