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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The roles of activated glia and of glial cytokines in the pathogenesis of Alzheimer's disease are reviewed.
Why it matters
This review describes how the glial cytokine IL-1 can promote processes linked to amyloid deposition and neuritic plaque formation, including upregulation of beta-amyloid precursor protein processing. It is a pathogenic review of possible mechanisms and reports no treatment trial or patient outcome.
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The discovery that the epsilon 4 allele of the apolipoprotein E (apoE) gene is a putative risk factor for Alzheimer disease (AD) in the general population has highlighted the role of genetic influences in this extremely common and disabling illness.
Why it matters
This autopsy study found that people with the APOE epsilon 4 allele and people with Down syndrome both have more amyloid deposits in the brain, but likely through different mechanisms. It shows that different genetic subgroups of Alzheimer's patients have measurably different patterns of brain pathology.
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We have investigated the possible effect of estrogen on the metabolism of the Alzheimer amyloid precursor protein (APP).
Why it matters
In a cell line with high estrogen receptors, treatment with 17 beta-estradiol increased release of a soluble amino-terminal fragment of APP, suggesting non-amyloidogenic processing. This is cell-culture work and does not show that estrogen prevents or treats Alzheimer's disease.
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Abnormal metabolic processing of the beta/A4 amyloid precursor protein (APP) has been implicated in the pathogenesis of Alzheimer disease.
Why it matters
This study examined the subcellular distribution of amyloid precursor protein in rat brain tissue and cultured cells to clarify its trafficking pathways. It is basic laboratory research and does not test or provide any treatment, cure or prevention for Alzheimer's disease.
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The pattern of cerebral degeneration in Alzheimer's disease (AD) patients suggests that basic auditory capacities should be normal in AD, whereas progressively higher levels of auditory function should be increasingly impaired.
Why it matters
This study found that people with mild to moderate Alzheimer's disease had specific hearing-related deficits compared with healthy elderly controls, but these deficits did not relate to age, dementia severity, or how long they had been ill. It is a small study of 19 patients and does not test any treatment, so it does not show how to cure or prevent Alzheimer's disease.
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Microtubule-associated protein tau is known to be hyperphosphorylated in Alzheimer disease brain and this abnormal hyperphosphorylation is associated with an inability of tau to promote the assembly of microtubule in the affected neurons.
Why it matters
This study measured phosphoprotein phosphatase activity in postmortem brains and suggested that a deficiency in this system might contribute to abnormal tau phosphorylation in Alzheimer's disease. It describes a possible mechanism but does not test any treatment.
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Clinical and neuropathological evaluation of elderly subjects with dementia has traditionally concentrated upon the focal distribution of brain disease, ignoring changes in the complex connections that link brain areas and that are crucial for cognition.
Why it matters
Using EEG coherence, this study found that Alzheimer-type dementia involves diminished connections between brain areas linked by long fiber tracts, supporting the idea that it is a disconnection syndrome. It offers no treatment, cure, or prevention, and only describes differences in brain connectivity between dementia types.
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A strong immunoreactivity for ferritin was observed in the neuritic (senile) plaques in Alzheimer's disease hippocampus.
Why it matters
This study found ferritin accumulation in the neuritic plaques of Alzheimer's disease hippocampus, almost exclusively associated with proliferated microglia that were also positive for HLA-DR. It describes brain tissue findings but does not report a treatment, cure, or prevention for Alzheimer's disease.
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The 4.2-kilodalton (kDa) polypeptide associated with the cerebral amyloid deposits of Alzheimer's disease (AD) derives from a much larger protein that is encoded by a gene on chromosome 21.
Why it matters
This study used antibodies to map where the amyloid precursor protein is found in normal and Alzheimer's brain tissue, finding it concentrated in neuronal lysosomes. It is descriptive mapping work and does not test any treatment or show how to prevent the disease.
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The clinical and biological features of Alzheimer disease are not uniform in their expression; heterogeneity is evident in the disease's clinical, anatomic, and physiologic characteristics.
Why it matters
This review describes that Alzheimer's disease is not uniform and that subtypes exist based on features such as inheritance, age of onset, and brain metabolism. It does not report any treatment, cure, or prevention, and notes that similar brain abnormalities are found in people 45 or older with Down syndrome.
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Alzheimer disease is the most common cause of dementia in adults.
Why it matters
In 10 people with Alzheimer-type dementia compared with six healthy age-matched controls, brain scans showed relatively less glucose uptake in the temporoparietal cortex on both sides. This describes a metabolic feature of the disease and does not test any treatment, cure, or prevention.
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45/100
Among 5712 adults (mean [SD] age, 63.47 (8.15) years; unweighted 3663 [53.92%] female), higher ln(ptau-181) was associated with ECog-12 memory (unstandardized β = 0.088; 95% CI, 0.005-0.170).
Why it matters
Plasma biomarkers p-tau181, NfL, and GFAP, but not Aβ42/40, were associated with greater subjective cognitive decline in Hispanic and/or Latino adults. These findings underscore their potential utility in early detection strategies.
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Thirty-two patients met inclusion criteria (lecanemab, N=15; donanemab, N=17).
Why it matters
In 32 patients receiving lecanemab or donanemab in routine practice, PET scans showed substantial amyloid clearance, and greater amyloid reduction was associated with greater MMSE improvement in adjusted analyses. This is a small real-world study, and it did not find that amyloid reduction was significantly linked to baseline amyloid burden, ARIA, or APOE-ε4 status.
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Donanemab provides clinical benefits but is unlikely to be cost-effective under current Australian thresholds.
Why it matters
This modelling study estimated that donanemab for early Alzheimer disease would substantially increase healthcare costs compared with standard care in Australia. It is a simulation based on published inputs rather than a trial of patient outcomes, so it speaks to cost and value rather than whether the drug works.
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Thirteen differentially expressed CSF proteins in A+T+ individuals correlated positively with tryptophan metabolites and pyroglutamate, and negatively with regulatory T cells, isobutyrate, and dendritic cells.
Why it matters
In cerebrospinal fluid and blood samples, thirteen proteins linked to metabolism and neuronal function tracked with Alzheimer's pathology and with tryptophan metabolites. This is biomarker research and does not show that changing these pathways treats or prevents the disease.
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Compared with men, women had greater amyloid burden (B = 0.05; 95% CI, 0.02-0.07; P < .001), Braak stages III and IV (B = 0.05; 95% CI, 0.02-0.08; P = .003) and Braak stages V and VI (B = 0.09; 95% CI, 0.06-0.12; P < .001) tau burden, and AD signature thickness (B = 0.04; 95% CI, 0.02-0.05; P < .001).
Why it matters
In a diverse community-based cohort, women had greater amyloid and tau burden but better preserved structural brain integrity than men. Sex differences in tau burden were more pronounced among APOE ε4 carriers, and findings were not modified by age or race and ethnicity.
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Transcranial direct current stimulation (tDCS) is a promising non-invasive intervention for mild cognitive impairment (MCI).
Why it matters
In 55 people with mild cognitive impairment, higher transcranial direct current stimulation electrical field strength was associated with improved white matter integrity in specific tracts, with greater plasticity in Aβ-positive individuals and APOE ε4 non-carriers. APOE ε4 status moderated the relationship between field strength and executive function, but this is a small prospective study and does not establish a treatment for Alzheimer's disease.
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Regardless of method or adjustment, the resulting heritability estimates were highly variable across populations.
Why it matters
This study found that estimates of how much Alzheimer disease is inherited varied widely across different populations, and including APOE ε4 status reduced those estimates. It highlights that population-specific and unmeasured factors such as lifestyle and environment contribute to these differences, but it does not test any treatment or prevention.
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The CSF and plasma cohorts were on average 71.4(±8.5) and 72.2 (±9.3) years of age, 49.1%/50.8% was female, and 263/453 (0.59%/51.8%) were cognitively impaired, respectively.
Why it matters
This study describes how CSF and plasma tau markers change across the Alzheimer's continuum, with %p-tau217 changing early before Aβ-PET positivity and %p-tau205 and MTBR-tau243 tracking later tau-PET changes. These are biomarker trajectories for detection and monitoring, not treatments, cures, or prevention.
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Monoclonal antibodies such as lecanemab and donanemab show reduction in amyloid plaque and slowing of cognitive and functional decline (modest) in early AD (mild cognitive impairment or mild dementia).
Why it matters
Lecanemab and donanemab modestly slow cognitive and functional decline in early Alzheimer disease, while aducanumab showed mixed results and is not approved by Health Canada. Tau-targeting and anti-inflammatory agents are still under investigation and have not yet shown definitive benefit.
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BackgroundMost adults with Down syndrome will develop Alzheimer's disease (AD) due to the triplication of the amyloid precursor protein in the 21 st chromosome.
Why it matters
Using Medicaid and Medicare data and machine learning, this case-control study identified age, dual enrollment, incident epilepsy or ulcer, hypothyroidism, schizophrenia and hyperlipidemia as predictors of Alzheimer's disease diagnosis in adults with Down syndrome. These are risk associations for prediction, not evidence of a treatment, cure or prevention.
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A total of 64 patients were enrolled in this ongoing real-world study.
Why it matters
In 64 Chinese patients with early Alzheimer's disease, lecanemab caused mostly mild side effects, and cognitive scores stayed stable over 6 months while plasma amyloid-β 42 and 40 rose. The authors note the high dropout rate and lack of a control group mean these preliminary results must be interpreted cautiously.
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Mixed dementia is caused most often by the coexistence of Alzheimer's disease (AD) and vascular dementia (VaD) pathologies.
Why it matters
This review summarizes the pathophysiology of mixed Alzheimer's disease and vascular dementia and describes animal, cell culture and brain organoid models used to study it. It reports no findings on treating, curing or preventing Alzheimer's disease.
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45/100
Alzheimer disease (AD) is characterized by amyloid-β plaques (A), tau tangles (T), and neurodegeneration (N), collectively defining the ATN framework.
Why it matters
This study compared plasma and imaging A/T/N biomarkers for predicting cognitive decline and assessed combining them across modalities. It is about prognosis and biomarker use, not about treating, curing or preventing Alzheimer's disease.
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We analyzed data from 3433 dementia-free participants with either magnetic resonance imaging or positron emission tomography (PET) data at baseline (mean [standard deviation] age: 65 [9] years, 36% non-Hispanic White [NHW], 27% Black, 37% Hispanic, and 63% women).
Why it matters
Among 3433 dementia-free participants, the distribution of neuroimaging markers such as amyloid and tau differed across racial/ethnic groups by sex/gender. The authors suggest an intersectional approach can help tailor prevention and treatment efforts, but the study itself reports marker differences, not treatment effects.
From across this topic
10 of the 5,172 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.
- Assessment of Demographic, Genetic, and Imaging Variables Associated With Brain Resilience and Cognitive Resilience to Pathological Tau in Patients With Alzheimer Disease
- CSF biomarkers of Alzheimer disease in HIV-associated neurologic disease
- Cerebrospinal fluid beta-amyloid 1-42 concentration may predict cognitive decline in older women
- Donepezil is associated with delayed nursing home placement in patients with Alzheimer's disease
- Mapping the impact of age and APOE risk factors for late onset Alzheimer's disease on long range brain connections through multiscale bundle analysis
- Review on Alzheimer-Suppressing Potential of different Medicinal plant
- The effectiveness and cost-effectiveness of donepezil, galantamine, rivastigmine and memantine for the treatment of Alzheimer's disease (review of Technology Appraisal No. 111): a systematic review and economic model
- Diet and Inflammation in Cognitive Ageing and Alzheimer's Disease
- Alzheimer's disease: synaptic dysfunction and Abeta
- The role of cerebral ischemia in Alzheimer's disease