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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Inflammation is increasingly implicated as a risk factor for dementia, stroke, and small vessel disease (SVD).
Why it matters
This systematic review found links between small vessel disease in the brain and markers of vascular inflammation, especially in stroke patients, and that higher systemic inflammatory markers predicted later small vessel disease severity. It is about risk associations, not about treating or curing Alzheimer's disease.
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Stroke, dementia, and hypertension are associated with late-onset epilepsy; however, the role of other vascular and lifestyle factors remains unclear.
Why it matters
In this cohort, midlife hypertension, diabetes, smoking, apolipoprotein E e4 genotype, stroke, and dementia were associated with higher risk of late-onset epilepsy, while physical activity and moderate alcohol intake were linked to lower risk. These findings are about epilepsy risk, not about treating, curing, or preventing Alzheimer's disease.
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Compared with controls, patients with idiopathic REM sleep behaviour disorder had decreased colonic 11 C-donepezil uptake (-0·322, 95% CI -0·112 to -0·531; p=0·0020), 123 I-MIBG heart:mediastinum ratio (-0·508, -0·353 to -0·664; p 18 F-DOPA uptake (Ki; -0·0023, -0·0009 to -0·0037; p=0·0013).
Why it matters
This imaging case-control study found that patients with idiopathic REM sleep behavior disorder had fully developed pathology in the peripheral autonomic nervous system and the locus coeruleus, equal to that in diagnosed Parkinson's disease. It concerns Parkinson's disease pathology and does not test any treatment for Alzheimer's disease.
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A total of 16 084 European adults from 8 cohort studies (mean age range, 56.9±12.3-82.1±4.2 years) of the European Eye Epidemiology (E3) consortium.
Why it matters
This study investigated factors affecting retinal nerve fiber layer thickness measurements in a European population. It does not address treating, curing, or preventing Alzheimer's disease.
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APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease.
Why it matters
In mice engineered to develop tau damage, those carrying the human APOE4 gene version had more tau, more brain shrinkage and more inflammation than mice with APOE2 or APOE3, while mice with no APOE were "largely protected"; in lab dishes, APOE4 support cells released more of the inflammatory signal TNF-α and killed more neurons. The authors conclude that APOE affects tau-driven damage "independently of amyloid-β", and report that in people, carrying ε4 "is associated with" more severe brain degeneration in one tau disease and faster progression in Alzheimer's. These are animal, cell and association findings with no treatment tested, so they point to a possible mechanism but do not show that targeting APOE4 would treat or prevent Alzheimer's in people.
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Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02).
Why it matters
In autopsied brains, eating seafood at least once a week was linked to less Alzheimer pathology, but only among APOE epsilon4 carriers, and fish oil supplements showed no significant link. Higher brain mercury was not linked to more neuropathology.
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65/100
Baseline CSF levels of NGRN in patients with AD (median level, 2381 pg/mL [interquartile range, 1651-3416 pg/mL]) were higher than in cognitively normal participants (median level, 1712 pg/mL [interquartile range, 1206-2724 pg/mL]) (P = .04).
Why it matters
In 163 memory-clinic patients from the Amsterdam Dementia Cohort who each had two spinal-fluid samples about two years apart, levels of neurogranin, a proposed marker of synapse loss, were higher in Alzheimer's disease than in cognitively normal people (median 2381 vs 1712 pg/mL, P = .04) and tracked closely with tau. Over time, neurogranin rose within cognitively normal participants but not in people with later-stage MCI or Alzheimer's, which the authors say "suggests that NGRN may reflect presymptomatic synaptic dysfunction or loss." The authors call it "a promising biomarker", but the group ranges overlapped, and this study tested diagnosis and monitoring, not a treatment.
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Meta-analysis of the 2 family-based and the 5 case-control cohorts yielded a p value of 0.0029, while the overall summary estimate (using case-control data only) resulted in an odds ratio of 1.67 (95% confidence interval 0.95-2.92) for the association between the TREM2 R47H and increased AD risk.
Why it matters
Testing family and case-control cohorts of Caucasian people, this study confirmed that the rare TREM2 R47H variant is associated with Alzheimer's risk (p value of 0.0029). However, the estimated effect (odds ratio of 1.67) was substantially smaller than first reported. This tempers earlier claims that R47H raises risk about as much as the APOE ε4 gene variant.
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Type 2 diabetes is associated with cognitive dysfunction and structural brain changes.
Why it matters
Across 86 studies of people with type 2 diabetes who did not have dementia, higher HbA1c and more variable blood glucose went along with somewhat poorer thinking scores. The link was weak, though: HbA1c generally explained less than 10% of the differences in cognition. Few studies followed people long enough to look at dementia or brain changes on MRI, so the authors say randomised trials are still needed to show whether lowering blood sugar protects long-term cognition.
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In response to KKM treatment, 68 genes were found to be differentially expressed (19 up-regulated, 49 down-regulated) after adjusting for potentially confounded differences in sex, illness burden, and BMI.
Why it matters
In this randomized trial, 45 family dementia caregivers were assigned to Kirtan Kriya Meditation or relaxing music for 12 minutes daily for 8 weeks, and 39 completed the study. In the meditation group, 68 genes were differentially expressed, with down-regulated transcripts including pro-inflammatory cytokines, suggesting a possible reversal of a stress-related inflammatory pattern.
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We suggest that 6 months of dietary n-3 FA supplementation affected expression of genes that might influence inflammatory processes and could be of significance for AD.
Why it matters
In a subgroup of 16 patients from the OmegAD study, 6 months of DHA-rich n-3 fatty acid supplementation changed expression of genes that might influence inflammation and could be of significance for Alzheimer's disease. This is a small gene-expression study and does not show that supplementation treats, cures, or prevents Alzheimer's disease.
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Vascular cognitive impairment is an umbrella term for cognitive dysfunction associated with and presumed to be caused by vascular brain damage.
Why it matters
This review of 32 neuropathological studies found microinfarcts were common in vascular dementia (62%), Alzheimer's disease (43%), and mixed dementia (33%), compared with 24% in nondemented older people. It concerns brain tissue findings after death and notes that detecting these lesions in living people would require high-resolution MRI, so it offers no treatment or cure.
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These findings show that frontotemporal lobar degeneration (FTLD) is a highly heritable disorder but heritability varies between the different syndromes.
Why it matters
This study found that frontotemporal lobar degeneration is highly heritable, with 41.8% of patients having some family history, but heritability varied between different clinical subtypes. Mutations were found in the MAPT and GRN genes, but not in the other genes tested, so the genetic causes of many cases remain unknown.
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The TAR DNA-binding protein 43 (TDP-43) has been identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin inclusions (FTLD-U), defining a novel class of neurodegenerative conditions: the TDP-43 proteinopathies.
Why it matters
In a screen of 296 patients with TDP-43-related brain diseases, three TARDBP gene changes turned up only in familial ALS (3 of 92, 3.3%), not in 24 sporadic ALS or 180 other TDP-43 disease patients, and were absent from 825 controls. Patient cell lines showed more caspase-cleaved TDP-43 fragments than controls, which the authors say "support TARDBP mutations as a cause of ALS"; the mechanism they propose is stated as speculation. This is ALS genetics, not a finding about Alzheimer's disease, and it tests no treatment.
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The treatment of ischaemic stroke with neuroprotective drugs has been unsuccessful, and whether these compounds can be used to reduce disability after recurrent stroke is unknown.
Why it matters
In the PRoFESS trial, patients who had had an ischaemic stroke were randomly assigned to aspirin plus extended-release dipyridamole or clopidogrel, and to telmisartan or placebo, to investigate putative neuroprotective effects on disability and cognitive function after recurrent stroke. This concerns stroke treatment and cognition after stroke, not treating, curing or preventing Alzheimer's disease.
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The preponderance of epidemiologic and tissue compositional studies supports a protective effect of omega-3 EFA intake, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in mood disorders.
Why it matters
This review found evidence supporting omega-3 fatty acids in mood disorders, but results for dementia remained inconclusive. It does not establish that omega-3 fatty acids prevent or treat dementia.
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MarkVCID2 enrolled 1883 individuals age 73.4 ± 7.5 years, 65.0% female, 24.2% Hispanic, and 27.1% non-Hispanic Black.
Why it matters
This paper describes the design and baseline characteristics of a study enrolling 1883 diverse participants to validate biomarkers of small vessel disease over 3 years. No results on treating, curing or preventing Alzheimer's disease are reported yet.
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After 12 months, no statistically significant difference was observed between MLI+EGCG and MLI+placebo in the PACC-exe (adjusted mean difference [AMD]: 0.12; 95%CI: -0.01, 0.24; p=0.061).
Why it matters
Adding green tea extract with EGCG to a lifestyle program did not significantly improve the main cognitive score after 12 months compared with lifestyle alone. Some benefit appeared after a washout, but this was exploratory and not the main finding.
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Rising global concentrations of environmental microplastics and nanoplastics (MNPs) drive concerns for human exposure and health outcomes.
Why it matters
This study detected microplastics and nanoplastics in human kidney, liver, and brain tissue, with higher concentrations in brains and even greater accumulation in decedent brains with a documented dementia diagnosis. It does not test any treatment, cure or prevention for Alzheimer's disease, and the authors call for more research into exposure, uptake and clearance pathways.
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Our findings illuminate the potential benefits of ChEI treatment in DLB patients.
Why it matters
This cohort study of 1,095 people with dementia with Lewy bodies found that cholinesterase inhibitor use significantly slowed cognitive decline compared with memantine and nonuse, and was associated with lower risk of death in the first year after diagnosis. It suggests cholinesterase inhibitors may help slow cognitive decline in this specific type of dementia, though the mortality benefit was not sustained after one year.
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The mean (SD) age was 73.9 (7.35) years among the 237 ADNI participants and 70.2 (9.7) years among the 130 Avid-A05 participants.
Why it matters
This cohort study found that in ApoE4 carriers, tau accumulation related to amyloid was accelerated at lower amyloid levels, suggesting ApoE4 may facilitate earlier spreading of tau across connected brain regions. It does not report any treatment, cure, or prevention of Alzheimer's disease.
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Why it matters
Updates neuroimaging standards for research into small vessel disease, covering advances since 2013.
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Our findings reveal that specific gut microbial features are closely associated with cognitive impairment and decreased hippocampal volume, which may play an important role in dementia development.
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Parkinson's disease (PD) is the most common movement disorder, with resting tremor, rigidity, bradykinesia and postural instability being major symptoms 1 .
Why it matters
This study reports the cryo-electron microscopy structures of α-synuclein filaments from human brains with Lewy pathology, establishing the existence of distinct molecular conformers of assembled α-synuclein in neurodegenerative disease. The work concerns Parkinson's disease, Parkinson's disease dementia, dementia with Lewy bodies and multiple system atrophy, and is structural biology rather than a treatment, cure or prevention for Alzheimer's disease.
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Among 300 participants with DS and a control group of 37 non-DS siblings, mean (SD) age was 45.0 (10.1) years, and 167 (49.6%) were men.
Why it matters
In this cross-sectional study of adults with Down syndrome, plasma p-tau217 and GFAP were associated with tau-PET and amyloid-PET status. It is a diagnostic biomarker study and does not report any treatment, cure, or prevention of 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.
- Modulation of apolipoprotein E structure by domain interaction: differences in lipid-bound and lipid-free forms
- Sevoflurane and Isoflurane induce structural changes in brain vascular endothelial cells and increase blood-brain barrier permeability: Possible link to postoperative delirium and cognitive decline
- REST regulates DYRK1A transcription in a negative feedback loop
- Neuropathology of White Matter Lesions, Blood-Brain Barrier Dysfunction, and Dementia
- The glymphatic system clears amyloid beta and tau from brain to plasma in humans
- Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography
- Enlarged amygdala volume and reduced hippocampal volume in young women with major depression
- Brain-Derived Neurotrophic Factor and Major Depressive Disorder: Evidence from Meta-Analyses
- Imaging of Synaptic Density in Neurodegenerative Disorders
- Degeneration in vivo of rat hippocampal neurons by wild-type Alzheimer amyloid precursor protein overexpressed by adenovirus-mediated gene transfer