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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Understanding how plasma tau biomarkers are influenced by co-pathologies and comorbidities is crucial for their accurate implementation.
Why it matters
In 102 brain donors, plasma p-tau217 was associated with neurofibrillary tangles, and plasma tau levels decreased as Lewy body pathology progressed. This is a postmortem correlation study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Glymphatic activity in bvFTD correlated strongly with vascular dysfunction and astrocytic activation, and was associated with brain changes and clinical severity.
Why it matters
In behavioral variant frontotemporal dementia, glymphatic activity was strongly linked to vascular dysfunction and astrocyte activation, and these factors together related to brain changes and clinical severity. The findings describe complex relationships among these mechanisms but do not test or offer a treatment.
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Diabetes is a significant modifiable risk factor for cognitive dysfunction.
Why it matters
This is a protocol for a randomized trial comparing liraglutide, empagliflozin, and linagliptin for achieving mild cognitive impairment remission in people with type 2 diabetes. It has not yet produced results, so it cannot yet say whether any of these drugs treat, cure, or prevent Alzheimer's disease.
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The plasma PlGF level was significantly elevated in patients with SIVD compared with CUCs, and showed a high accuracy with an area under the curve of 0.893.
Why it matters
Plasma placental growth factor was higher in people with subcortical ischemic vascular dementia and was linked to worse cognition, partly through white matter hyperintensity volume. This is a potential diagnostic biomarker, not a treatment, and the study does not show that targeting it changes disease course.
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Pancreatic cancer (PC), particularly pancreatic ductal adenocarcinoma (PDAC), is a significant global health issue with high mortality rates.
Why it matters
This review is about the exposome and pancreatic cancer, including lifestyle and environmental risk factors for pancreatic ductal adenocarcinoma. It does not address Alzheimer's disease.
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46/100
TDP-43_SAA was positive in 29/65 patients with sporadic MND, 9/21 patients with genetic MND, 6/17 OND patients and 3/22 controls.
Why it matters
TDP-43 seeding activity was detected in olfactory mucosa from some patients with motor neuron disease, and plasma TDP-43 levels were higher in sporadic MND patients than controls and decreased as disease progressed. The authors state further research is needed, and this is a biomarker study, not a treatment or cure.
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• Patients with Parkinson's disease (PD) and cognitive impairment demonstrated a significantly greater burden of white matter hyperintensities (WMH), with the highest burden observed in those with PD dementia.
Why it matters
In people with Parkinson's disease, greater amounts of white matter hyperintensities were linked to worse cognitive scores, with the highest burden in those who had Parkinson's disease dementia. This is an observational study, so it cannot show whether these brain changes cause the cognitive problems or how to treat them.
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46/100
Excessive intake of dietary fats is strongly associated with an increased risk of various chronic diseases, such as obesity, diabetes, hepatic metabolic disorders, cardiovascular disease, chronic intestinal inflammation, and certain cancers.
Why it matters
This review is about how high-fat diets affect gut bacteria and chronic diseases such as obesity, diabetes and cardiovascular disease, not Alzheimer's disease, so it provides no information on Alzheimer's treatment, cure or prevention. It suggests probiotics as a possible add-on therapy for the effects of high-fat diets.
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Behavioral variant of Frontotemporal Dementia (bvFTD) and Bipolar Disorder (BD) share overlapping symptoms, complicating diagnosis.
Why it matters
This study found that miRNA signatures in neural-enriched extracellular vesicles can differentiate behavioral variant frontotemporal dementia from bipolar disorder, especially in C9orf72-related cases. The authors state that further research is needed to validate these findings and explore their clinical application, so this is not yet a treatment or cure.
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The maturation and stabilization of appropriate synaptic connections is a vital step in neural circuit development; however, the molecular signals underlying these processes are not fully understood.
Why it matters
In mice, astrocyte glypican 5 was required for normal synapse maturation and stabilization, and its absence caused structural and functional changes in brain connections. The authors note implications for disorders with altered synaptic function including Alzheimer's disease, but this is animal work and does not show a treatment.
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= 0.120). These findings suggest that DESH and high EI, often considered biomarkers for iNPH, may lack specificity and may be found in a subset of patients with PSP or LBD leading to unnecessary neurosurgery for iNPH.
Why it matters
This study found that DESH and high Evan's index, which are often considered biomarkers for idiopathic normal pressure hydrocephalus, may also appear in some patients with progressive supranuclear palsy or Lewy body dementia. This lack of specificity could lead to unnecessary neurosurgery for idiopathic normal pressure hydrocephalus.
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Genetic diversity in the apolipoprotein E (ApoE) gene has been identified as the major susceptibility genetic risk factor for sporadic Alzheimer’s disease (SAD).
Why it matters
This review states that the ApoE ε4 allele is a major risk factor for sporadic Alzheimer's disease while the ε2 allele is protective, and that ApoE affects amyloid clearance, tau pathology, and microglial responses. It summarizes existing knowledge and does not report a proven treatment, cure, or prevention.
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Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder.
Why it matters
In mouse models of amyloidosis and tauopathy, inhaled xenon changed microglia to an intermediate activation state, increased amyloid plaque compaction, reduced brain atrophy and neuroinflammation, and improved nest-building behavior. The authors say these results support translating xenon inhalation as a treatment for Alzheimer's disease, but this has not yet been shown in people.
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Neuraminidase 1 (NEU1) cleaves terminal sialic acids from sialoglycoproteins in endolysosomes and at the plasma membrane.
Why it matters
This laboratory work describes how the enzyme Neu1 affects microglia by changing sialylation of the Trem2 receptor. It is basic cell research about a possible mechanism and does not test any treatment in people.
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Metabolic changes play a crucial role in determining the status and function of macrophages, but how lipid reprogramming in macrophages contributes to tumor progression is not yet fully understood.
Why it matters
This study is about lipid-laden macrophages in human liver cancer, not Alzheimer's disease. It found these cells were linked to disease progression in liver cancer patients, but it provides no information on treating, curing or preventing Alzheimer's disease.
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Microglia are a specialized type of neuroimmune cells that undergo morphological and molecular changes through multiple signaling pathways in response to pathological protein aggregates, neuronal death, tissue injury, or infections.
Why it matters
This review states that human TREM2 mutations are associated with an increased risk of developing Alzheimer disease and that Trem2 plays dual roles in neuroinflammation and in disease-associated microglia. It reports no treatment tested in patients.
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Microglia, the brain's principal immune cells, have been implicated in the pathogenesis of Alzheimer's disease (AD), a condition shown to affect more females than males.
Why it matters
In aging mouse hippocampus, this study found female-biased neuroinflammation and microglial senescence. This is early animal work on aging and sex differences and does not show that any treatment prevents or cures Alzheimer's disease in people.
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Alzheimer's disease (AD) is the most common neurodegenerative disease, resulting in the loss of cognitive ability and memory.
Why it matters
TREM2 is a receptor found mainly on microglia, the brain's immune cells, and the review describes it as helping those cells grow, survive, move and clear away toxic substances and abnormal proteins. It reports that "the current academic view" sees TREM2 as protective in Alzheimer's, which makes it a candidate drug target at a time when, the authors note, most drugs "only provide symptom relief". This is a review of existing research: it names no tested treatment and reports no new results in patients.
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Microglia plays crucial roles in Alzheimer's disease (AD) development.
Why it matters
This study found that LILRB2 can negatively regulate TREM2 signaling and suppress microglia functions, and generated antagonistic LILRB2 antibodies to study these interactions. These are laboratory findings about microglial signaling and do not yet show a treatment, cure or prevention for Alzheimer's disease.
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Immune checkpoint blockade (ICB) has been improving patient outcomes of non-small cell lung cancer (NSCLC), but its effectiveness is highly subjective to individual tumor microenvironment.
Why it matters
This study is about non-small cell lung cancer and found that immunosuppressive TREM2-positive macrophages were linked to worse prognosis and poorer responses to anti-PD-1 immunotherapy. It has no relevance to treating, curing, or preventing Alzheimer's disease.
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The role of physical exercise in the prevention of Alzheimer's disease (AD) has been widely studied.
Why it matters
In APP/PS1 mice, long-term running exercise improved cognitive function and promoted microglial glucose metabolism and morphological plasticity in the hippocampus. It is an animal study, so it does not prove that exercise prevents or treats Alzheimer's disease in people.
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Progranulin (PGRN, encoded by the GRN gene) plays a key role in the development, survival, function, and maintenance of neurons and microglia in the mammalian brain.
Why it matters
This review describes progranulin's roles in neurons and microglia and notes that mutations reducing progranulin increase the risk of Alzheimer's and other diseases. It identifies a possible therapeutic target but reports no treatment that has been shown to cure or prevent Alzheimer's disease.
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Chronic psychological stress is one of the most important triggers and environmental risk factors for neuropsychiatric disorders.
Why it matters
This study examines microglial glucocorticoid receptors in female mice under chronic stress, not Alzheimer's disease. It provides no information on treating, curing or preventing Alzheimer's disease.
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There is an urgent need for objective markers of Alzheimer's disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression, and assess response to disease-modifying therapies.
Why it matters
In cerebrospinal fluid from 80 adults with Down syndrome, the synaptic protein VAMP-2 correlated with episodic memory, age and other Alzheimer-related markers. This is described as proof-of-concept for a potential marker of cognitive impairment, not a treatment, cure or prevention.
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Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are fatal neurodegenerative disorders that are thought to exist on a clinical and pathological spectrum.
Why it matters
This review describes how mutations in some genes causing frontotemporal dementia or ALS affect lysosome and endosome-lysosome function, linking lysosome dysfunction to these diseases. It concerns FTD and ALS mechanisms and offers no treatment, cure or prevention for Alzheimer's disease.
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.
- Microglia rescue neurons from aggregate-induced neuronal dysfunction and death through tunneling nanotubes
- Differential gene expression in ADAM10 and mutant ADAM10 transgenic mice
- Hippocampal abnormalities after prolonged febrile convulsion: a longitudinal MRI study
- Abundant tau filaments and nonapoptotic neurodegeneration in transgenic mice expressing human P301S tau protein
- Orexin-A is Associated with Increases in Cerebrospinal Fluid Phosphorylated-Tau in Cognitively Normal Elderly Subjects
- Brain perivascular macrophages: characterization and functional roles in health and disease
- beta-Amyloid-induced dynamin 1 degradation is mediated by N-methyl-D-aspartate receptors in hippocampal neurons
- Microstructural white matter changes in cognitively normal individuals at risk of amnestic MCI
- Tau Protein and Neurodegeneration
- Amyloid β-peptide is produced by cultured cells during normal metabolism