- 428studies, of 27,380 in the library
- 428peer-reviewed
- 1976–2026years published
- 54median usefulness score out of 100
These counts and lists are worked out from the library itself each time the page loads. A score rates how much weight a study can bear — its design, journal, evidence and recency — not whether its result is good news.
How the records spell this journal (2 spellings)
- Brain : a journal of neurology — 381 studies
- Brain — 47 studies
The 20 highest-scoring
- CSF proteomics of semorinemab Alzheimer's disease trials identifies cell-type specific signatures
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Tilavonemab in early Alzheimer's disease: results from a phase 2, randomized, double-blind study
This phase 2 randomized, double-blind, placebo-controlled trial tested the anti-tau antibody tilavonemab at three doses against placebo in patients with early Alzheimer's disease over 96 weeks. The available text does not report whether tilavonemab affected the primary endpoint.
- Sex differences in the genetic predictors of Alzheimer's pathology
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A comprehensive head-to-head comparison of key plasma phosphorylated tau 217 biomarker tests
In a head-to-head comparison, the mass spectrometry-based %p-tau217WashU test performed significantly better than all immunoassays at identifying amyloid-PET, tau-PET, and cognitive abnormalities. The authors suggest %p-tau217 could serve as a stand-alone confirmatory test, while some immunoassays may be better suited as triage tests needing a second confirmation.
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Plasma GFAP is an early marker of amyloid-β but not tau pathology in Alzheimer's disease
This longitudinal study found that plasma GFAP was an early marker of amyloid-beta but not tau pathology in Alzheimer's disease. It concerns a biomarker and does not test a treatment, cure or prevention.
- The hubs of the human connectome are generally implicated in the anatomy of brain disorders
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Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer's disease: implications for sequence of pathological events in Alzheimer's disease
This 2009 study repeated PIB and MRI imaging in people who were cognitively normal, had mild cognitive impairment or had Alzheimer's disease, to learn the order in which disease changes happen. PIB retention rose by a small amount each year in all participants (median 0.042 ratio units/year, P < 0.001), and the yearly rise did not differ between the three groups (P = 0.90); the authors concluded that "significant plaque deposition occurs prior to clinical decline." It is an observational imaging study: it tested no treatment, our record does not include its MRI results, and timing alone does not show that plaque causes the decline.
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Longitudinal plasma p-tau217 is increased in early stages of Alzheimer's disease
In the Swedish BioFINDER study, plasma p-tau217 increased over time in people with preclinical and prodromal Alzheimer's disease and in those with mild cognitive impairment who later converted to dementia, but it did not change in amyloid-negative participants or non-converters. This suggests p-tau217 could be used to monitor disease progression, but it is not a treatment, cure, or prevention.
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Time course of phosphorylated-tau181 in blood across the Alzheimer's disease spectrum
This study found that changes in blood p-tau181 occurred early and were associated with amyloid-beta pathology and with later widespread tau aggregation. It concerns a potential diagnostic and screening blood biomarker and does not test any treatment, cure, or prevention.
- Anterior temporal involvement in semantic word retrieval: voxel-based lesion-symptom mapping evidence from aphasia
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Risk and predictors of dementia and parkinsonism in idiopathic REM sleep behaviour disorder: a multicentre study
In this multicentre study, people with idiopathic REM sleep behaviour disorder converted to an overt neurodegenerative syndrome at 6.3% per year, with 73.5% converting after 12-year follow-up, and several markers predicted conversion. The findings are presented as a way to stratify patients for future neuroprotective trials, not as a treatment or cure.
- Data-driven neuropathological staging and subtyping of TDP-43 proteinopathies
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Head-to-head comparison of 10 plasma phospho-tau assays in prodromal Alzheimer's disease
This study compared several blood tests for the protein p-tau in people with mild cognitive impairment. A mass-spectrometry p-tau217 test was best at spotting people with amyloid in the brain (AUC 0.947, against 0.642–0.813 for five other assays) and matched spinal-fluid levels most closely (R = 0.891, against 0.755 for a second p-tau217 test). The authors say the best tests "rival the gold standards of Aβ-PET and CSF" but that the findings need further validation, so it does not establish any blood test as a stand-alone diagnosis.
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A multicentre longitudinal study of flortaucipir (18F) in normal ageing, mild cognitive impairment and Alzheimer's disease dementia
In this 18-month longitudinal study, cortical tau burden measured by flortaucipir PET increased significantly in amyloid-beta positive but not amyloid-beta negative participants, and both baseline tau and its change were associated with changes in cognitive performance. The authors describe these results as a preliminary characterization of how tau spreads in Alzheimer's disease.
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Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography
In 437 people without dementia from the ADNI research study, researchers measured amyloid in spinal fluid (CSF amyloid-β42) and on florbetapir PET brain scans, then repeated the PET scan after an average of 2.1 years. They asked whether either test picks up abnormal amyloid buildup before the other; the study's title reports that the spinal fluid test does, but the summary held here gives no figures for how much earlier. It is a study about the timing of tests, not about treatment, and it does not show who will go on to develop dementia.
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Minocycline reduces chronic microglial activation after brain trauma but increases neurodegeneration
In an experimental model, the antibiotic minocycline reduced chronic microglial activation after brain trauma but increased neurodegeneration. This suggests that simply suppressing microglia after injury may be harmful, but it is experimental work and does not establish a treatment for Alzheimer's disease.
- Cerebrospinal fluid biomarker panel for synaptic dysfunction in a broad spectrum of neurodegenerative diseases
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Serum GFAP levels correlate with astrocyte reactivity, post-mortem brain atrophy and neurofibrillary tangles
This cohort study found that serum GFAP levels were associated with post-mortem tau pathology independently of amyloid deposits, and were also associated with hippocampal sclerosis and argyrophilic grain disease. The authors state that further research is needed to replicate and validate these results in diverse populations, so this is biomarker and mechanistic evidence rather than a treatment or cure.
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The bivariate distribution of amyloid-β and tau: relationship with established neurocognitive clinical syndromes
This work supports a model in which amyloid appears first and tauopathy later, with tauopathy linked to clinical symptoms. It describes the sequence of brain changes in Alzheimer's disease and does not offer a treatment, cure, or prevention.
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The accumulation rate of tau aggregates is higher in females and younger amyloid-positive subjects
This longitudinal PET study found that the rate of tau accumulation was greater in females and younger amyloid-positive individuals, while amyloid accumulation was greater in APOE ε4 carriers and older individuals. The authors say these findings are important for designing clinical trials and understanding factors linked to faster tau aggregation.
See all 428 studies, with filters →
Newest additions
- The longevity gene APOE2 enhances pericyte function and reduces lipid droplets
- Photobiomodulation of immune crosstalk rescues neuroinflammation in Alzheimer's disease models
- The tau biomarker cascade is condensed in Down syndrome compared with sporadic Alzheimer's disease
- ApoE4 lowers the ptau217 threshold for tau aggregation and spread in an allele dose-dependent manner
- Imaging and plasma biomarkers for pathological accumulation in Down syndrome
- Plasma pTau 217/β-amyloid 1-42 ratio for enhanced accuracy and reduced uncertainty in detecting amyloid pathology
- Cofilin hyperphosphorylation triggers TDP-43 pathology in sporadic amyotrophic lateral sclerosis
- HDAC6 regulates BACE1 stability and NLRP3 inflammasome activation in Alzheimer's disease
- Transcriptomic signature of frontotemporal lobar degeneration with TDP-43 type C pathology
- Alzheimer and cardiovascular genetic scores and cognition: the FINGER randomized controlled trial
By review status
- Peer-reviewed — 428
Other journals
- JAMA Psychiatry34
- JAMA Internal Medicine47
- JAMA Neurology325
- Alzheimer's & Dementia1,310
- The BMJ78
- The Lancet99
- The Journal of Nutrition, Health & Aging46
- The New England Journal of Medicine81
- JAMA202
- The Lancet Neurology226
- Diabetes Care25
- Molecular Psychiatry107
- JAMA Network Open189
- Alzheimer's Research & Therapy373