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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46/100
Despite accumulating amyloid burden, cholinergic enzyme activity is stable in the precuneus during prodromal AD.
Why it matters
This postmortem study found that cholinergic enzyme activity in the precuneus was stable in mild cognitive impairment despite rising amyloid, and only declined in clinical Alzheimer's disease. Reduced enzyme activity was associated with more amyloid binding, lower cognitive scores, and the APOE*4 allele.
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In this article, the challenges faced by several noted population studies for Alzheimer dementia in operationalizing current clinical diagnostic criteria for Alzheimer's disease (AD) have been reviewed.
Why it matters
This article reviews challenges that population studies face in applying current clinical diagnostic criteria for Alzheimer's disease, including differences in case ascertainment, methodological biases, cultural and educational influences on test performance, inclusion of special populations, and detection of the earliest symptomatic stages. It suggests classification may improve with biomarkers for Alzheimer's disease if their sensitivity, specificity, and predictive value are established and if they suit epidemiological studies, but it reports no treatment, cure, or prevention.
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Melatonin secretion decreases in Alzheimer´s disease (AD) and this decrease has been postulated as responsible for the circadian disorganization, decrease in sleep efficiency and impaired cognitive function seen in those patients.
Why it matters
This review of clinical studies found that melatonin replacement has been shown effective to treat sundowning and other sleep-wake disorders in Alzheimer's disease patients, and it postulates melatonin as a useful add-on therapeutic tool in mild cognitive impairment. For Alzheimer's disease, it states that larger randomized controlled trials are necessary before effectiveness can be established.
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We investigated whether blood N-glycan changes can be used as a diagnostic biomarker for Alzheimer disease (AD).
Why it matters
A serum N-glycan called NA2F was decreased in Alzheimer disease patients compared with controls and showed moderate diagnostic accuracy, with a stronger decrease in females. This suggests a possible blood marker, but it is a diagnostic finding and does not test any treatment.
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46/100
Recent evidence suggests that high molecular weight soluble oligomeric Abeta (oAbeta) assemblies (also known as Abeta-derived diffusible ligands, or ADDLs) may represent a primary neurotoxic basis for cognitive failure in Alzheimer disease (AD).
Why it matters
This work studied the bioactivity of amyloid-beta oligomers formed endogenously from human APP and PS1 transgenes in experimental animals. It is animal-model research on toxicity mechanisms and does not establish any treatment, cure, or prevention for patients.
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Linkage studies, candidate gene and whole-genome association studies have resulted in a tremendous amount of putative risk genes for Alzheimer's disease (AD).
Why it matters
This review summarizes the genetics of Alzheimer's disease and states that, apart from the three causal genes (amyloid precursor protein and presenilin 1 and 2) and the risk gene APOE, no single functional risk variant had been identified. It describes the state of genetic knowledge and does not report a treatment, cure, or prevention.
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46/100
Neuroinflammation is a prominent feature of Alzheimer disease (AD) and other chronic neurodegenerative disorders.
Why it matters
This review describes neuroinflammation in Alzheimer's disease and mild cognitive impairment and notes that microglia might be shifted to an anti-inflammatory state. It reports no tested treatment or prevention.
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Accumulating evidence indicates that p38 mitogen-activated protein kinase (MAPK) could play more than one role in Alzheimer's disease (AD) pathophysiology and that patients suffering from AD dementia could benefit from p38 MAPK inhibitors.
Why it matters
This review proposes that p38 MAPK inhibitors could benefit patients with Alzheimer's dementia because the pathway contributes to neuroinflammation, excitotoxicity, synaptic plasticity and tau phosphorylation. It notes that behavioral improvements from p38 MAPK inhibition and in vivo evidence are still missing, so no treatment benefit has been demonstrated.
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Upon activation by calcineurin, the nuclear factor of activated T-cells (NFAT) translocates to the nucleus and guides the transcription of numerous molecules involved in inflammation and Ca(2+) dysregulation, both of which are prominent features of Alzheimer's disease (AD).
Why it matters
In postmortem human brain tissue, NFAT1 and NFAT3 shifted into the nucleus at different stages of Alzheimer's neuropathology and cognitive decline. This describes a signaling change, not a treatment, and cannot show that targeting it would help patients.
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DNA methylation occurs predominantly at cytosines that precede guanines in dinucleotide CpG sites; it is one of the most important mechanisms for epigenetic DNA regulation during normal development and for aberrant DNA in cancer.
Why it matters
This study checked whether DNA methylation of the MAPT, APP and PSEN1 genes could be measured reliably in postmortem brain, including samples with delays up to 48 hours. It is a feasibility study of a laboratory method and reports no treatment, cure or prevention for Alzheimer's disease.
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These results indicate that the epsilon4-positive APOE genotype not only represents a risk factor for Alzheimer disease (AD), but also results in higher levels of Abeta plaque deposition in epsilon4-positive patients with AD compared to age-matched epsilon4-negative patients with similar levels of cognitive impairment and brain atrophy.
Why it matters
Among patients with moderate Alzheimer disease, those carrying the APOE epsilon4 allele had stronger and more extended amyloid plaque deposition on PET imaging, while levels of brain atrophy were comparable between carriers and noncarriers. This describes how APOE genotype relates to plaque load in living patients but does not test any therapy.
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Alzheimer disease (AD) is a progressive neurodegenerative disorder whose clinical manifestations appear in old age.
Why it matters
This review discusses evidence that epigenetic and environmental factors, including early-life exposure to lead, may contribute to late-onset Alzheimer's disease along with oxidative stress. It is a review and does not report a proven treatment, cure or prevention.
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46/100
FA reduction in forceps minor was the most significant area of difference between AD and VaD.
Why it matters
This study found that reduced fractional anisotropy in the forceps minor and transcallosal prefrontal tracts helped differentiate vascular dementia from Alzheimer's disease. It is about using imaging to tell these dementias apart, not about treating, curing, or preventing Alzheimer's disease.
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Amyloid imaging represents a major advance in neuroscience, enabling the detection and quantification of pathologic protein aggregations in the brain.
Why it matters
Amyloid imaging with PET can detect beta-amyloid deposits in cognitively normal older individuals and in those with mild cognitive impairment or Alzheimer's disease. The review suggests amyloid imaging may help select patients for anti-amyloid therapies in the future, but it does not report on any treatment's effectiveness.
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Alzheimer disease beta-amyloid (Abeta) peptides are generated via sequential proteolysis of amyloid precursor protein (APP) by BACE1 and gamma-secretase.
Why it matters
This work examines how BACE1 targeting to cholesterol-rich lipid rafts affects beta-amyloid production, but the findings are drawn from cultured cells and neurons rather than patients. It does not establish a treatment or cure, and prior cholesterol-depletion studies produced conflicting results, so no clear therapeutic direction is provided.
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These results suggest that neuronal injury markers such as VLP-1 may have utility as biomarkers for AD.
Why it matters
CSF levels of the brain injury marker VLP-1 were higher in Alzheimer patients than controls, and combining it with amyloid-beta and tau markers performed better than any one alone. This was a small study of 33 patients and 24 controls, so it does not by itself establish a diagnostic test.
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46/100
Two-thirds of MCI-multidomains, but only half of MCI-amnestic progress to AD.
Why it matters
In this three-year population-based study, MCI-multidomains showed the highest progression to Alzheimer's disease, and MCI-amnestic reached similar predictivity only when using a modified definition. The authors also identified a group with only global cognitive deficits who were not detected by current operational criteria for mild cognitive impairment.
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A majority of mutations within the beta-amyloid region of the amyloid precursor protein (APP) gene cause inherited forms of intracerebral hemorrhage.
Why it matters
This report describes the clinical and neuropathological features of the Arctic amyloid precursor protein mutation in one Swedish and one American family. It characterizes an inherited form of early-onset Alzheimer's disease and does not test any treatment, cure, or prevention.
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Multiple pathogenic factors may contribute to the pathophysiology of Alzheimer's disease (AD).
Why it matters
In this small study of 34 MCI patients, 45 Alzheimer's patients, and 28 controls, inflammatory markers differed between groups, with higher IL-6 in Alzheimer's disease and higher IFN-alpha only in mild cognitive impairment. It reports blood marker differences and does not show that any treatment, cure, or prevention works.
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The genetics of Alzheimer disease (AD) to date support an age-dependent dichotomous model whereby earlier age of disease onset ( or = 65 years) representing most cases of AD has yet to be explained by a purely genetic model.
Why it matters
This review explains that APOE is the strongest known genetic risk factor for later-onset Alzheimer's disease, but it is neither sufficient nor necessary to cause the disease. It states that many other reported genetic risk variants still await replication in large populations before their role is clear.
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Subtle and spatially complex deformation patterns of hippocampus between patients with AD and healthy control subjects can be detected by machine learning methods.
Why it matters
This small study of 19 Alzheimer's patients and 20 controls found specific shape changes in the hippocampus, especially the CA1 region, using machine learning. It is a structural imaging study and does not test any treatment, cure, or prevention.
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A number of studies reported that oxidative and nitrosative damage may be important in the pathogenesis of Alzheimer's disease (AD).
Why it matters
This study found higher levels of protein nitration in the hippocampus and inferior parietal lobule of people with amnestic MCI compared with controls. It suggests nitrosative damage occurs early and may matter for progression, but no treatment was tested.
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46/100
Alzheimer disease (AD) is multi-factorial and heterogeneous.
Why it matters
This review discusses the role of neurofibrillary degeneration of abnormally hyperphosphorylated tau in Alzheimer disease and related tauopathies, and considers therapeutic and prevention implications. It is a conceptual review and does not report a tested treatment, cure, or prevention.
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To clarify the involvement of the posterior cingulate cortex (PCC) in Alzheimer's disease (AD), we analyzed brain volume loss by voxel-based morphometry.
Why it matters
Using brain scans, this study classified Alzheimer's patients into four subgroups based on patterns of brain shrinkage, including a pattern involving the posterior cingulate cortex that was linked to early onset disease. The authors say these patterns raise doubts about Alzheimer's being a single disease or a single progression path, and no treatment was tested.
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Alzheimer's disease is a progressive neurodegenerative disorder characterised by the gradual onset of dementia.
Why it matters
This review describes therapeutic strategies being tested in clinical trials, such as reducing beta-amyloid burden or toxicity, but states that it is not yet known which approaches will be efficacious. It also notes that current structural neuroimaging relies on late features like atrophy, highlighting the need for earlier and more specific diagnosis.
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.
- Imaging and cerebrospinal fluid biomarkers in early preclinical alzheimer disease
- Age-related changes in the default mode network are more advanced in Alzheimer disease
- Disruption of functional brain networks in Alzheimer's disease: what can we learn from graph spectral analysis of resting-state magnetoencephalography?
- Advanced glycation end products in Alzheimer's disease and other neurodegenerative diseases
- Machine-learning based strategy identifies a robust protein biomarker panel for Alzheimer’s disease in cerebrospinal fluid
- Cerebrospinal fluid neurogranin: relation to cognition and neurodegeneration in Alzheimer's disease
- Quantitative assessment of synaptic density in the outer molecular layer of the hippocampal dentate gyrus in Alzheimer's disease
- The missing improvers: Tau pathology, neuroplasticity, and the case for tau-informed patient selection before amyloid immunotherapy
- Alzheimer's Disease and Frontotemporal Dementia: A Review of Pathophysiology and Therapeutic Approaches