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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70/100
A single traumatic brain injury is associated with an increased risk of dementia and, in a proportion of patients surviving a year or more from injury, the development of hallmark Alzheimer's disease-like pathologies.
Why it matters
In 52 cases of traumatic brain injury with survivals from 10 hours to 47 years, this study examined the neuroinflammatory response and white matter degeneration over time. It links traumatic brain injury to later dementia risk and Alzheimer's-like pathologies but reports no treatment, cure or prevention for Alzheimer's disease.
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Abnormal aggregates of the synaptic protein, α-synuclein, are the dominant pathology in syndromes known as the synucleinopathies.
Why it matters
This review describes how abnormal α-synuclein deposits underlie synucleinopathies such as Parkinson's disease and dementia with Lewy bodies, and how additional pathologies may explain differences in clinical presentation. It is about understanding these diseases, not about treating, curing, or preventing Alzheimer's disease.
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69/100
Among 2766 participants (mean [SD] age, 69.9 [3.8] years; 486 [17.9%] Black, 196 [7.1%] Hispanic, and 2007 [73.9%] White), 1311 developed the combined end point of MCI or dementia (849 participants with MCI and 752 participants with dementia).
Why it matters
In this cohort of older women, higher plasma p-tau217 was associated with developing MCI or dementia up to 25 years later. The authors say age, race, APOE ε4, and hormone therapy use should be considered when examining these associations.
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69/100
CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217.
Why it matters
Chronic kidney disease was associated with higher plasma p-tau217 concentrations, which could confound its use as a marker of amyloid pathology in people with kidney impairment. The effect was mitigated by using %p-tau217, indicating limitations for standard p-tau217 measurements in individuals with significant renal impairment.
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The primary outcome was difference in the change in Neuropsychiatric Inventory apathy scores for oxytocin versus placebo periods in the per-protocol population after 6 weeks of treatment.
Why it matters
In this phase 2 trial, intranasal oxytocin given every third day was well tolerated and was associated with a small reduction in apathy in people with frontotemporal dementia. The findings are from a per-protocol analysis.
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69/100
Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials.
Why it matters
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.
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69/100
Peripheral glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are sensitive markers of neuroinflammation and neuronal damage.
Why it matters
This study evaluated whether plasma GFAP and NfL levels predict dementia in UK Biobank participants. It is observational and does not show that measuring these markers or acting on them prevents dementia.
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An increased tau positron emission tomography (PET) signal in the medial temporal lobe (MTL) has been observed in older individuals in the absence of amyloid-β (Aβ) pathology.
Why it matters
This study examined the course of medial temporal tau deposition seen on PET in older individuals without amyloid-beta pathology and its link to Alzheimer's disease. It is an observational cohort study and does not test any treatment, cure, or prevention.
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Overall, we showed that SDB was associated with MTL atrophy in cognitively asymptomatic older adults engaged in the Alzheimer continuum, which may increase the risk of developing memory impairment over time.
Why it matters
In cognitively unimpaired older adults, sleep-disordered breathing was associated with atrophy in medial temporal lobe regions, and lower hippocampal and CA1 volumes were linked to worse episodic memory at follow-up. This is an observational association study, not a treatment, cure, or prevention trial.
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Patients in the CBS-AD group had a longer diagnostic latency, relatively benign clinical trajectory, greater cognitive impairment, and higher APOE-ε4 allele frequency than those in the CBS-non-AD group (AUC, 0.80-0.87; P Conclusions and relevance These findings suggest that studies focusing on the PSP-RS subtype are likely to miss a large number of patients with underlying PSP tau pathology.
Why it matters
Among patients with atypical parkinsonian syndromes, those with corticobasal syndrome and Alzheimer's disease pathology had a longer diagnostic delay, more cognitive impairment, and higher APOE-ε4 frequency. This is about diagnosis and does not show a treatment, cure, or prevention.
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These data support the use of cNfL as a biomarker of neuroaxonal damage and indicate that age-specific and sex-specific (and in some cases disease-specific) reference values may be needed.
Why it matters
This review of over 10,000 people found CSF neurofilament light elevated in many neurological conditions compared with healthy controls. It supports its use as a general marker of nerve damage and notes that age- and sex-specific reference values may be needed; it is not a treatment.
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Low dose ω3-PUFA supplementation, either alone or in combination with a multidomain lifestyle intervention comprising physical activity counselling, had no significant effects on muscle strength over 3 years in elderly people.
Why it matters
In this 3-year secondary analysis of the MAPT trial with 1679 participants, omega-3 supplementation and a multidomain lifestyle intervention had no significant effect on muscle strength. The study found no benefit for this outcome and does not address treating or preventing Alzheimer's disease.
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TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system.
Why it matters
Soluble TREM2 in spinal fluid is a stand-in measure of how microglia, the brain's immune cells, are working. This cross-sectional study grouped people at early stages of Alzheimer's, with and without symptoms, using the NIA-AA biomarker framework. It reports that sTREM2 is raised early and that the rise is associated with tau-related neurodegeneration but not with amyloid-β pathology. The stored text gives no figures, and as a one-time observational comparison it shows association rather than cause and tests no treatment.
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LIPUS treatment can be an alternative to surgery for established nonunions.
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69/100
Low frequency coding variants in TREM2 are associated with increased Alzheimer disease (AD) risk, while loss of functions mutations in the gene lead to an autosomal recessive early-onset dementia, named Nasu-Hakola disease (NHD).
Why it matters
In this case-control study, cerebrospinal fluid soluble TREM2 was higher in Alzheimer disease cases than controls and correlated with cerebrospinal fluid total tau and phosphorylated tau, while carriers of Nasu-Hakola disease-associated TREM2 variants had significantly lower levels. This describes an association between a biomarker and disease status and mutation status, and does not show that measuring or targeting soluble TREM2 treats, cures, or prevents Alzheimer disease.
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Vascular cognitive impairment without dementia is very common among the aged and tends to progress to dementia, but there have been no proper large-scale intervention trials dedicated to it.
Why it matters
This trial tested dl-3-n-butylphthalide in people with vascular cognitive impairment without dementia caused by subcortical ischemic small vessel disease, a condition that can progress to dementia. Preclinical studies had suggested it was effective for cognitive impairment of vascular origin, and the trial was designed to assess this in patients.
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We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms.
Why it matters
This large multiethnic genetic analysis identified several genetic loci associated with white matter hyperintensities on MRI, a marker linked to higher risk of stroke, dementia, and death. It concerns genetic influences on a brain marker, not treatment or prevention of Alzheimer's disease.
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TREM and TREM-like receptors are a structurally similar protein family encoded by genes clustered on chromosome 6p21.11.
Why it matters
This meta-analysis examined a missense variant in TREML2 and reported that it protects against Alzheimer's disease. It identifies a genetic factor linked to disease risk but does not test any treatment or prevention in people.
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The APOE ϵ4 allele is a strong risk factor across the LBD spectrum and occurs at an increased frequency in pDLB relative to PDD.
Why it matters
In 909 autopsied brains, the APOE ε4 gene variant was more common in every dementia group than in controls (7.2% of gene copies), including dementia with Lewy bodies and Parkinson disease dementia in people whose brains showed little or no Alzheimer-type change (31.9% and 19.1%). After adjusting for age and sex, carrying ε4 was linked to about 6 times higher odds of "pure" Lewy body dementia and about 3 times higher odds of Parkinson disease dementia. The authors say this "suggests that ϵ4 increases the likelihood of presenting with dementia" in these diseases, possibly through routes "unrelated to amyloid processing", but this is an association, not proof of cause.
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69/100
Primary clinical efficacy outcomes were not significant.
Why it matters
In this phase 2 trial, the 250 mg dose of ELND005 showed no significant differences from placebo on the primary measures of cognition or daily living. The authors state that primary clinical efficacy outcomes were not significant, though safety and biomarker results will guide future studies.
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The eMERGE (electronic MEdical Records and GEnomics) Network is an NHGRI-supported consortium of five institutions to explore the utility of DNA repositories coupled to Electronic Medical Record (EMR) systems for advancing discovery in genome science. eMERGE also includes a special emphasis on the ethical, legal and social issues related to these endeavors.
Why it matters
This describes a research network that links DNA samples to electronic medical records, and dementia is one of the conditions being studied with genome-wide association genotyping. It is a description of infrastructure and methods, not a treatment, cure, or prevention finding.
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69/100
Despite evidence of target engagement as indicated by an increase in serum insulin-like growth factor-1, the human growth hormone secretagogue MK-677 25 mg was ineffective at slowing the rate of progression of Alzheimer disease.
Why it matters
In this double-blind, multicenter trial of 563 patients with mild to moderate Alzheimer disease, MK-677 increased serum IGF-1 levels but showed no significant differences from placebo on the CIBIC-plus or on change from baseline scores on the ADAS-Cog, ADCS-ADL, or CDR-sob. The treatment had no clinical effect on AD progression.
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Two regions achieved genome-wide significance with TDP-43: apolipoprotein E (APOE) and TMEM106B. Three loci reached genome-wide significance with HS: APOE, TMEM106B, and granulin precursor (GRN).
Why it matters
This genetic study found that TDP-43 proteinopathy and hippocampal sclerosis share risk genes, including APOE and TMEM106B, with effects on hippocampal sclerosis partly mediated through TDP-43. It identifies shared genetic risk factors but does not test any treatment, cure, or prevention.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by amyloid-beta (Aβ) accumulation and neuroinflammation.
Why it matters
This sub-analysis of a phase 2 trial looked at spinal fluid from 30 people with Alzheimer's given resveratrol and 21 given placebo over 52 weeks. Resveratrol was linked to lower levels of markers of nerve damage and inflammation, including TREM2 and MMP-9. The authors say resveratrol may have anti-inflammatory and protective effects, but whether these biomarker changes translate into clinical benefit still needs study.
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Our study suggests a possible utility of plasma Aβ42/40, P-tau181, and P-tau231 as a noninvasive biomarkers to assess amyloid copathology in DLB, and plasma GFAP and NfL as monitoring biomarkers for cognitive symptoms in DLB.
Why it matters
In 562 people with dementia with Lewy bodies, Alzheimer's disease, or healthy controls, plasma amyloid ratio and p-tau differed by amyloid status in the Lewy body group. The study examined how these blood biomarkers relate to spinal fluid amyloid, cognition, and core features in dementia with Lewy bodies, but the available summary does not report whether they predict cognitive decline.
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.
- RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention
- CNS inflammation and macrophage/microglial biology associated with HIV-1 infection
- Effect of apolipoprotein E genotype and diet on apolipoprotein E lipidation and amyloid peptides: randomized clinical trial
- Phagocytosis executes delayed neuronal death after focal brain ischemia
- β-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects
- Characterizing tau deposition in chronic traumatic encephalopathy (CTE): utility of the McKee CTE staging scheme
- Association of Apolipoprotein E ε4 With Transactive Response DNA-Binding Protein 43
- Differential Associations of Apolipoprotein E ε4 Genotype With Attentional Abilities Across the Life Span of Individuals With Down Syndrome
- Astrocytic estrogen receptors and impaired neurotrophic responses in a rat model of perimenopause
- A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation