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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Episodic memory is the first and most severely affected cognitive domain in Alzheimer's disease (AD), and it is also the key early marker in prodromal stages including amnestic mild cognitive impairment (MCI).
Why it matters
This study compared memory tests and found that combining certain verbal learning and story memory measures classified MCI and predicted progression to Alzheimer's disease more accurately than single tests. It is about improving diagnosis and identifying who may progress, not about treating or preventing the disease.
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In generalized estimating equation models (adjusted for age, race/ethnicity, and years of education), higher cholesterol (total cholesterol and LDL-C) concentrations and history of diabetes were associated with faster cognitive decline.
Why it matters
In this cohort of patients with new Alzheimer disease, higher cholesterol and a history of diabetes were linked to faster cognitive decline. It points to vascular factors as possibly influencing how quickly the disease progresses, but it does not test any treatment.
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In the oldest old, the presence of the APOE epsilon2 allele (APOE2) was associated with a somewhat reduced risk of dementia, but paradoxically was associated with increased Alzheimer disease (AD) neuropathology.
Why it matters
In 85 people aged 90 and older who came to autopsy, APOE epsilon 4 carriers were more likely to be diagnosed with dementia, while APOE epsilon 2 carriers were not. However, APOE epsilon 2 carriers were more likely to meet neuropathologic criteria for Alzheimer's disease despite having intact cognition, suggesting the relationship between this allele, cognition and brain pathology is complex in the oldest old.
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The progressive development of Alzheimer's disease (AD)-related lesions such as neurofibrillary tangles,amyloid deposits and synaptic loss within the cerebral cortex is a main event of brain aging.
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50/100
Amyloid plaques and neurofibrillary tangles (NFTs) are the pathological hallmarks of Alzheimer disease (AD).
Why it matters
This review argues that existing data support the idea that both amyloid plaques and neurofibrillary tangles contribute to cognitive impairment in Alzheimer's disease. It notes that the disease does not progress in a linear way and that some people with dementia lack these hallmark plaques and tangles, while some without cognitive impairment have severe Alzheimer-type pathology at autopsy.
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AF contributes to stroke and secondary cognitive decline.
Why it matters
In this cross-sectional study, stroke-free people with atrial fibrillation performed worse on learning and memory tasks and had hippocampal atrophy compared with people without atrial fibrillation. This identifies atrial fibrillation as a risk factor for cognitive impairment even without stroke, but does not test whether treating it prevents dementia.
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50/100
Emotion recognition progresses from a deficit in low-intensity fearful facial recognition in a-MCI phase to a deficit in all intensities and emotions in mild AD.
Why it matters
In this case-control study, people with amnestic mild cognitive impairment had more trouble recognizing low-intensity fearful faces than comparison subjects, and this deficit was explained by short-term verbal memory impairment. This is a cognitive finding and does not test any treatment or prevention.
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Cerebral amyloid angiopathy (CAA) is characterized by the deposition of the amyloid beta-protein (A beta) within cerebral vessels.
Why it matters
This paper describes how amyloid beta builds up in brain blood vessels (cerebral amyloid angiopathy), including a capillary form tied to the APOE epsilon 4 allele and often seen in Alzheimer's disease. In a mouse model, this capillary amyloid was linked to blocked capillaries and disturbed cerebral blood flow, suggesting a possible second way amyloid harms the brain beyond its direct toxic effects, but no treatment or prevention is tested here.
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50/100
Elevation of the proinflammatory cytokine Interleukin-1 (IL-1) is an integral part of the local tissue reaction to central nervous system (CNS) insult.
Why it matters
This review describes elevated IL-1 as part of the brain's neuroinflammatory response to injury and in chronic neurodegenerative disease. It reports no treatment or prevention effect and offers no clinical intervention.
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Tensor-based morphometry (TBM) creates three-dimensional maps of disease-related differences in brain structure, based on nonlinearly registering brain MRI scans to a common image template.
Why it matters
This study used brain MRI scans to map the pattern of brain shrinkage in 40 people with Alzheimer's disease, 40 with mild cognitive impairment, and 40 healthy controls. It is a descriptive imaging study and does not test any treatment, so it does not show how to treat, cure, or prevent Alzheimer's disease.
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Amyotrophic lateral sclerosis (ALS) is a motor neuron disease that has sporadic and inherited forms.
Why it matters
This review describes cognitive and behavioural symptoms in amyotrophic lateral sclerosis and evidence that ALS and frontotemporal dementia overlap clinically, radiologically, pathologically and genetically. It reports no treatment, cure or prevention.
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Many proteins suspected of causing neurodegenerative diseases exist in diverse assembly states.
Why it matters
In mice, accelerating amyloid-beta fibrillization reduced oligomer levels and functional deficits, suggesting that shifting amyloid-beta assembly states may be helpful. This is an animal study, so it does not establish a treatment, cure, or prevention for Alzheimer's disease in humans.
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50/100
Oxidative stress and neuronal energy depletion are characteristic biochemical hallmarks of Alzheimer's disease (AD).
Why it matters
In this small open-label study, nine patients with Alzheimer's disease taking 600mg alpha-lipoic acid daily alongside standard cholinesterase inhibitors showed stable cognitive scores over 12 months. Because the study was open-label and involved only nine patients, it cannot show whether alpha-lipoic acid actually slows or prevents Alzheimer's disease.
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50/100
Statistical interdependencies between magnetoencephalographic signals recorded over different brain regions may reflect the functional connectivity of the resting-state networks.
Why it matters
This small study of 18 Alzheimer patients and 18 controls found specific patterns of altered resting-state brain connectivity, with loss of long-distance connections in some frequency bands and local increases in others. It is an observational comparison and does not test any treatment, so it cannot show whether changing these connectivity patterns would affect the disease.
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Lewy bodies (LBs) are alpha-synuclein-immunoreactive neuronal inclusions with a predilection for specific cortical and subcortical regions, including the amygdala.
Why it matters
In 347 Alzheimer's disease brains examined after death, 149 (43%) had Lewy bodies: 87 met criteria for Lewy body disease, and 62 more had Lewy bodies in the amygdala with only sparse alpha-synuclein pathology elsewhere. Compared with the Lewy body disease cases, these amygdala cases had a significantly lower alpha-synuclein burden but did not differ in age at death, disease duration, sex ratio, tangle stage, plaque density or APOE ε4 frequency, which the authors say suggests a distinct, isolated form of alpha-synucleinopathy. The study looked only at brain tissue, not at symptoms or treatment, so it informs how Alzheimer's pathology is classified, not how the disease is diagnosed or treated in life.
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Patients wore CPAP for 4.8 hours per night.
Why it matters
In 30 patients with Alzheimer's disease and obstructive sleep apnea, CPAP was tolerated, with patients wearing it about 4.8 hours per night, and more depressive symptoms were linked to worse adherence. This is a small study about treating sleep apnea, not about treating, curing, or preventing Alzheimer's disease.
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Deposition of iron in the brain is proposed to play a role in the pathophysiology of the normal aging process and neurodegenerative diseases.
Why it matters
This review discusses how MRI can detect excess iron in the brain, which is seen in normal aging and in conditions including Alzheimer disease and Parkinson disease. It is a review of an imaging method and does not test any treatment, cure, or prevention.
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To determine which clinical feature(s) [among visual hallucinations (VH), extrapyramidal signs (EPS) and visuospatial impairment] in the earliest stages of disease best predicted a diagnosis of dementia with Lewy bodies (DLB) at autopsy, first-visit data of 23 pathologically proven DLB and 94 Alzheimer's disease cases were compared.
Why it matters
Among people with early-stage dementia, visual hallucinations at first presentation were the best positive predictor of dementia with Lewy bodies at autopsy, while lack of visuospatial impairment was the best negative predictor. This is about telling different types of dementia apart, not about treating, curing, or preventing Alzheimer's disease.
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Alzheimer's disease (AD) is the most common form of neurodegenerative dementia and affects up to 15 million people worldwide.
Why it matters
This review reports that excess brain cholesterol has been associated with increased formation and deposition of amyloid-beta peptide, and that genetic polymorphisms in cholesterol metabolism may contribute to Alzheimer's disease risk and pathogenesis. It examines the potential of statins in prevention and treatment, but does not show that statins work.
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Human genetic data have associated angiotensin-converting enzyme (ACE) with Alzheimer disease (AD), and purified ACE has been reported to cleave synthetic amyloid beta-protein (Abeta) in vitro.
Why it matters
In cells, angiotensin-converting enzyme promoted the breakdown of secreted amyloid beta 40 and 42, and an ACE inhibitor raised amyloid beta levels. This is cell-based evidence that ACE activity affects amyloid clearance, not proof that ACE inhibitors cause or treat Alzheimer's in patients.
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From the modest but important breakthroughs in the treatment of Alzheimer's disease (AD), diagnostic focus has increasingly shifted to the accurate detection of the earliest phase of the illness.
Why it matters
This review discusses challenges in diagnosing preclinical Alzheimer's disease and predicting who with mild cognitive impairment will develop it. It reports no treatment or prevention results.
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In nondemented individuals, entorhinal cortex atrophy is associated with risk of Alzheimer disease.
Why it matters
In 58 older people without dementia followed for up to five years, shrinkage of the entorhinal cortex predicted who would develop Alzheimer disease, while hippocampal size and its rate of decline did not. This points to entorhinal cortex atrophy as a risk marker, not a treatment.
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The authors assessed whether measures of hippocampal water diffusivity at baseline can predict future progression to Alzheimer disease (AD) in amnestic mild cognitive impairment (aMCI).
Why it matters
In amnestic mild cognitive impairment, higher baseline hippocampal water diffusivity was associated with greater risk of progressing to Alzheimer disease. This suggests a possible way to identify who will progress, but it offers no treatment or cure.
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50/100
The results suggest that brain response differences are not due to poorer general memory abilities, differential atrophy, or brain response during control conditions, but instead appear to be directly influenced by APOE genotype.
Why it matters
In this small functional MRI study of 20 nondemented older adults, those with an APOE ε4 allele showed greater magnitude and extent of brain response during learning of new pictures than those without. The authors say the results are consistent with a compensatory hypothesis, but this is a small imaging study and does not show that any treatment, cure, or prevention is available.
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We review accumulating evidence that cerebrovascular amyloid deposition (cerebral amyloid angiopathy [CAA]) is an independent risk factor for cognitive dysfunction.
Why it matters
This review reports evidence that cerebral amyloid angiopathy is an independent risk factor for cognitive dysfunction, including after controlling for age and Alzheimer's disease pathology. It describes a risk association and does not show any treatment, cure or prevention.
From across this topic
9 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 9. The same 9 appear here every time.
- Variant of TREM2 associated with the risk of Alzheimer's disease
- Clinical trials of new drugs for Alzheimer disease
- Mediterranean diet and risk for Alzheimer's disease
- Early Detection of Alzheimers Disease Using Deep Learning
- Mitochondrial dysfunction gene expression, DNA methylation, and inflammatory cytokines interaction activate Alzheimer's disease: a multi-omics Mendelian randomization study
- Precision Medicine Approach to Alzheimer's Disease: Rationale and Implications
- Discordance Between Genetic Ancestry and Self-Reported Race Impacts Inference of Neuropsychiatric Burden in Alzheimer's Disease
- Decreased peripheral brain-derived neurotrophic factor levels in Alzheimer's disease: a meta-analysis study (N=7277)
- Whole-brain analysis reveals increased neuroanatomical asymmetries in dementia for hippocampus and amygdala