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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75/100
This large GWAS of WMH burden in community-based cohorts of individuals of European descent identifies a novel locus on chromosome 17.
Why it matters
White-matter spots on brain MRI (WMHs) are linked to later dementia, stroke and depression, but few genes behind them were known. Pooling genome scans from 9,361 stroke-free adults of European descent, and confirming in 3,024 more, this study found one region on chromosome 17 (17q25) tied to more WMH; each variant added only 4–8% of the average burden. It points to where researchers should look, not to a test or treatment — and it did not measure dementia itself.
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Patients taking rivastigmine were significantly less apathetic and anxious, and had fewer delusions and hallucinations while on treatment than controls.
Why it matters
In this 20-week Lancet trial, 120 people with dementia with Lewy bodies in the UK, Spain and Italy took rivastigmine (up to 12 mg a day) or a placebo; those on rivastigmine were less apathetic and anxious, had fewer delusions and hallucinations, and were faster and better on attention-heavy tests, and 63% of them (37 people) versus 30% on placebo (18) improved by at least 30% from baseline. The differences tended to disappear once the drug was stopped, and nausea, vomiting and loss of appetite were more common on rivastigmine, though the authors judged it safe and well tolerated when the dose was adjusted individually. The trial measured symptom relief during treatment only, so it does not show that rivastigmine slows, cures or prevents this form of dementia.
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We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression.
Why it matters
This study tested whether plasma neurofilament light identifies asymptomatic carriers of familial frontotemporal lobar degeneration mutations at risk of disease progression. It is observational and does not provide a treatment or cure.
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74/100
Hippocampal volume increase in response to aerobic exercise has been consistently observed in animal models.
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A non-synonymous genetic rare variant, rs75932628-T (p.R47H), in the TREM2 gene has recently been reported to be a strong genetic risk factor for Alzheimer's disease (AD).
Why it matters
This multi-center study found that the TREM2 p.R47H variant was more common in Alzheimer's disease patients than controls, confirming it as a risk factor. It is a genetic association study and does not test any treatment or prevention.
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Previous Cochrane reviews have considered the use of cholinesterase inhibitors in both Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB).
Why it matters
This review assessed cholinesterase inhibitors in dementia with Lewy bodies, Parkinson's disease dementia and cognitive impairment in Parkinson's disease, based on the idea that these conditions involve severe loss of acetylcholine. It concerns symptom treatment in these related conditions, not curing or preventing Alzheimer's disease.
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Analysis of error types provides useful information about the stages and processes involved in normal and aphasic word production.
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Conjugated equine estrogens with or without MPA are associated with greater brain atrophy among women aged 65 years and older; however, the adverse effects are most evident in women experiencing cognitive deficits before initiating hormone therapy.
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Over the last decade a significant number of studies have reported smaller hippocampal volume in individuals with symptoms of post-traumatic stress disorder (PTSD) relative to control groups, and in some cases hemispheric asymmetries in this effect have been noted.
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In two randomized crossover studies involving 48 healthy, cognitively normal adults (registered on ClinicalTrials.gov), researchers measured brain and blood markers after normal sleep versus sleep deprivation.
Why it matters
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.
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Despite undetectable TPI-287 levels in CSF, CSF biomarkers demonstrated decreased chitinase-3-like protein-1 (YKL-40) levels in the 4RT treatment arm (mean [SD], -8.4 [26.0] ng/mL) compared with placebo (mean [SD], 10.4 [42.3] ng/mL; median difference, -14.6 [95% CI, -30.0 to 0.2] ng/mL; P = .048, Mann-Whitney test).
Why it matters
In this trial of 68 participants with Alzheimer disease, progressive supranuclear palsy, or corticobasal syndrome, TPI-287 levels were undetectable in cerebrospinal fluid, and only the 4-repeat tauopathy group showed decreased YKL-40 levels compared with placebo. The authors conclude that basket trials are a useful approach for early tau therapeutic development, so this is an early-stage finding and not evidence of clinical benefit in Alzheimer disease.
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Among older persons with AMD, oral supplementation with LCPUFAs or lutein/zeaxanthin had no statistically significant effect on cognitive function.
Why it matters
In this large randomized trial, supplements of omega-3 fatty acids or lutein/zeaxanthin had no statistically significant effect on cognitive function in older people with age-related macular degeneration. This means these supplements did not help prevent cognitive decline in this group.
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We investigated the effects of renin-angiotensin system blockade on cognitive function in patients aged 55 years and older with established atherosclerotic cardiovascular disease or diabetes with end-organ damage in two clinical trials.
Why it matters
This analysis of two large trials examined whether blood pressure drugs that block the renin-angiotensin system affected cognitive function in people at high cardiovascular risk. The study text does not report the cognitive results, so it cannot show whether these drugs help prevent cognitive decline.
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African heritage diets are increasingly being replaced by Western-style dietary patterns because of urbanization, economic development, increased access to processed foods, globalization and changing social norms.
Why it matters
This randomized trial in 77 healthy men in Tanzania examined switching between an African heritage diet and a Western-style diet, not Alzheimer's disease. It found the Western-style diet promoted a pro-inflammatory state while switching back to the heritage diet or consuming a fermented banana beverage had a largely anti-inflammatory effect.
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SNAP-25 and 14-3-3 zeta/delta also had the strongest associations with tau-PET, amyloid-β-PET and cortical thickness at baseline and were associated with longitudinal changes in these imaging biomarkers [β(standard error, SE) = -0.056(0.0006) to 0.058(0.005), P < 0.0001].
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The risk of developing Alzheimer's disease (AD) significantly increases in individuals carrying the APOEε4 allele.
Why it matters
This study found that rare variants in the FN1 gene may reduce Alzheimer risk related to APOE ε4, and zebrafish experiments suggested fibronectin loss-of-function reduced gliosis and improved clearance of toxic proteins. The work points to the extracellular matrix as a possible target, but it is early laboratory and genetic research, not a treatment.
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Circulating NfL and GFAP may, independently and jointly, provide useful clinical insight regarding dementia risk and prognosis.
Why it matters
In 1712 dementia-free older adults followed for 19 years, being in the highest versus lowest tertile of serum NfL or GFAP was associated with higher risk of incident dementia and dementia-specific mortality, and the joint highest tertile was associated with even higher risk. This suggests these blood markers may provide clinical insight into dementia risk and prognosis, but it does not show that lowering them prevents or treats dementia.
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In response to sleep loss (+17.2%), compared with normal sleep (+1.8%), the evening to morning ratio was increased for t-tau ( p = 0.035).
Why it matters
In 15 healthy young men, one night of sleep loss increased the evening-to-morning ratio of plasma total tau, while Aβ40, Aβ42, NfL, and GFAP did not change between sleep conditions. This is a small exploratory study and does not test any treatment, cure, or prevention.
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72/100
Survivors of a traumatic brain injury can deteriorate years later, developing brain atrophy and dementia.
Why it matters
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.
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In patients with mild vascular dementia, anodal tDCS of the left DLPFC is able to produce additional effects to cognitive training on visual short-term memory, verbal working memory, and executive control.
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Hippocampal sclerosis of aging (HS-Aging) is a high-morbidity brain disease in the elderly but risk factors are largely unknown.
Why it matters
This study found an association between the ABCC9 gene and hippocampal sclerosis of aging, a brain disease in the elderly. It is a genetic association study, so it does not show that changing this gene would treat or prevent the disease.
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Genome-wide association studies (GWAS) have identified a region upstream the BIN1 gene as the most important genetic susceptibility locus in Alzheimer's disease (AD) after APOE.
Why it matters
This study found that a genetic variant upstream of the BIN1 gene increased BIN1 expression and Alzheimer's disease risk, and that the variant was linked to tau but not amyloid loads in brains. The authors propose BIN1 affects risk by influencing tau pathology.
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A mean value of 85.7% was achieved for overall diagnostic accuracy, 82.4% for positive predictive value, and 87.5% for negative predictive value.
Why it matters
This study assessed the accuracy of a dopamine transporter imaging test for diagnosing dementia with Lewy bodies. It concerns diagnosis of Lewy body disease, not the treatment, cure or prevention of Alzheimer's disease.
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These findings are consistent with smaller hippocampal volume in adult subjects with chronic PTSD.
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Subject to the usual caveats inherent in studies with small sample size, this pilot phase 2 study supports further investigation of this novel treatment strategy using a metal-protein-attenuating compound.
Why it matters
In this small pilot phase 2 trial of 36 patients with moderately severe Alzheimer disease, clioquinol treatment was associated with significantly less worsening than placebo in the more severely affected group, and plasma Abeta42 declined in the clioquinol group while rising in the placebo group. The authors state that the small sample size limits these findings and that further investigation of this metal-protein-attenuating compound is needed.