Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Triggering receptor expressed on myeloid cells 2 (TREM2) plays crucial roles in Alzheimer's disease (AD) by regulating microglia migration toward, and phagocytosis of oligomeric amyloid-β (oAβ) and amyloid plaques.
Why it matters
A TREM2 agonist antibody, made stronger by engineering, increased microglial phagocytosis and reduced amyloid pathology in a mouse model of Alzheimer's disease. This is animal research on a potential drug approach and has not been shown to work in people.
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We evaluated the relationship between baseline CSF p-tau181 and the rate of tau PET change in the temporal meta-ROI and entorhinal cortex (ERC) and how it varied by amyloid level (CSF Aβ42 or amyloid PET) among 143 individuals from the Mayo Clinic Study of Aging and Mayo Alzheimer Disease Research Center.
Why it matters
Among 143 people, higher CSF p-tau181 and amyloid markers were linked to faster tau PET accumulation, with the entorhinal cortex changing more in non-demented participants. This is an observational imaging study and does not test any treatment, cure, or prevention.
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Post-translational modifications (PTMs) have emerged as key modulators of protein phase separation and have been linked to protein aggregation in neurodegenerative disorders.
Why it matters
This laboratory work found that Casein kinase 1delta-mediated TDP-43 hyperphosphorylation or C-terminal phosphomimetic mutations reduced TDP-43 phase separation and aggregation, making condensates more liquid-like and dynamic, contrary to the usual assumption. It is early mechanistic research on TDP-43 in ALS and frontotemporal dementia and does not address treating, curing or preventing Alzheimer's disease.
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This study reveals an important role of astrocytic apoE3 and apoE4 on the deposition and accumulation of Aβ plaques as well as on certain Aβ-associated downstream effects.
Why it matters
In a mouse model of amyloidosis, selectively reducing astrocyte apoE3 and apoE4 strongly reduced amyloid-beta plaque deposition and produced less compact plaques. This is an animal study and reports no treatment, cure or prevention in people.
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Synucleinopathies are clinically and pathologically heterogeneous disorders characterized by pathologic aggregates of α-synuclein in neurons and glia, in the form of Lewy bodies, Lewy neurites, neuronal cytoplasmic inclusions, and glial cytoplasmic inclusions.
Why it matters
This review sorts the α-synuclein diseases into two groups: Lewy body disease (Parkinson's disease, Parkinson's disease with dementia and dementia with Lewy bodies) and multiple system atrophy. It describes how lab seeding tests such as RT-QuIC and PMCA "offer exciting opportunities for molecular diagnosis using readily accessible peripheral tissue samples," but it reports no accuracy figures. It also says "there are currently no disease-modifying therapies for the synucleinopathies," and it does not address Alzheimer's disease directly.
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Disrupted hippocampal performance underlies psychiatric comorbidities and cognitive impairments in patients with neurodegenerative disorders.
Why it matters
In postmortem human samples from several neurodegenerative diseases, adult-born dentate granule cells showed abnormal development and changes in differentiation markers. This describes what happens in disease tissue and does not establish a treatment or cure for Alzheimer's disease.
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Converting checkpoint inhibitor (CPI)-resistant individuals to being responsive requires identifying suppressive mechanisms.
Why it matters
This study targeted TREM2 on tumor-associated macrophages to improve cancer immunotherapy, not Alzheimer's disease. It does not test any Alzheimer's treatment, cure, or prevention.
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The increasing availability of single-cell data revolutionizes the understanding of biological mechanisms at cellular resolution.
Why it matters
This paper presents NEBULA, a fast statistical method for differential or co-expression analysis of large-scale multi-subject single-cell data. It is a computational tool and provides no direct information about treating, curing or preventing Alzheimer's disease.
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The primary cohort included 91 AAs and 868 NHWs.
Why it matters
This study compared cerebrospinal fluid soluble TREM2 levels and associated genetic variants between African American and non-Hispanic White participants. It describes racial differences in an immune-related marker, not a treatment, cure, or prevention for Alzheimer's disease.
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ApoE4, a strong genetic risk factor for Alzheimer disease, has been associated with increased risk for severe COVID-19.
Why it matters
In human stem cell models, ApoE4 was associated with a higher rate of SARS-CoV-2 infection in neurons and astrocytes, and remdesivir inhibited the infection in these cells. This is laboratory work about COVID-19 and ApoE4, not a study of treating or preventing Alzheimer disease.
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Triggering receptor expressed on myeloid cells 2 (TREM2) sustains microglia response to brain injury stimuli including apoptotic cells, myelin damage, and amyloid β (Aβ).
Why it matters
In 5XFAD mice, engaging TREM2 with the antibody hT2AB activated microglia, and the R47H variant impaired ligand binding and microglial responses to amyloid-β pathology. This is mouse work testing a tool antibody and does not demonstrate a treatment for people.
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52/100
Primary age-related tauopathy (PART) is a neurodegenerative entity defined as Alzheimer-type neurofibrillary degeneration primarily affecting the medial temporal lobe with minimal to absent amyloid-β (Aβ) plaque deposition.
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52/100
Identifying factors underlying resistance to immune checkpoint therapy (ICT) is still challenging.
Why it matters
This study found that TREM2-high macrophages and gamma-delta T cells were more common in melanoma patients who did not respond to immune checkpoint therapy. It is about cancer immunotherapy and provides no information about treating, curing or preventing Alzheimer's.
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52/100
The presubiculum captures unique AD-related biological variation that is not reflected in total hippocampal volume.
Why it matters
In 127 clinically normal older individuals, presubiculum volume linked amyloid and tau pathology to memory performance, with hippocampal amyloid modifying the relationship. This is an observational imaging study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Organelle-specific autophagy is one of the major subtypes of autophagy, selectively targeting different organelles for quality control.
Why it matters
This review discusses organelle-specific autophagy and its reported benefit in inflammatory disorders by removing damaged organelles and maintaining homeostasis. It is a general review and does not report any treatment, cure or prevention for Alzheimer's disease.
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This multimodal approach enhanced the system's performance and provided a clinically informative method for neuroimaging analysis.
Why it matters
In 44 people with behavioural-variant frontotemporal dementia and 60 healthy people scanned at three centres with different MRI setups, a fully automated computer pipeline combining brain-structure and resting-brain-activity scans sorted people into the right group 91% of the time (it caught 83.7% of patients and correctly cleared 96.6% of healthy people). The study compared patients only with healthy people, not with Alzheimer's or other conditions that look similar, so it shows promise for a research tool rather than a ready clinical test. It does not test any treatment, cure or prevention.
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Stress granules (SGs) form during cellular stress and are implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD).
Why it matters
In cell and motor neuron experiments, certain small molecules prevented the RNA-dependent recruitment of TDP-43 into stress granules, a process linked to ALS and frontotemporal dementia. This is early laboratory work and does not show any treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is the most common form of progressive and irreversible dementia, and accurate diagnosis of AD at its prodromal stage is clinically important.
Why it matters
This research developed a new method called radiomics to improve computer-aided diagnosis of Alzheimer's disease and mild cognitive impairment using brain scans. It is about improving diagnosis, not about treating, curing, or preventing the disease.
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Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death.
Why it matters
This review describes necroptosis, a regulated necrotic cell death mediated by RIPK1, RIPK3 and MLKL, and states that it promotes further cell death and neuroinflammation in several neurodegenerative diseases including Alzheimer disease. It explains a disease mechanism and reports no treatment, cure or prevention.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative diseases that overlap in their clinical presentation, pathology and genetics, and likely represent a spectrum of one underlying disease.
Why it matters
This review describes neuroinflammation in ALS and FTD, which overlap as a disease spectrum, and notes that inflammation appears early. It reports no treatment that cures or prevents these diseases.
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Alzheimer's disease (AD) is an intractable progressive neurodegenerative disease characterized by cognitive decline and dementia.
Why it matters
In a mouse model of Alzheimer's disease, the Caspase-1 inhibitor VX-765 reversed memory impairment and hyperactivity, but memory deficits returned about a month after the drug was stopped. This is early animal research, so it does not yet show that the drug would work or be safe in people.
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The discovery that repeat expansions in the C9orf72 gene are a frequent cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) has revolutionized our understanding of these diseases.
Why it matters
This review proposes that C9orf72-related ALS and FTD arise from a combination of loss and gain of function plus downstream cellular pathways. It is a summary of mechanisms, not a trial, and suggests no specific treatment.
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SUVs in the pons and the inferior cerebellum indicated consistent clearance across all 51 subjects.
Why it matters
This study characterized a tau PET radioligand in 51 people and found its binding pattern matched known stages of tau pathology, with minimal off-target binding in the brain. It is a technical imaging study and does not test any treatment, though it may help measure tau in future research.
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Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system (CNS).
Why it matters
This study is about multiple sclerosis and found that the CSF1R inhibitor BLZ945 enhanced remyelination and prevented demyelination in mice. It provides no evidence about treating, curing, or preventing Alzheimer's disease.
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52/100
The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer disease.
Why it matters
In APP/PS1-21 mice, reducing apoE with an antisense oligonucleotide before plaque deposition decreased amyloid pathology, while starting treatment at the onset of amyloid deposition increased plaque size and reduced plaque-associated neuritic dystrophy without changing overall plaque load. These are mouse results showing that timing of apoE reduction matters, and they do not establish a treatment for people.
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.
- An Increased Percentage of Long Amyloid β Protein Secreted by Familial Amyloid β Protein Precursor (βApp 717 ) Mutants
- String Vessel Formation is Increased in the Brain of Parkinson Disease
- The 14-3-3 brain protein in cerebrospinal fluid as a marker for transmissible spongiform encephalopathies
- Tau PET imaging in Black and Latino participants with and without cognitive impairment
- Dietary antioxidants and other dietary factors in the etiology of Parkinson's disease
- β-Amyloid peptide increases levels of iron content and oxidative stress in human cell and Caenorhabditis elegans models of Alzheimer disease
- Effects of low versus high frequencies of repetitive transcranial magnetic stimulation on cognitive function and cortical excitability in Alzheimer's dementia
- Soluble TREM2 induces inflammatory responses and enhances microglial survival
- Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease
- Scavenger receptor class B type I (SR-BI) regulates perivascular macrophages and modifies amyloid pathology in an Alzheimer mouse model