Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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To assess the relationship between dementia, neuronal loss, and neuropathological findings in Alzheimer's disease (AD), we counted the number of neurons, senile plaques, and neurofibrillary tangles in a high-order association cortex.
Why it matters
Counting cells in one region of the brain's outer layer (the superior temporal sulcus) in 34 people with Alzheimer's and 17 people without dementia, this 1997 study found that more than half of the neurons were lost in Alzheimer's. Neuron loss and tangles both rose with how long and how severe the illness was, and the neuron loss was many times greater than the number of tangles. Plaque counts and amyloid burden did not track neuron loss, tangles or disease duration. The authors say this suggests neuron loss contributes directly to the memory and thinking problems, but the study measured links, not cause, and tested no treatment.
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A candidate gene for the chromosome 1 Alzheimer's disease (AD) locus was identified (STM2).
Why it matters
Researchers identified a candidate gene (STM2) for the familial form of Alzheimer's disease linked to chromosome 1, and found a point mutation in it in affected people from Volga German families. The gene closely resembles a chromosome 14 Alzheimer's gene, which the authors say strongly supports the idea that mutations in both genes cause disease.
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These findings support previous contentions that a "preclinical phase" of detectable cognitive deficits can precede the clinical diagnosis of probable AD by many years, and they also support the hypothesis that problems with secondary verbal memory are among the first signs of AD.
Why it matters
In this 13-year prospective study, most screening neuropsychological measures were individually related to later Alzheimer's disease diagnosis, but only measures of verbal memory and immediate auditory attention span remained significantly related in stepwise regression. The results suggest cognitive changes can be detected years before clinical diagnosis, which may help identify people early, but the study reports no treatment or cure.
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Clinicians accurately predicted AD pathological findings or their absence in most cases.
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Gene dosage of the apolipoprotein E (APOE) epsilon 4 allele is a major risk factor for familial Alzheimer disease (AD) of late onset (after age 60).
Why it matters
This study found that the APOE epsilon2 allele appears to protect against late-onset Alzheimer's disease, while the epsilon4 allele increases risk, with the two versions acting in opposite directions. It supports the idea that apolipoprotein E is directly involved in the disease, but it does not test any treatment or prevention.
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This study measured the annual rate of cognitive change in patients with Alzheimer's disease and determined the effects of clinical variables on that rate.
Why it matters
This longitudinal study measured the annual rate of cognitive change in 111 patients with Alzheimer's disease and compared two cognitive scales. It describes measurement and predictors of decline but does not test any treatment, cure, or prevention.
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This statistical prediction is recommended for use in combination with clinical judgment to certify DAT patients for Medicare hospice coverage.
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False-positive (FP) plasma results may lead to overtreatment and false-negative (FN) results to missed or delayed disease-modifying therapies.
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Alzheimer's disease (AD) is a major cause of dementia and cognitive decline.
Why it matters
Using longitudinal imaging from over 1000 measurements in the DELCODE study, loss of episodic memory network deactivation was linked to amyloid and tau positivity and appeared before cognitive decline. The authors conclude that synaptic dysfunction and neurodegeneration are independent drivers of cognitive decline, providing a rationale for targeting synaptic dysfunction, but no treatment is tested.
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Overall, the available evidence suggests that natural compounds confer multitarget neuroprotective effects that directly engage with key pathological mechanisms underlying AD.
Why it matters
This systematic review of 41 lab studies, 25 in animals and 16 in cells, found that natural compounds such as plant chemicals and herbal formulas consistently showed protective effects against Alzheimer's-related changes, including less oxidative stress, inflammation and amyloid-β clumping. The authors note that problems with absorption, standardization and proof of clinical benefit remain, and that well-controlled clinical trials are needed before these can be considered treatments.
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59/100
BackgroundAlzheimer's disease (AD) accounts for the majority of dementia-related disorders among aging populations.
Why it matters
This review found that task-based EEG shows consistent brain wave changes in people with mild cognitive impairment and Alzheimer's disease, such as reduced event-related potential amplitudes and disrupted connectivity. These EEG measures may help detect cognitive impairment early, but the review does not evaluate any treatment or cure.
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Meta-analyses of epidemiological studies have suggested that Alzheimer's disease (AD) may be linked with exposure to extremely low frequency (ELF) magnetic fields (MF).
Why it matters
This cohort study found no association between residential extremely low frequency magnetic fields from indoor transformer stations and Alzheimer's disease risk (hazard ratio 1.02). It is an observational study of exposure and risk, not a treatment, cure, or prevention trial.
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Microglia are resident immune cells of the brain and are implicated in the etiology of Alzheimer's disease (AD) and other diseases.
Why it matters
Analysing primary microglia from 189 human postmortem brains, this study found gene expression changes associated with multiple Alzheimer's disease phenotypes, including dementia severity and neuropathological lesions, plus changes in gene-gene coordination and disease subtypes. It furthers understanding of microglia in Alzheimer's disease biology and nominates candidate targets, but identifies no treatment, cure or prevention.
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The pTau217/Aβ42 ratio demonstrated the highest diagnostic accuracy, with an AUC of 0.927 (0.900-0.954).
Why it matters
A blood test measuring the ratio of two proteins, pTau217 and Aβ42, was better at detecting brain amyloid than measuring either protein alone. The authors say this ratio could be useful, but it needs to be validated in more and different clinical settings before it can be widely used.
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Higher structural stiffness of the carotid artery is associated with cognitive decline, whereas both structural and load‐dependent stiffness are associated with brain structural abnormalities common in Alzheimer disease‐related dementias.
Why it matters
This cohort study found that greater structural carotid artery stiffness was associated with greater longitudinal cognitive decline and structural brain abnormalities related to Alzheimer's disease and related dementias. It identifies a vascular risk factor but does not test a treatment, cure, or prevention.
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Early onset hallucinations were significantly more common in pLBD than pAD (OR 0.069 [95% CI 0.012-0.397], p = 0.003) or mixed AD+LBD (OR 0.09 [95% CI 0.010-0.771], p = 0.028) and there was a greater increase in the odds of hallucinations over time in pAD and AD+LBD than pLBD such that there was was no difference in the prevalence of late-onset hallucinations between pLBD, pAD or AD+LBD.
Why it matters
In this post-mortem cohort, hallucinations early in disease were more common in pure Lewy body disease than in pure Alzheimer's disease or mixed disease, and were linked to specific brain pathology. Later hallucinations increased in Alzheimer's and mixed disease, suggesting different underlying causes over time.
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AD was common in both AD-related syndromes (110/125 [88%]) and FTLD-related syndromes (45/198 [23%]).
Why it matters
This clinicopathological study measured three blood biomarkers (p-tau217, NfL, and GFAP) in 349 autopsied individuals, including people with syndromes usually linked to frontotemporal lobar degeneration. It examined whether these blood tests can detect Alzheimer's disease pathology in people whose clinical syndrome is not typical Alzheimer's, but the available summary does not report how well the biomarkers performed.
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Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time.
Why it matters
This review states that immune processes appear to play a pivotal role in Alzheimer's disease, based on experimental, epidemiological, neuropathological and genetic evidence. It reports no treatment, cure or prevention and describes mechanisms rather than tested therapies.
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59/100
Alzheimer's disease (AD) is the leading cause of dementia globally, having a pathophysiology that is complex and multifactorial.
Why it matters
This systematic review gathers evidence on four kinds of non-coding RNAs, molecules that regulate genes without making proteins, in Alzheimer's disease. They are involved in amyloid-beta clumping, tau changes, inflammation and other disease processes, and may serve as markers for early detection and as new treatment targets. The authors stress that more research is needed to confirm their clinical usefulness.
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Higher baseline p-tau181 and NfL were associated with significantly faster decline in most cognitive, physical, and functional outcomes (+1 SD p-tau181: β MMSE = -0.055, 95% CI -0.067 to -0.043, β FCSRT = -0.034, 95% CI -0.043 to -0.025, β fluency = -0.029, 95% CI -0.038 to -0.020, β SPPB = -0.040, 95% CI -0.057 to -0.022, and β 4IADL = -0.115, 95% CI 0.091-0.140. +1 SD NfL: β MMSE = -0.039, 95% CI -0.053 to -0.025, β FCSRT = -0.022, 95% CI -0.032 to -0.012, β fluency = -0.014, 95% CI -0.024 to -0.004, and β 4IADL = 0.077, 95% CI 0.048-0.105).
Why it matters
In this cohort, higher baseline p-tau181 and NfL were linked to faster decline in several cognitive, physical, and functional measures. The study only describes how these blood markers relate to later decline; it does not test any treatment or prevention.
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Alzheimer disease (AD) is primarily associated with accumulations of amyloid plaques and tau tangles in gray matter, however, it is now acknowledged that neuroinflammation, particularly in white matter (WM), significantly contributes to the development and progression of AD.
Why it matters
In 310 older participants, this cross-sectional study used a diffusion imaging measure to look at white matter neuroinflammation across the Alzheimer's continuum and its links to pathology and cognition. It explores a possible contributor to disease but does not test any treatment or prevention.
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We characterized the world's second case with ascertained extreme resilience to autosomal dominant Alzheimer's disease (ADAD).
Why it matters
This case report describes a man with an inherited Alzheimer-causing mutation who remained cognitively intact until age 67 and carried a rare RELN variant called COLBOS. The finding suggests a role for RELN signaling in resilience to dementia, but it comes from a single case and mouse work, so it is very early.
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An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course.
Why it matters
This genetic analysis aimed to identify which modifiable risk factors are causally linked to Alzheimer's disease to guide prevention and drug targeting. It is an analysis of genetic associations and does not report a treatment, cure, or proven prevention.
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Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus.
Why it matters
This study identified two genetic regions on chromosomes 17 and 18 linked to Alzheimer's disease in African American individuals, and found that inheriting African ancestry at the 17p13.2 region was associated with lower risk. These findings highlight genes like MINK1, KIF1C, and BCL2 that may matter for Alzheimer's risk in this population.
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The positive association of choline for cognition has been reported in both animal and human studies, yet the associations of choline with the risks of incident dementia or Alzheimer's disease (AD) in humans is unclear.
Why it matters
This study tested whether lower or higher dietary choline intake is associated with increased or decreased risks of incident dementia and Alzheimer's disease using Framingham Heart Study Offspring Cohort data. It is observational, so it cannot show that changing choline intake would prevent dementia or Alzheimer's disease.
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.
- Associations of Longitudinal Changes in Blood Biomarkers of Dementia With the Proportion of Genetically Inferred African Ancestry
- Alzheimer‐related neuropathology is improved by treatment with longevity‐enhancing treatments in aged male EFAD mice
- Discovery of Parkinson's disease states and disease progression modelling: a longitudinal data study using machine learning
- Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease
- The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
- Hypercortisolemia and glucocorticoid receptor-signaling insufficiency in Alzheimer's disease initiation and development
- The Use of Tau PET to Stage Alzheimer Disease According to the Braak Staging Framework
- Associations between plasma complement C1q and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact adults: The CABLE study
- 2014 Alzheimer's disease facts and figures
- Plasma proteomics reveals stage-dependent biological remodelling in Alzheimer's disease