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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Apolipoprotein (APOE) e4 genotype is an accepted risk factor for accelerated cognitive aging and dementia, though its neurostructural substrates are unclear.
Why it matters
This cross-sectional UK Biobank study examined whether carrying the APOE e4 allele is associated with brain imaging measures such as white matter hyperintensity volume. It reports associations with brain structure only, so it does not show that treating or preventing anything changes Alzheimer's disease.
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Atherosclerotic lesions are known for their cellular heterogeneity, yet the molecular complexity within the cells of human plaques has not been fully assessed.
Why it matters
This study used single-cell RNA and ATAC sequencing on human carotid atherosclerotic plaques and identified 14 cell populations. It concerns atherosclerosis and does not test any treatment, cure or prevention for Alzheimer's disease.
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Innate immunity is associated with Alzheimer's disease 1 , but the influence of immune activation on the production of amyloid-β is unknown 2,3 .
Why it matters
This work identifies IFITM3 as a protein that binds to γ-secretase and increases amyloid-β production when inflammatory cytokines induce it in neurons and astrocytes. The findings are about a mechanism in cells and mouse models, not a proven treatment, cure, or prevention for people.
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Braak stages of tau neurofibrillary tangle accumulation have been incorporated in the criteria for the neuropathological diagnosis of Alzheimer's disease.
Why it matters
This study evaluated 18F-MK-6240 PET for detecting tau tangles and notes that first-generation tau PET agents had low sensitivity for early Braak stages. It is about imaging, not about treating, curing or preventing Alzheimer's disease.
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Checkpoint immunotherapy unleashes T cell control of tumors, but is undermined by immunosuppressive myeloid cells.
Why it matters
This study found that Trem2-/- mice were more resistant to tumor growth and more responsive to anti-PD-1 immunotherapy, and anti-TREM2 treatment curbed tumor growth in combination with anti-PD-1. It concerns cancer immunotherapy and does not test any treatment, cure or prevention for Alzheimer's disease.
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Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) triggered by autoimmune mechanisms.
Why it matters
This study examined TREM2 in myelin debris clearance in multiple sclerosis, not Alzheimer's disease. It does not test any Alzheimer's treatment, cure, or prevention.
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58/100
Neuronal circuit assembly requires the fine balance between synapse formation and elimination.
Why it matters
Brain immune cells called microglia trim away extra synapses as brain circuits form, but what marks a synapse for removal was "still undefined." In lab dishes of hippocampal neurons grown with microglia, this study reports that phosphatidylserine exposed on the neuron surface acts as an "eat-me" signal. Covering it up with Annexin V, or removing the receptor TREM2 from microglia, only "partially" prevented synapse removal. This is basic biology of normal brain development, not an Alzheimer's study or a treatment.
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Tissue-resident and recruited macrophages contribute to both host defense and pathology.
Why it matters
This study examines how macrophages diversify in diet-induced non-alcoholic steatohepatitis in the liver, including induction of Trem2 expression. It is about liver disease, not Alzheimer's, and offers no treatment insight.
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The AD set included 23,092 cases and 30,920 controls, the ALS set included 7391 cases and 12,442 controls, and the PD set included 8498 patients and 9161 controls.
Why it matters
Pooling 35 studies, this meta-analysis found that the R47H variant of the TREM2 gene was associated with a higher risk of Alzheimer's, but not of ALS or Parkinson's disease. The authors suggest this points to different disease processes behind different neurodegenerative conditions, helping place TREM2 specifically within Alzheimer's biology.
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Although white matter hyperintensities have traditionally been viewed as a marker of vascular disease, recent pathology studies have found an association between white matter hyperintensities and Alzheimer's disease pathologies.
Why it matters
In 434 participants without dementia, this study examined which white matter hyperintensity regions on MRI were associated with amyloid and tau on PET. It is an imaging association study and does not test any treatment, cure or prevention.
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Cell-cell communication via ligand-receptor signaling is a fundamental feature of complex organs.
Why it matters
This study used single-cell RNA sequencing of mouse liver cells and identified NASH-associated macrophages marked by high TREM2 expression. It concerns liver disease and does not test any treatment, cure or prevention for Alzheimer's disease.
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This study reviewed the structure, function, analytical aspects, and age-dependent normal ranges of neurofilaments, providing a comprehensive overview of neurofilament light chain as a marker of axonal injury across various neurological disorders.
Why it matters
A review of neurofilaments as biomarkers in neurological disorders.
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A major challenge in the field of neurodegenerative diseases and brain aging is to identify the body's intrinsic mechanism that could sense the central nervous system (CNS) damage early and protect the brain from neurodegeneration.
Why it matters
This paper proposes that microglia use a sensory mechanism, including the Trem2 signaling pathway, to detect damage in the brain. It is a proposal based on accumulating evidence, not a demonstrated treatment or cure.
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Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms.
Why it matters
In plasma samples from 28 Alzheimer's disease patients and matched controls, astrocyte-derived exosomes showed higher levels of several complement proteins. This is a small study of a possible inflammatory mechanism and does not show that targeting complement would treat, cure, or prevent Alzheimer's disease.
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The mechanisms underpinning concussion, traumatic brain injury, and chronic traumatic encephalopathy, and the relationships between these disorders, are poorly understood.
Why it matters
This study examined brain injury and tau pathology in young athletes after concussion and in a mouse model of impact head injury, not Alzheimer's disease treatment. It does not test any Alzheimer's treatment, cure, or prevention.
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In idiopathic normal pressure hydrocephalus, we found delayed enhancement (P < 0.05) and decreased clearance of gadobutrol (P < 0.05) at the Sylvian fissure.
Why it matters
In people with idiopathic normal pressure hydrocephalus, this study found delayed enhancement and decreased clearance of gadobutrol at the Sylvian fissure. It reports a finding about fluid clearance in that condition, not a treatment, cure, or prevention for Alzheimer's disease.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and overlapping clinical and pathological features.
Why it matters
This study identified TIA1 mutations in ALS and frontotemporal dementia that alter stress granule dynamics and promote TDP-43 accumulation. It concerns ALS and frontotemporal dementia, not Alzheimer's disease, and does not test any treatment, cure, or prevention.
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In this study, we report the experience of the only reference clinical next-generation sequencing lab in Saudi Arabia with the first 1000 families who span a wide-range of suspected Mendelian phenotypes.
Why it matters
This report describes genetic testing in 1000 Saudi Arabian families with suspected inherited disorders, finding disease-causing variants in 34% and suggesting that more may be found if candidate genes are confirmed. It is about genetic diagnosis broadly, not about treating, curing, or preventing Alzheimer's disease.
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Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of clinical symptoms.
Why it matters
In a mouse model of tauopathy, T cells entered the hippocampus and were linked to neuroinflammation and cognitive decline. This is animal research, so it does not yet show a treatment or cure for people.
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Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and frontotemporal lobar dementia are among the most pressing problems of developed societies with aging populations.
Why it matters
This review suggests that neuroinflammation, involving glial cells and the blood-brain barrier, contributes to neurodegeneration in diseases including Alzheimer's disease, and that therapies targeting glial cells might help. It is a discussion of a possible approach, not a proven treatment, cure or prevention.
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Genetic mutations in TAR DNA-binding protein 43 (TARDBP, also known as TDP-43) cause amyotrophic lateral sclerosis (ALS), and an increase in the presence of TDP-43 (encoded by TARDBP) in the cytoplasm is a prominent histopathological feature of degenerating neurons in various neurodegenerative diseases.
Why it matters
In neurons from people with ALS or frontotemporal dementia, TDP-43 accumulated in mitochondria and impaired respiratory complex I, and blocking this mitochondrial localization improved phenotypes in mutant TDP-43 mice. This is laboratory and animal work proposing a possible therapeutic target, not a proven treatment for patients.
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Physical and cognitive exercise may prevent or delay dementia in later life but the neural mechanisms underlying these therapeutic benefits are largely unknown.
Why it matters
In this trial of 100 older adults with mild cognitive impairment, progressive resistance training but not computerized cognitive training significantly improved global cognition and reversed progression of white matter hyperintensities, while cognitive training but not resistance training attenuated memory decline. The findings indicate physical and cognitive training work through different mechanisms, but this addresses delay or prevention rather than cure.
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58/100
Neuronal inclusions of poly(GA), a protein unconventionally translated from G4C2 repeat expansions in C9ORF72, are abundant in patients with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) caused by this mutation.
Why it matters
In this mouse study, animals with poly(GA) pathology showed neurodegeneration and behavioral abnormalities resembling frontotemporal dementia and ALS, and the poly(GA) clumps trapped HR23 and nucleocytoplasmic transport proteins. This is animal research on C9ORF72-related disease, not Alzheimer's disease, and does not test any treatment, cure, or prevention for Alzheimer's.
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SEE THAL AND VANDENBERGHE DOI101093/BRAIN/AWW057 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Post-mortem Braak staging of neurofibrillary tau tangle topographical distribution is one of the core neuropathological criteria for the diagnosis of Alzheimer's disease.
Why it matters
In 173 older adults ranging from cognitively normal to Alzheimer's disease, scans with the tau PET tracer 18F-AV-1451 could be sorted into patterns resembling the Braak stages that pathologists use after death: a simple set of rules gave a "plausible" stage for 149 people (86%), and 12 more (7%) showed predefined variant patterns. The estimated stage was significantly associated with amyloid status, diagnosis and global cognition. The study reports no comparison with autopsy and no follow-up scans, so it shows that tau PET can look like Braak staging, not that it measures a person's stage. It is an imaging method, not a treatment.
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The impact of APOE4 on brain metabolism and structure is modified by sex.
Why it matters
In healthy elderly controls, APOE4 carriers had lower CSF amyloid-beta1-42 and higher CSF p-tau181p than non-carriers, with no APOE-by-sex interaction on these CSF markers. However, there was a significant APOE-by-sex interaction on brain metabolism and structure, with female APOE4 carriers showing more widespread hypometabolism and cortical thinning than male carriers.
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.
- Specific Resting-State Brain Networks in Mesial Temporal Lobe Epilepsy
- Hippocampal atrophy in major depression: a function of childhood maltreatment rather than diagnosis?
- Neurodegenerative and neurological disorders by small inhaled particles
- Neuroprotective role of Origanum majorana essential oil loaded in mixed surfactants based nano emulsion against lipopolysaccharide-induced Alzheimer in mice
- Systematic review of differentially abundant proteins in people with Lewy body dementia
- Evaluating the impact of age and treatment on neuroinflammation-related proteins in mouse models of proteinopathies
- Corticonigral degeneration with neuronal achromasia presenting with primary progressive aphasia: ultrastructural and immunocytochemical studies
- Olfactory impairment predicts cognitive decline in early Parkinson's disease
- Homozygous TREM2 mutation in a family with atypical frontotemporal dementia
- Human early-onset dementia caused by DAP12 deficiency reveals a unique signature of dysregulated microglia