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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In a community-based cohort of 70-year olds, P-NfL was associated with both prevalent and incident CKD, while CSF and/or imaging measures did not differ by CKD status.
Why it matters
In this cohort of 70-year-olds, plasma neurofilament light was associated with both existing and new chronic kidney disease, while CSF and imaging measures did not differ by kidney disease status. This suggests kidney function may need to be considered when interpreting plasma neurofilament light levels, but it does not report any treatment, cure, or prevention of Alzheimer's disease.
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The clinical diagnosis of synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), is challenging, especially at an early disease stage, due to the heterogeneous and often non-specific clinical manifestations.
Why it matters
In 439 spinal-fluid samples from people with parkinsonism or dementia, an RT-QuIC test detected misfolded α-synuclein in 95.3% of Lewy body disorders (dementia with Lewy bodies, Parkinson's disease, and the possible early-stage syndromes iRBD and pure autonomic failure). It was negative in 98% of 101 autopsy-confirmed cases without Lewy body pathology. Nearly all multiple system atrophy samples tested negative, so the test points to Lewy body disease specifically. It is not a test for Alzheimer's disease or a treatment.
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Cognitive testing follow-up occurred for 1 to 18 years (mean [SD], 0.98 [2.25] years); autopsy-verified diagnoses were available for 120 of 845 participants with diseases (14.2%).
Why it matters
CSF neurofilament light levels were associated with cognitive impairment in patients with dementia, motor neuron disease and movement disorders, and correlated inversely with baseline MMSE scores. It is a marker of neuroaxonal degeneration, not a treatment, cure or prevention.
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68/100
Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging.
Why it matters
In this cohort, higher midlife levels of circulating inflammatory markers were associated with smaller brain volumes and reduced episodic memory 24 years later. This links midlife systemic inflammation to later brain structure and memory, but does not show that treating inflammation prevents Alzheimer's disease.
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These samples were graded on an ordinal scale and genotyped for variants associated with synucleinopathies.
Why it matters
This retrospective study of brain tissue compared people with synucleinopathies who had different amounts of co-existing Alzheimer's disease pathology, graded by NIA-AA neuropathological criteria. It looked at whether those levels, and genetic variants linked to synucleinopathies, went along with the time from first motor symptoms to dementia and with overall survival, after adjusting for age at death and sex. Our record contains only the methods, not the results, so check the original paper for what was found; as a look back at post-mortem tissue, it can show associations but not causes or treatment effects.
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This study investigated a subtype of reactive astrocytes called A1 and discovered that they are induced by classically activated neuroinflammatory microglia.
Why it matters
Reports that activated microglia induce reactive astrocytes that are toxic to nerve cells. It describes how one kind of brain cell acts on another and does not test any treatment in people.
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A variant within a DNase hypersensitive site 5' of TREM2, rs9357347-C, associates with reduced AD risk and increased TREML1 and TREM2 levels (uncorrected P = 6.3 × 10 -3 and 4.6 × 10 -2 , respectively).
Why it matters
This study found that a variant near TREM2, rs9357347-C, was associated with reduced Alzheimer's disease risk and increased TREML1 and TREM2 brain gene expression. It identifies a possible genetic link but does not provide a treatment or cure.
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Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients.
Why it matters
In people newly diagnosed with Parkinson's disease, those with mild cognitive impairment had more widespread cortical thinning and hippocampal atrophy over 18 months than those without cognitive impairment. The authors suggest structural imaging biomarkers may help identify those at risk of Parkinson's disease dementia earlier, though this concerns Parkinson's disease rather than Alzheimer's disease.
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68/100
Arterial stiffness was associated with Aβ plaque deposition in the brain, independent of BP and APOE ε4 allele.
Why it matters
In dementia-free very elderly adults, greater arterial stiffness was associated with having amyloid plaques in the brain, independent of blood pressure and APOE ε4. This is an observational association and does not show that reducing arterial stiffness would treat, cure, or prevent Alzheimer's disease.
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Their results on motor testing from the preceding years were plotted, and then assessed with regression analysis, to determine when markers first deviated from normal values.
Why it matters
This study examined when motor markers first deviate from normal in patients with idiopathic REM sleep behavior disorder, and found that 25% showed evidence of possible prodromal parkinsonism. It concerns the start of parkinsonism and does not test any treatment for Alzheimer's disease.
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Patients with the repeat expansion had significantly more co-morbid FTD than patients without the repeat (50%vs 12%), and a distinct pattern of non-motor cortex changes on high-resolution 3 T magnetic resonance structural neuroimaging.
Why it matters
This population-based cohort study found that patients with ALS and the C9orf72 repeat expansion had significantly more co-morbid frontotemporal dementia and a distinct pattern of non-motor cortex changes on neuroimaging. It concludes that these patients seem to present a recognisable phenotype with earlier disease onset, cognitive and behavioural impairment, and reduced survival.
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IER is as effective as CER with regard to weight loss, insulin sensitivity and other health biomarkers, and may be offered as an alternative equivalent to CER for weight loss and reducing disease risk.
Why it matters
In this randomized trial in 107 overweight or obese premenopausal women, intermittent and continuous energy restriction were equally effective for weight loss over 6 months. It measured dementia risk biomarkers among other outcomes but reports no result on treating, curing, or preventing Alzheimer's disease.
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67/100
These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer's disease.
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A total of 172 patients were included (86 each in the sotatercept and placebo groups).
Why it matters
This trial tested sotatercept in adults with pulmonary arterial hypertension at high risk of death, not Alzheimer's disease. It found sotatercept lowered the risk of death, lung transplantation or hospitalization for worsening pulmonary arterial hypertension compared with placebo, and the trial was stopped early for efficacy.
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Insoluble tau aggregates within neurofibrillary tangles are a defining neuropathological feature of Alzheimer’s disease (AD) and closely correlate with clinical symptoms.
Why it matters
In three cohorts, plasma eMTBR-tau243 was elevated at the mild cognitive impairment stage and increased further in dementia, and it was strongly associated with tau PET binding and cognitive performance, outperforming other plasma tau biomarkers. This is a blood biomarker for detecting and tracking tau tangles, not a treatment, cure or prevention.
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CSF-soluble misfolded α-synuclein aggregates (seeds) are readily detected in people with Parkinson's disease by α-synuclein seed amplification assay (synSAA), but identification of seeds associated with multiple system atrophy for diagnostic purposes has proven elusive.
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Neurofilament proteins have been validated as specific body fluid biomarkers of neuro-axonal injury.
Why it matters
This review says blood and fluid levels of neurofilament proteins are a validated sign of nerve-fibre damage, and that sensitive blood tests have brought measurement "to the doorstep of routine clinical practice" for tracking disease activity, treatment response and prognosis. The marker rises in many conditions — including multiple sclerosis, ALS, stroke, brain injury and frontotemporal dementia as well as Alzheimer's — so a high level signals damage, not a specific diagnosis, and the authors stress that normal ageing and other confounders must be considered when reading a result. It describes a monitoring tool, not a treatment.
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Females are disproportionately affected by dementia due to Alzheimer's disease.
Why it matters
This study examined whether biological sex affects how amyloid-beta and phosphorylated tau interact to drive tau tangle buildup in the brain. It found that females may accumulate tangles faster than males despite similar amyloid levels, which could help explain why women are disproportionately affected by Alzheimer's dementia.
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67/100
Additionally, our results indicate that AD subjects carrying APOE ε4 are more responsive to the neuroprotective effects of physical activity.
Why it matters
In this analysis of 95 participants with mild to moderate Alzheimer's disease from a randomized exercise trial, levels of neuroprotective proteins proBDNF, BDNF, and humanin increased in neuron-derived extracellular vesicles in the exercise group, especially in APOE ε4 carriers. The findings suggest that exercise may trigger neuroprotective effects, but the study did not measure whether this translates into cognitive improvement or disease modification.
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Aggregated insoluble tau is one of two defining features of Alzheimer's disease.
Why it matters
CSF MTBR-tau243 was most strongly associated with tau PET and cognition and least with amyloid PET, and in combination with p-tau205 explained most of the variance in tau PET burden. The authors propose it as a specific biomarker of tau aggregate pathology that may be used in interventional trials, but it is not itself a treatment.
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Transcranial pulse stimulation (TPS) is a recent development in non-invasive brain stimulations (NIBS) that has been proven to be effective in terms of significantly improving Alzheimer patients' cognition, memory, and execution functions.
Why it matters
This small pilot trial tested transcranial pulse stimulation in 30 adults with major depression, not in people with Alzheimer's disease. It found reduced depressive symptoms, but it does not show any effect on treating, curing, or preventing Alzheimer's disease.
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Both high baseline GFAP (hazard ratio 3·6, 95% CI 2·2-5·7; p 42/40 , both GFAP (2·6, 1·4-5·0; p=0·0026) and amyloid β 42/40 (2·1, 1·2-3·6; p=0·0091) were independently associated with incident dementia whereas NfL was not (1·4, 0·8-2·5; p=0·28).
Why it matters
In cognitively normal older people, higher baseline GFAP predicted incident dementia and steeper cognitive decline, while neurofilament light did not predict dementia but may serve as a monitoring marker. These are prognostic biomarkers and not a treatment, cure, or prevention.
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Neurodegenerative disorders such as Alzheimer's disease (AD), Lewy body diseases (LBD), and the amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD) spectrum are defined by the accumulation of specific misfolded protein aggregates.
Why it matters
Pooling 2600 human central nervous system samples from 26 Alzheimer's, 21 Lewy body disease and 13 ALS-FTD datasets, researchers found a shared gene activity pattern: immune and inflammation genes were turned up, while genes for mitochondrial energy production and protein clean-up were turned down. The authors suggest that neuroinflammation and failing energy and protein-disposal systems are consistent features across these different neurodegenerative diseases.
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Further investigations are needed, especially trials providing stronger interventions (such as exercise training and a controlled diet) and also embracing the sensorial domain of IC.
Why it matters
In this 3-year secondary analysis of the MAPT trial with 1445 participants, omega-3 supplementation and a multidomain intervention did not prevent decline in intrinsic capacity. The study found no benefit of these interventions for maintaining function in older adults.
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A rare coding variant (rs72824905, p.P522R) conferring protection against Alzheimer's disease (AD) was identified in the gene encoding the enzyme phospholipase-C-γ2 (PLCG2) that is highly expressed in microglia.
Why it matters
In 3595 patients with mild cognitive impairment, carriers of the PLCG2 p.P522R variant showed a slower rate of cognitive decline than non-carriers. This is an observational genetic study and reports no treatment, cure or prevention.
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.
- Regional profiles of the candidate tau PET ligand 18F-AV-1451 recapitulate key features of Braak histopathological stages
- Smartphone Passive Digital Phenotyping in Frontotemporal Lobar Degeneration
- Cortical synaptic changes and gliosis in normal aging, Alzheimer's disease and frontal lobe degeneration
- Accumulation of TDP-43 causes karyopherin-α4 pathology that characterises amyotrophic lateral sclerosis
- Longitudinal Dynamics of the Blood Proteome Within the Alzheimer Spectrum in Down Syndrome
- Genetic association of the low-density lipoprotein receptor-related protein gene (LRP), an apolipoprotein E receptor, with late-onset Alzheimer's disease
- The neurodegeneration mutant löchrig interferes with cholesterol homeostasis and Appl processing
- Isolation, characterization, and regional mapping of microclones from a human chromosome 21 microdissection library
- The role of TREM2 R47H as a risk factor for Alzheimer's disease, frontotemporal lobar degeneration, amyotrophic lateral sclerosis, and Parkinson's disease
- Cloning and characterization of HIV-1-inducible astrocyte elevated gene-1, AEG-1