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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Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease.
Why it matters
In this meta-analysis of 22 studies, the APOE-ε2 allele was associated with a higher prevalence of Parkinson's disease, while the APOE-ε4 allele was not. This differs from Alzheimer's disease, where APOE-ε4 increases prevalence and APOE-ε2 is protective.
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Overproduction of IL-6, a proinflammatory cytokine, is associated with a spectrum of age-related conditions including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, periodontal disease, frailty, and functional decline.
Why it matters
In this longitudinal study, caregivers of spouses with dementia had an average rate of increase in the inflammatory cytokine IL-6 about four times as large as noncaregivers, and this steeper rise persisted even years after the spouse's death. It describes a possible mechanism linking chronic stress to inflammation, not a treatment, cure, or prevention for Alzheimer's disease.
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The criteria ought to provide the foundation for research work into the neuropsychology, neuropathology, genetics, molecular biology, and epidemiology of these important clinical disorders that account for a substantial proportion of cases of primary degenerative dementia occurring before the age of 65 years.
Why it matters
This 1998 international workshop consensus set out research diagnostic criteria for three syndromes of frontotemporal lobar degeneration: frontotemporal dementia, progressive nonfluent aphasia and semantic dementia. Each has listed core and supportive features, with broad inclusion and exclusion rules for the condition as a whole. The authors describe these disorders as accounting for "a substantial proportion" of degenerative dementia beginning before age 65. The paper is expert agreement, not a test of accuracy or of any treatment, and it is about FTD rather than Alzheimer's disease.
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Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer beta-amyloid (Abeta) precursor protein containing a Lys670 --> Asn, Met671 --> Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age.
Why it matters
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.
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Mary Poppins famously asserted that "a spoonful of sugar helps the medicine go down," but this bon mot is likely wrong in almost every way.
Why it matters
This editorial discusses how diet, glucose regulation and GLP-1 receptor agonists relate to stroke and dementia risk. It presents commentary rather than new trial results on treating, curing or preventing Alzheimer's disease.
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Alzheimer's disease (AD) has a strong genetic component, with APOE ε4 being the most established risk factor through its effects on beta-amyloid (Aβ) metabolism and microglial function.
Why it matters
This study found that the ABI3S209F variant was associated with increased risk of Alzheimer's disease and neurodegenerative disorders, and that carriers with APOE ε4 had higher brain amyloid burden. It is a genetic and imaging study in asymptomatic older adults and does not test any treatment, cure, or prevention.
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61/100
A total of 365 participants (mean [SD] age, 75.4 [7.9] years; 192 female [52.6%]) in the ADNI tau-PET group and 524 participants (mean [SD] age, 77.1 [7.9] years; 268 male [51.1%]) in the ADNI p-tau217 group were selected from the 998 individuals who were Aβ+ in the ADNI cohort and used to generate tau-clinical mismatch models with 55.6% to 57.1% classified as canonical (CDR-SB commensurate to tau), 23.7% to 24.7% as resilient (CDR-SB tau).
Why it matters
Models of tau-clinical mismatch identified people with accelerated disease course due to copathology and those with greater cognitive resilience to pathology. These models may help predict individual cognitive trajectories, including during antiamyloid therapy.
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The LBD-present group had higher QSM values in the SNc (P = 0.008) than the LBD-absent group with no differences in SNr.
Why it matters
This study found that higher QSM values in the substantia nigra pars compacta distinguished Lewy body disease cases with good accuracy and correlated with parkinsonism severity, providing neuropathological confirmation of a biomarker. It could facilitate more precise diagnoses but no treatment or cure.
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At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS).
Why it matters
In people with amyloid-beta, a higher free-water fraction in the choroid plexus was linked to worse glymphatic function, more tau, synaptic loss, brain atrophy, and worse cognition, and it increased faster over time than in controls. This identifies a possible imaging marker of disease progression but does not test any treatment.
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WMHs in the frontoparietal and anterior periventricular region were associated with blood pressure traits, WMH genetic risk score (GRS), baseline and decline in general cognitive performance, incident all-cause dementia, and ischemic stroke.
Why it matters
This longitudinal study found that white matter hyperintensities in different brain regions were linked to different risk factors and outcomes, including dementia and stroke. The authors say that accounting for where these hyperintensities are located is key to understanding the mechanisms behind small vessel disease and moving toward personalized treatments.
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Recent studies suggest the existence of brain-first and body-first subtypes within the Lewy body disorder (LBD) spectrum, including Parkinson's disease.
Why it matters
This postmortem study of Lewy body disease describes brain-first and body-first subtypes, including two body-first subtypes with vagal or sympathetic predominance. It concerns Lewy body disease, not Alzheimer's disease, and does not test any treatment, cure or prevention.
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Thirty-five patients with probable DLB, 37 patients with MCI-LB, and 100 individuals without cognitive impairment were included.
Why it matters
Brain hypometabolism begins to evolve during the prodromal stages of dementia with Lewy bodies, with changes paralleling symptomatic progression. These data may inform clinical practice and trials planning, based on a case-control study of 72 patients with DLB or MCI-LB and 100 individuals without cognitive impairment.
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Expression profiles of amacrine cells (interneurons within the retina) were robustly enriched in schizophrenia genetic risk across mammalian species and in different developmental stages.
Why it matters
This study found no consistent associations between retinal cell types and Alzheimer disease genetic risk. It does not provide evidence for using retinal cell profiles to study or predict Alzheimer disease.
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Choline alfoscerate exhibits additional cognitive improvement in both cognitive and noncognitive domains, supporting the findings of the ASCOMALVA trial.
Why it matters
Adding choline alfoscerate to donepezil was linked to better memory and noncognitive scores than donepezil alone at 12 and 24 weeks in this small 119-patient trial. It does not show a cure or prevention, and the comparison with other nootropics was less clear.
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Pathological hallmarks of Alzheimer's disease (AD) precede clinical symptoms by years, indicating a period of cognitive resilience before the onset of dementia.
Why it matters
In mice with tauopathy, removing the Cgas gene reduced the microglial interferon response and preserved synapses and plasticity. This is animal research, so it does not yet show any treatment or prevention benefit in people.
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The analysis included 26 original articles describing (1050 rodents) with AD-like symptoms.
Why it matters
Across 26 studies of 1050 rodents with Alzheimer-like symptoms, animals given cannabinoid agonists did better on a learning task (shorter escape latency) and had lower levels of glial cell markers such as glial fibrillary acid protein and Iba1. Inflammatory markers fell clearly in wild-type mice but not significantly in transgenic mice. Since these are animal results, the authors call for population studies and well-designed clinical trials to see whether cannabinoid agents help people.
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61/100
Brain regions with higher synaptic density are associated with a higher 18F-AV-1451 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminishes with disease severity.
Why it matters
In people with progressive supranuclear palsy or corticobasal degeneration, two tau-related brain diseases, brain regions with more synapses were linked to higher binding of the tau scan tracer 18F-AV-1451. This link weakened as the disease became more severe. The finding hints at how tau build-up and synapse loss relate over the course of these conditions, but the record gives few details.
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Gut microbiota composition was associated with amyloid and p-tau status.
Why it matters
This study investigated associations between gut microbiota composition and Alzheimer's disease biomarkers using machine learning in patients with dementia, mild cognitive impairment and subjective cognitive decline. It found modest prediction and some microbial associations, but it is about correlations with biomarkers, not treatment or cure.
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White matter hyperintensities (WMHs) are commonly assumed to represent non-specific cerebrovascular disease comorbid to neurodegenerative processes, rather than playing a synergistic role.
Why it matters
This longitudinal study compared how white matter hyperintensities relate to grey matter atrophy and cognitive decline in normal aging, mild cognitive impairment, Alzheimer's dementia, frontotemporal dementia, and Parkinson's disease. It is observational, so it cannot show that reducing white matter hyperintensities would slow or prevent dementia.
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Although all p-tau variants increased across the AD continuum, p-tau217 Lilly showed the greatest dynamic range (13-fold increase vs 1.9-5.4-fold increase for other p-tau variants for AD dementia vs non-AD).
Why it matters
Comparing CSF p-tau variants, p-tau217 showed the largest increase across the Alzheimer's continuum and stronger links to amyloid and tau PET than the other variants. This is a biomarker comparison for diagnosis and does not test any treatment, cure, or prevention.
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Plasma proteins affect biological processes and are common drug targets but their role in the development of Alzheimer's disease and related dementias remains unclear.
Why it matters
This study examined thousands of plasma proteins for links to cognitive decline and 20-year risk of dementia in two cohort studies. It does not show that targeting these proteins prevents or treats dementia, and the findings are about associations that may point to future research.
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61/100
Alzheimer's disease is characterized by β-amyloid plaques and tau tangles.
Why it matters
In 88 people whose brains were examined after death, both amyloid plaques and tau tangles were independently linked to higher blood P-tau217, while levels were not raised in 9 people with other (non-Alzheimer's) tau diseases. In 426 living people scanned with PET (BioFINDER-2), P-tau217 tracked amyloid in early disease and both amyloid and, more strongly, tau in later disease. This is an association study supporting P-tau217 as a blood marker of Alzheimer's brain changes; it tests no treatment, and the non-Alzheimer's comparison is small.
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Alzheimer's disease (AD) is the most prevalent cause of dementia 1 .
Why it matters
In 5xFAD mice, ablating meningeal lymphatic vessels affected microglia responses and the outcome of anti-amyloid immunotherapy. This is animal research and does not establish a treatment, cure or prevention for Alzheimer's disease in humans.
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TREM2 is a receptor for lipids expressed in microglia.
Why it matters
In a mouse model of amyloid buildup, an antibody that activates human TREM2 increased microglia proliferation and reduced pathology. This is animal work, so it does not show that TREM2 activation helps people with Alzheimer's.
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Synucleinopathies are neurodegenerative diseases that are associated with the misfolding and aggregation of α-synuclein, including Parkinson's disease, dementia with Lewy bodies and multiple system atrophy 1 .
Why it matters
This laboratory study showed that an assay measuring α-synuclein aggregates in cerebrospinal fluid could tell Parkinson's disease apart from multiple system atrophy with high sensitivity. It concerns diagnosis of these synucleinopathies, not 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.
- Immunohistochemical characterization of microglia in Nasu-Hakola disease brains
- Astrocytic pathology of methionine sulfoximine-induced encephalopathy
- Cerebrospinal fluid levels of MMP-2, 7, and 9 are elevated in association with human immunodeficiency virus dementia
- Profiles of extracellular miRNA in cerebrospinal fluid and serum from patients with Alzheimer's and Parkinson's diseases correlate with disease status and features of pathology
- Frontotemporal dementia as a consequence of GRN mutations: From disease cause to models to therapies
- CSF sAPPβ, YKL-40, and neurofilament light in frontotemporal lobar degeneration
- Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2
- Refractory Status Epilepticus in a Patient With Aducanumab-Induced Amyloid-Related Imaging Abnormalities
- A pilot randomized controlled double-blind trial of intermittent theta burst stimulation (iTBS) repetitive transcranial magnetic stimulation (rTMS) to improve memory in mild cognitive impairment (MCI): a study protocol
- Depletion of GSH in glial cells induces neurotoxicity: relevance to aging and degenerative neurological diseases