- 46studies on this subject, of 27,380 in the library
- 43peer-reviewed
- 1995–2026years published
- 56.5median 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 we score a study.
The 20 highest-scoring studies
-
Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer's disease
In three cohorts totalling 1,016 cognitively unimpaired individuals, amyloid-beta was associated with increased plasma phosphorylated tau and an Alzheimer's-like pattern of tau accumulation only in people positive for astrocyte reactivity. The findings suggest astrocyte reactivity as an upstream event linking amyloid-beta with initial tau pathology and may help select participants for trials, but no treatment is tested.
-
The glymphatic system clears amyloid beta and tau from brain to plasma in humans
In 48 healthy adults, sleep-related brain-fluid dynamics and deep sleep predicted how much amyloid-beta and tau moved from the brain into the blood overnight. This is a small mechanistic study in healthy volunteers, not a trial testing whether improving sleep prevents Alzheimer's disease.
-
The TREM2 agonistic antibody AL002 in early Alzheimer's disease: a phase 2 randomized trial
In this phase 2 trial of 381 participants with early Alzheimer's disease, the TREM2 agonistic antibody AL002 did not meet the primary endpoint of change in the Clinical Dementia Rating-Sum of Boxes score versus placebo, although it showed target engagement in the central nervous system. The most frequent treatment-emergent adverse events were MRI changes resembling amyloid-related imaging abnormalities, so this treatment was negative for clinical benefit in this trial.
-
Glymphatic system dysfunction predicts amyloid deposition, neurodegeneration, and clinical progression in Alzheimer's disease
In participants with Alzheimer's disease dementia, mild cognitive impairment and normal controls, a lower ALPS index was associated with faster amyloid PET burden change, higher risk of amyloid-positive transition and clinical progression, and faster cognitive decline, with the associations fully mediated by amyloid PET and brain atrophy. The findings suggest glymphatic failure may precede amyloid pathology and predict progression, but no treatment, cure or prevention is tested.
-
Lewy body pathology exacerbates brain hypometabolism and cognitive decline in Alzheimer's disease
Among 795 cognitively impaired participants, those with both Alzheimer's disease and Lewy body pathology showed worse baseline cognition and faster global cognitive decline and cortical hypometabolism than those with only Alzheimer's pathology. The authors say that detecting Lewy body pathology in vivo could enhance prognostic evaluations and have implications for clinical trial design.
-
Amyloid-associated hyperconnectivity drives tau spread across connected brain regions in Alzheimer's disease
Combining amyloid PET, resting-state functional MRI and longitudinal tau-PET in controls and amyloid-positive patients, this study found that amyloid-beta induces hyperconnectivity of temporal lobe tau epicenters to vulnerable posterior brain regions, and that this precedes neocortical tau spreading. It identifies a mechanism by which amyloid-beta promotes tau spread, which may inform therapeutic efforts, but no treatment is tested.
-
Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer's disease
In people with inherited Alzheimer's disease, the rate of change of serum neurofilament light distinguished mutation carriers from non-carriers about a decade earlier than single measurements and predicted brain shrinkage and cognitive change. This is a marker of progression, not a treatment or cure.
-
Microglia modulate Aβ-dependent astrocyte reactivity in Alzheimer's disease
Across 101 individuals studied with PET and plasma biomarkers, amyloid-beta pathology was associated with astrocyte reactivity only in the presence of microglial activation, and these effects related to cognitive impairment through tau phosphorylation and aggregation. This describes a pathway linking microglial activation, astrocytes and tau in the disease process, without testing any treatment, cure or prevention.
-
Tau accumulation and its spatial progression across the Alzheimer's disease spectrum
Tau generally followed the expected Braak spreading order, but which exact regions were affected varied a lot between people, and tau spread fastest in the mild cognitive impairment stage. This suggests treatments aimed at tau may need to account for individual differences in where it spreads, especially early on.
-
Microglial mechanisms drive amyloid-β clearance in immunized patients with Alzheimer's disease
Using spatial transcriptomics in human brain tissue, this study identified distinct microglial states associated with amyloid-beta clearance and found upregulation of TREM2 and APOE in microglia across immunization approaches, correlating with antibody responses and amyloid-beta removal. These findings describe mechanisms seen in immunized patients and point to possible molecular targets, but they do not show that targeting them treats or prevents Alzheimer's disease.
-
Limbic-predominant age-related TDP-43 encephalopathy in the oldest old: a population-based study
In this population-based study, limbic-predominant age-related TDP-43 encephalopathy neuropathologic change stages were significantly associated with dementia and lower MMSE scores, and its attributable risk was higher than that of Alzheimer's disease neuropathologic change (24.2% versus 18.6%). The study shows this pathology is very common and a major determinant of dementia in the general late-life population, but it examines brain tissue after death and tests no treatment.
-
Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles
Describes a triple-transgenic model of Alzheimer's disease that develops both plaques and tangles. A disease model is a research tool for testing ideas and candidate treatments, and is not a treatment itself.
-
Long-term physical exercise facilitates putative glymphatic and meningeal lymphatic vessel flow in humans
In healthy volunteers, 12 weeks of long-term exercise increased putative glymphatic influx at the putamen and increased putative meningeal lymphatic vessel size and flow, alongside changes in inflammation- and immune-related plasma proteins. The results suggest increased glymphatic and meningeal lymphatic flow as a possible mechanism for exercise's neuroprotective effects on cognition, but this was a small imaging study in healthy volunteers and did not test whether exercise prevents Alzheimer's disease.
-
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
This study in transgenic mice found that mice overexpressing a mutant form of human amyloid precursor protein showed normal learning and memory at 3 months but impairment by 9 to 10 months, accompanied by elevated Aβ and amyloid plaques. It is an animal study and does not directly address treating, curing, or preventing Alzheimer's disease in humans.
-
Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment
A blood test for GFAP identified which patients with mild cognitive impairment had underlying Alzheimer's pathology and predicted who later developed dementia. This points to GFAP as a possible blood marker for identifying patients for trials or monitoring, not as a treatment.
-
Early Alzheimer's Disease with frequent neuritic plaques harbors neocortical tau seeds distinct from primary age-related tauopathy
In 38 patients with Braak-matched Alzheimer's disease neuropathologic change or primary age-related tauopathy, tau seeding and post-translational modification profiles were associated with amyloid-beta neuritic plaque density and differentiated the two conditions in neocortex. The data suggest tau seed modifications relate to disease trajectory and may explain more severe cognitive dysfunction in late-stage Alzheimer's disease, but no treatment is tested.
-
ApoE4 lowers the ptau217 threshold for tau aggregation and spread in an allele dose-dependent manner
This study found that plasma ptau217 elevations were linked to faster tau-PET spread in an ApoE4 allele dose-dependent manner, and that a higher ApoE4 allele count was linked to lower ptau217 thresholds marking transition to tauopathy. It clarifies how the key genetic risk factor for sporadic Alzheimer's disease relates to tau aggregation and spread, but offers no treatment, cure or prevention.
-
Norepinephrine-mediated slow vasomotion drives glymphatic clearance during sleep
This study identified tightly synchronized oscillations in norepinephrine, cerebral blood volume and cerebrospinal fluid as the strongest predictors of glymphatic clearance during NREM sleep, and found that the sleep aid zolpidem suppressed norepinephrine oscillations and glymphatic flow. It describes how sleep architecture drives brain waste clearance, which is relevant to understanding clearance mechanisms but does not test an Alzheimer's treatment, cure or prevention.
-
Alzheimer's disease transcriptional landscape in ex vivo human microglia
Analysing primary microglia from 189 human postmortem brains, this study found gene expression changes associated with multiple Alzheimer's disease phenotypes, including dementia severity and neuropathological lesions, plus changes in gene-gene coordination and disease subtypes. It furthers understanding of microglia in Alzheimer's disease biology and nominates candidate targets, but identifies no treatment, cure or prevention.
-
Immune checkpoint TIM-3 regulates microglia and Alzheimer's disease
In mouse models, deleting Havcr2 in microglia increased phagocytic activity and ameliorated cognitive impairment and reduced amyloid-beta pathology in 5xFAD mice. These findings in a transgenic animal model highlight the therapeutic potential of targeting microglial TIM-3, but no human treatment or prevention is demonstrated.
See all 46 studies in Laboratory science, with filters →
Newest additions on this subject
- Arc mediates intercellular tau transmission via extracellular vesicles
- Clonal expansion of cytotoxic CD8⁺ T cells in lecanemab-associated ARIA
- Peripheral cancer attenuates amyloid pathology in Alzheimer's disease via cystatin-c activation of TREM2
- Systemic complement factors in aging, Alzheimer's disease and other dementias: a longitudinal study over 10 years
- Neuropathologic Profiles and Associated Cognitive Trajectories in Community-Living Older Adults
- Utility of the Amygdalar Atrophy Scale to Identify Patients With Limbic-Predominant Age-Related TDP-43 Encephalopathy in a Memory Clinic
- The Alzheimer's therapeutic Lecanemab attenuates Aβ pathology by inducing an amyloid-clearing program in microglia
- Lymphoid gene expression supports neuroprotective microglia function
- Interplay between astrocyte reactivity and APOE ε4 status is associated with accelerated pTau-related tau pathology in Alzheimer's disease
- The gain-of-function TREM2-T96K mutation increases risk for Alzheimer's disease by impairing microglial function
All 46 studies in Laboratory science, newest first →
What the library holds on this subject
By review status
| Status | Studies |
|---|---|
| Peer-reviewed | 43 |
| Regulatory decision — not a study | 1 |
| Retracted — do not rely on it | 2 |
By strength of evidence
| Rated in our summary | Studies |
|---|---|
| moderate | 16 |
| early | 15 |
| low | 5 |
| high | 4 |
| preliminary | 3 |
| not rated | 2 |
| null-result | 1 |
Most frequent journals
| Journal | Studies |
|---|---|
| Nature Communications | 6 |
| Cell | 4 |
| Nature Medicine | 4 |
| Nature Neuroscience | 4 |
| Brain | 3 |
| Nature | 3 |
| Science | 3 |
| Journal of Neuroscience | 2 |
| Molecular Neurodegeneration | 2 |
| Neuron | 2 |
Studies by year published
| Year | Studies | Bar |
|---|---|---|
| 2026 | 8 | |
| 2025 | 16 | |
| 2024 | 6 | |
| 2023 | 1 | |
| 2022 | 2 | |
| 2021 | 1 | |
| 2020 | 1 | |
| 2019 | 1 | |
| 2016 | 1 | |
| 2015 | 1 | |
| 2014 | 1 | |
| 2012 | 2 | |
| 2008 | 1 | |
| 2006 | 1 | |
| 2003 | 1 | |
| 1996 | 1 | |
| 1995 | 1 |
Counts the 46 studies with a usable publication date. The library is a large sample of published work, not a complete index, so these counts describe the library, not the whole field.
Other subjects in the library
- Getting a diagnosis
- Biomarkers
- Clinical trials
- Prevention and risk
- Caregiving
- How common it is
- Costs and economics
- Genetics
- Disease mechanisms
- Vascular contributions
- Prevention trials
- Clinical safety
- Health systems and care delivery
- End-of-life care
- Risk factors
- Digital health tools
- Treatments
- Disparities
- Mild cognitive impairment
- Risk genes beyond APOE
- Brain scans and imaging
- TREM2 and immune genetics
- Cognitive tests and assessment
- Lewy body dementia
- Down syndrome and Alzheimer's
- Long-term cohort studies
- Inflammation and the immune system
- Tau biomarkers
- Brain tissue and pathology
- Drug development
- Hippocampus size on brain scans