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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There is a need for an accessible biomarker that can complement current cerebrospinal fluid and imaging biomarkers in an accurate and early diagnosis of Alzheimer disease (AD).
Why it matters
This study found no difference in salivary total tau levels between people with Alzheimer's disease, mild cognitive impairment, and healthy elderly controls. It plainly shows that salivary total tau was not associated with Alzheimer's disease in this sample and does not support its use as a diagnostic biomarker.
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Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder associated with dementia and cognitive impairment most common in elderly population.
Why it matters
This review states that neuroinflammation associated with amyloid-beta deposition in the brain is a major hallmark of neurodegenerative disease pathology and that the exact mechanism is not yet elucidated. It discusses natural products with anti-neuroinflammatory potential but does not report an established treatment or cure.
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Analyses revealed high overlap between components, regional and quantitative hypoperfusion, and hypometabolism in patients with AD compared with HC participants in precuneus, parietal, temporal, and occipital cortex.
Why it matters
In patients with Alzheimer's disease, reduced blood flow and reduced glucose metabolism overlapped in several cortical regions compared with healthy controls, while in mild cognitive impairment only FDG PET showed reduced metabolism in the precuneus. This is a comparison of imaging methods and does not test any treatment.
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Acupuncture has been used in the therapy of Alzheimer disease (AD); however, its neural mechanisms are still unclear.
Why it matters
In 14 Alzheimer disease patients, acupuncture at two acupoints changed regional brain activity and strengthened functional connectivity between the hippocampus and precentral gyrus compared with before stimulation. This was a small study of brain activity changes only, so it does not show whether acupuncture affects the course of Alzheimer's disease.
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In younger controls, SUV peak was observed in the temporal lobe with values of approximately 3.0 for 11 C-RO-963, 1.5 for 11 C-RO-643, and 3.5 for 18 F-RO-948.
Why it matters
This study characterized three tau radiopharmaceuticals and found that 18F-RO-948 showed better contrast between areas of high and low tau accumulation and could distinguish Alzheimer's disease subjects from healthy controls. It is a diagnostic imaging study and does not report any treatment, cure, or prevention of Alzheimer's disease.
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Ample epidemiological evidence suggests a strong correlation among diet, lifestyle factors and the onset and consolidation of dementia and Alzheimer's disease (AD).
Why it matters
This review of human studies reports that healthy dietary patterns such as the Mediterranean, DASH, and MIND diets are associated with lower risk of neurocognitive impairment and Alzheimer's disease. It discusses the beneficial effects of overall diet composition rather than single nutrient supplements for prevention or delay of Alzheimer's disease and dementia.
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These results show significant differences in neurogranin and total-tau between typical and atypical patients, which may relate to factors other than disease topography.
Why it matters
In 114 participants, cerebrospinal fluid neurogranin was higher in both typical and atypical Alzheimer's disease than in controls, and both neurogranin and total-tau were higher in typical than atypical cases. This is a biomarker comparison study and does not test any treatment.
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The study objective was to evaluate the safety and efficacy of deep brain stimulation (DBS) at the ventral capsule/ventral striatum (VC/VS) region to specifically modulate frontal lobe behavioral and cognitive networks as a novel treatment approach for Alzheimer's disease (AD) patients.
Why it matters
This non-randomized phase I open-label trial of only three Alzheimer's patients tested deep brain stimulation of the ventral capsule/ventral striatum to modulate frontal lobe networks, comparing them with matched ADNI groups. It is very early safety and feasibility work and does not establish that this treatment is effective.
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After controlling for comorbidities, treated AD patients have better survival, lower institutionalization, and sometimes fewer resource utilizations, suggesting that treatment and improved care management could be beneficial for newly-diagnosed AD patients from economic and clinical perspectives.
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Identifying individuals destined to develop Alzheimer's dementia within time frames acceptable for clinical trials constitutes an important challenge to design studies to test emerging disease-modifying therapies.
Why it matters
This study developed a machine learning method using a single amyloid PET scan to assess progression to dementia within 24 months, with 84% accuracy. The authors say it has immediate applications for population enrichment in clinical trials of disease-modifying therapies, but it does not itself test any treatment, cure or prevention.
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Almost 47 million people suffer from dementia worldwide, with an estimated new case diagnosed every 3.2 seconds.
Why it matters
This review states that currently used Alzheimer's drugs only alleviate symptoms and do not treat the underlying causes of dementia, and that a worldwide effort is under way to find treatments to stop, slow, or prevent the disease. It does not report any new treatment or cure.
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Alzheimer's disease (AD) is a gradually debilitating disease that leads to dementia.
Why it matters
This work examines oxysterols and their possible involvement in neuroinflammation across Alzheimer's disease stages, but it states that the molecular mechanisms are still unclear and no reliable biomarkers exist for early diagnosis. It provides no treatment, cure or prevention.
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Proteolysis of the amyloid precursor protein (APP) liberates various fragments including the proposed initiator of Alzheimer disease-associated dysfunctions, amyloid-β.
Why it matters
This review argues that the accepted view of amyloid precursor protein cleavage by alpha-, beta- and gamma-secretases is too simple, given newly discovered secretases and additional metabolites. It is a summary of basic biology and does not report a treatment, cure or prevention for Alzheimer's disease.
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47/100
The results for both (11)C-PiB and (18)F-NAV4694 can now be expressed in centiloids, an important step that should allow better clinical and research use of Aβ imaging.
Why it matters
This study worked out how to express results from two amyloid PET tracers on the same centiloid scale, and found the two tracers correlated strongly. This is a measurement advance for comparing scans across sites, not a treatment, cure, or prevention.
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Chromosome 21, triplicated in Down Syndrome, contains several genes that are thought to play a critical role in the development of AD neuropathology.
Why it matters
This review explains that people with Down syndrome, who have an extra copy of chromosome 21 including the APP gene, develop amyloid plaques early and later develop other Alzheimer's-like brain changes such as tangles, inflammation, and neuron loss. It also notes evidence of compensatory responses that may delay dementia onset, but it does not report a treatment or cure.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia.
Why it matters
This review states that the precise mechanism by which amyloid-beta causes neurotoxicity remains unknown and that the contribution of neuroinflammation to disease progression is still not understood. It reports no treatment, cure or prevention.
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Alzheimer's disease (AD) patients and those with high-risk mild cognitive impairment are increasingly considered to have dysfunction syndromes.
Why it matters
This imaging study found that connections within and between brain networks were impaired in people with Alzheimer's disease, and that the interaction between sensorimotor and attention functions was affected first at the mild cognitive impairment stage. The authors suggest these connectivity patterns might serve as biomarkers or predictors of disease progression, but this is a small study of 89 people and does not test any treatment.
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47/100
The ATP-binding cassette transporter A7 (ABCA7) has been identified as a susceptibility factor of late onset Alzheimer disease in genome-wide association studies.
Why it matters
In cell and mouse studies, loss of the ABCA7 gene increased beta-secretase cleavage and amyloid-beta production, and crossing ABCA7-deficient mice with an Alzheimer's mouse model increased soluble amyloid-beta. This laboratory work indicates a role for ABCA7 in amyloid processing but does not establish a treatment or prevention for people.
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47/100
Anosognosia in AD is due not only to functional changes within cortical midline structures involved in self-referential processes (OFC, PCC), but also to disconnection between these regions as well as with the medial temporal lobe.
Why it matters
In 23 patients with probable Alzheimer's disease, unawareness of memory deficits was associated with reduced metabolism in the orbitofrontal and posterior cingulate cortices and reduced connectivity between these regions and the medial temporal lobe. The findings suggest a disruption of communication between self-related and memory-related brain networks, but they do not test any treatment, cure or prevention.
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We hypothesized that de novo variants (DNV) might participate in the genetic determinism of sporadic early-onset Alzheimer disease (EOAD, onset before 65 years).
Why it matters
In 14 sporadic early-onset Alzheimer's disease trios, the researchers found de novo copy number variations and non-synonymous de novo variants, several of which targeted genes in a biological network centered on amyloid beta. This is a small genetic study, so it suggests possible genetic contributors but does not establish a treatment, cure or prevention.
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Alzheimer's disease (AD) is recognized to have a long presymptomatic period, during which there is progressive accumulation of molecular pathology, followed by inexorable neuronal damage.
Why it matters
This review describes diffusion imaging as a promising but still early method for detecting grey matter changes in Alzheimer's disease before visible shrinkage. It is about early diagnosis and tracking, not about treating or preventing the disease.
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Although amyloid plaques and neurofibrillary pathology play important roles in Alzheimer disease (AD), our understanding of AD is incomplete, and the contribution of microglia and iron to neurodegeneration is unknown.
Why it matters
In postmortem Alzheimer disease brain tissue studied with ultra-high-resolution 7T MRI and histology, small MRI signal changes in the subiculum were best explained by microscopic iron together with activated microglia. This is a tissue study suggesting microglial-mediated neurodegeneration may occur in the hippocampus, not a test of any treatment, cure, or prevention.
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We conclude that variations in morphologies among microglial cells, and cells of macrophage lineage, can help guide future work connecting neuroinflammatory mechanisms with specific neurodegenerative disease subtypes.
Why it matters
This autopsy study defined five microglia morphological phenotypes and compared hippocampal microglia in Alzheimer's disease, dementia with Lewy bodies, hippocampal sclerosis of aging, and normal controls. It describes microglial differences across these conditions but does not test any treatment, cure, or prevention.
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Exposure to air pollutants, including particulate matter, results in activation of the brain inflammatory response and Alzheimer disease (AD)-like pathology in dogs and humans.
Why it matters
In mice, only 9 months of exposure to fine airborne particulate matter increased BACE protein, APP processing, and Aβ1-40 levels, along with some inflammatory markers. This is an animal study and does not show that air pollution causes Alzheimer's disease in people or that any treatment, cure, or prevention works.
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Multiple different pathological protein aggregates are frequently seen in human postmortem brains and hence mixed pathology is common.
Why it matters
This postmortem study found that people with mixed Alzheimer's and Lewy body disease who were diagnosed clinically as Alzheimer's had higher tau loads than those diagnosed as Lewy body dementia. It describes differences in pathology between clinical groups but does not evaluate any treatment.
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.
- Different cerebrospinal fluid levels of Alzheimer-type biomarker Aβ42 between general paresis and asymptomatic neurosyphilis
- Comparative performance of plasma pTau181/Aβ42, pTau217/Aβ42 ratios, and individual measurements in detecting brain amyloidosis
- Multimodal techniques for diagnosis and prognosis of Alzheimer's disease
- Association of Longitudinal Changes in Cerebrospinal Fluid Total Tau and Phosphorylated Tau 181 and Brain Atrophy With Disease Progression in Patients With Alzheimer Disease
- Image analysis of beta-amyloid load in Alzheimer's disease and relation to dementia severity
- Correlating antemortem amyloid PET burden, postmortem MRI volumes, with neuropathological measures: Insights from Down syndrome and Alzheimer's disease cohorts
- Alzheimer's disease: clinical trials and drug development
- Determining eligibility for anti‐amyloid treatments using blood biomarkers
- Inflammatory Alterations and Multidomain Cognition in Alzheimer Disease and Related Dementias