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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48/100
A subset of a dementia subgroup with characteristics predominantly associated with DM-related factors may underlie a pathophysiology different from AD, although these patients were clinically diagnosed as having AD.
Why it matters
In this small longitudinal study, a subgroup of patients with diabetes-related dementia showed a different pattern of blood flow change and mostly did not show amyloid binding on PET, unlike the Alzheimer disease group. This suggests some dementia tied to diabetes-related factors may have a disease process different from Alzheimer disease.
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Alzheimer's disease (AD) and Parkinson's disease (PD) are the two common neurodegenerative diseases characterized by progressive neuronal dysfunction in the presence of pathological microglial activation.
Why it matters
This imaging study compared microglial activation and neuronal function in small groups of people with Alzheimer's disease, mild cognitive impairment, Parkinson's disease dementia and controls. It is a small study that describes associations between brain inflammation and neuronal function, not a treatment or cure.
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As preclinical Alzheimer's disease becomes a target for therapeutic intervention, the overlap between imaging abnormalities associated with typical ageing and those associated with Alzheimer's disease needs to be recognised.
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A growing body of evidence supports an intriguing clinical/epidemiological connection between Alzheimer disease (AD) and type 2 diabetes (T2D).
Why it matters
This review proposes that inflammation, insulin resistance, and mitochondrial dysfunction are common features in Alzheimer's disease and type 2 diabetes, and suggests this may lead to treatments. It reports no tested treatment, cure, or prevention.
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Alzheimer disease (AD) is the most common cause of dementia in people over 60 years old.
Why it matters
This review discusses the hypothesis that neuroinflammation contributes to Alzheimer's disease and suggests natural anti-inflammatory components as possible agents for prevention or as a coadjuvant for treatment. It is a discussion of a framework and does not report testing of any treatment, cure, or prevention.
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Development of molecular imaging agents for fibrillar β-amyloid positron-emission tomography during the past decade has brought molecular imaging of Alzheimer disease pathology into the spotlight.
Why it matters
Amyloid PET imaging can detect β-amyloid deposition many years before Alzheimer's symptoms appear and can track its progression over time. It is most useful for distinguishing Alzheimer's disease from frontotemporal lobar degeneration, but may not reliably separate dementias that commonly share overlapping β-amyloid pathology, such as dementia with Lewy bodies and vascular dementia.
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A link between Alzheimer's disease (AD) and metabolic disorders has been established, with patients with type 2 diabetes at increased risk of developing AD and vice versa.
Why it matters
This review discusses a link between Alzheimer's disease and metabolic disorders, with patients with type 2 diabetes at increased risk of developing Alzheimer's disease and vice versa. It reviews evidence that targeting neuroinflammation may provide novel therapeutic avenues for Alzheimer's disease.
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Late-onset Alzheimer's disease (AD) is a sporadic disorder with increasing prevalence in aging.
Why it matters
This covers the report by two independent research groups that variants of the TREM2 gene are linked to a higher risk of late-onset Alzheimer's, with an odds ratio similar to that of APOE ε4, then the only known major genetic risk factor. TREM2 is a receptor on innate immune cells. Using Direct RNA Sequencing, the authors confirmed it is a major microglia-specific gene in the brain, which points to the brain's immune cells as part of the story. The record gives no odds-ratio figure or sample sizes, and the paper tests no treatment, so it describes a risk link, not a way to prevent or treat the disease.
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48/100
Exposure to vascular risk factors has a gradual deleterious effect on brain MRI and cognitive measures.
Why it matters
This study explored whether patterns of brain MRI findings and cognitive test results can predict future stroke and Alzheimer's disease in people who were initially free of both. Such prediction could help identify high-risk individuals, but it does not offer a treatment or cure.
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Metabolic disorders and aging promote accumulation of amylin amyloid in the cerebrovascular system and gray matter, altering microvasculature and tissue structure.
Why it matters
This study found amylin oligomers and plaques in brain tissue of diabetic patients and also amylin deposition in blood vessels and brain tissue of some late-onset Alzheimer's patients without apparent diabetes. It is a tissue-based finding about a possible second amyloid, not evidence that any treatment cures or prevents Alzheimer's disease.
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Classical immunohistochemical studies in the Alzheimer disease (AD) brain reveal prominent glial reactions, but whether this pathological feature is due primarily to cell proliferation or to a phenotypic change of existing resting cells remains controversial.
Why it matters
In brain tissue from 40 Alzheimer patients and 32 nondemented subjects, the higher numbers of activated astrocytes and microglia reflected a phenotypic change of existing cells rather than cell proliferation. This describes a feature of the disease process and does not report any treatment, cure or prevention.
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Alzheimer disease (AD) is an age-related neurodegenerative disease.
Why it matters
This review gathers evidence that amyloid-beta (1-42), the main component of the plaques found in Alzheimer's brains, is linked to oxidative stress, which the authors call another hallmark of the disease. It reports that recent studies are "consistent with the notion" that one building block of the peptide (methionine at position 35) is critical to this oxidative damage and nerve-cell toxicity. It is a review of a proposed disease mechanism: it reports no new patient data and does not test any treatment or prevention.
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48/100
There is no evidence for individual risk prediction and even less for specific treatments.
Why it matters
This review states there is no evidence for individual risk prediction and even less for specific treatments, and that dementia screening in asymptomatic subjects should not be used outside of clinical studies. It describes MRI measures of regional gray matter volume as a proxy for neuronal loss and a basis of functional impairment in specific networks.
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Western countries are experiencing aging populations and increased longevity; thus, the incidence of dementia and Alzheimer's disease (AD) in these countries is projected to soar.
Why it matters
This review states there is strong evidence linking regular physical activity to higher cognitive function, less cognitive decline and reduced risk of Alzheimer's disease or dementia. It also says these associations need further investigation, particularly through long-term interventional studies, and that the underlying mechanisms are largely unknown.
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48/100
Estimate the probabilities, for Alzheimer's disease (AD) patients, of transitioning between stages of disease severity (mild, moderate, severe, dead) and care settings (community, institutional).
Why it matters
This study used data from a large registry to estimate the chances that Alzheimer's patients move between stages of severity and care settings over time. It is a descriptive tool for understanding disease progression and planning care, not a test of any treatment or cure.
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48/100
Adiponectin, an adipocytokine released by the adipose tissue and has important roles in the metabolic regulation and inflammatory control, may play an important roles in the physiopathology of psychiatric and neurodegenerative disorders.
Why it matters
This study measured blood adiponectin levels in people with mild cognitive impairment, Alzheimer's disease, and healthy elders. Levels were lower in the mild cognitive impairment and Alzheimer's disease groups, but circulating adiponectin did not predict cognitive decline in controls or progression to Alzheimer's disease in those with mild cognitive impairment.
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48/100
Investigation of dopaminergic transporter loss in vivo using (123)I-N-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl) nortropane single photon emission computed tomography has been widely used as a diagnostic aid in Lewy body disease.
Why it matters
In autopsy-confirmed cases of Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease dementia, striatal image uptake was associated with nigral dopaminergic neuronal density but not with α-synuclein, tau, or amyloid β burden. This suggests reduced uptake on dopaminergic imaging may reflect neuronal loss rather than the presence of these pathological lesions.
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Our findings show that the presence of Aβ in the brain, known to occur in about one-third of asymptomatic elderly individuals, is actually a pathologic state associated with accelerated atrophy.
Why it matters
Cognitively normal older adults with high amyloid on PET had faster brain shrinkage over 18 months than those with low amyloid. This supports the idea that amyloid in asymptomatic people is a pathologic state, but it does not show that removing amyloid helps.
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The aim of this study was to explore the relationship between cerebrospinal fluid Alzheimer's disease (AD) markers and depression in elderly people.
Why it matters
This study explored the relationship between cerebrospinal fluid Alzheimer's markers and depression in 183 elderly participants with Alzheimer's disease or subjective cognitive impairment. It is an observational study of depression and markers, not a treatment, cure, or prevention for Alzheimer's disease.
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48/100
Weight loss is a frequent complication of Alzheimer's disease (AD) and a strong predictor of adverse outcomes in patients suffering from this disease.
Why it matters
This study followed 414 community-dwelling patients with probable Alzheimer's disease for 4 years to see whether weight loss predicted rapid cognitive decline. The provided text does not report the results, so it is unknown whether weight loss was linked to faster decline.
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The role of structural brain magnetic resonance imaging (MRI) is becoming more and more emphasized in the early diagnostics of Alzheimer's disease (AD).
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Alzheimer's disease (AD) is the 3rd most costly disease and the leading cause of dementia.
Why it matters
This review argues that small soluble Aβ oligomers, rather than amyloid plaques, are the toxins that disrupt synapses and cause memory failure in Alzheimer's disease. It presents the oligomer hypothesis as a new basis for the cause, diagnosis, and treatment of the disease, though it does not report a new treatment or cure.
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Gene ontology over-representation and functional gene network analyses indicate an increase in synaptic activity and changes in plasticity during the very early pre-symptomatic stage of the disease.
Why it matters
This gene expression study found changes in synaptic and plasticity genes in the prefrontal cortex before Alzheimer's pathology appears, with ApoE4 affecting the timing of these changes. It suggests possible new targets for therapy but does not test any treatment.
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These data support the hypothesis that neuronal endosomal dysfunction is associated with preclinical AD.
Why it matters
In brain tissue from people with mild cognitive impairment and Alzheimer's disease, genes controlling early endosomes (rab5) and late endosomes (rab7) were increased in CA1 neurons, and this increase tracked with worse cognition before death. Cell experiments suggested that higher rab5 lowers the neurotrophin receptor TrkB, pointing to endosomal dysfunction as a possible early process in the disease.
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MRI research examining structural brain atrophy in Alzheimer's disease (AD) generally focuses on medial temporal and cortical structures, but amyloid and tau deposits also accumulate in the caudate.
Why it matters
Using MRI scans from 400 people, this study mapped caudate atrophy, which was lower in mild cognitive impairment and Alzheimer's disease than in controls and was associated with age and clinical dementia measures. It describes a structural correlate of disease and does not test any treatment, cure or prevention.
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.
- Using virtual reality to characterize episodic memory profiles in amnestic mild cognitive impairment and Alzheimer's disease: influence of active and passive encoding
- Antibody-Based In Vivo PET Imaging Detects Amyloid-β Reduction in Alzheimer Transgenic Mice After BACE-1 Inhibition
- A Review of Clinical Biomarker Insights: Advances in Diagnosis and Prognosis of Early Alzheimer
- Validation of blood biomarkers for Alzheimer Disease in Thai Cohort
- Evaluating Clinical Foundation Models for Early Alzheimer's Disease and Related Dementia Prediction from Longitudinal EHRs
- Defective DNA base excision repair in brain from individuals with Alzheimer's disease and amnestic mild cognitive impairment
- Neuropsychological correlates of capacity determinations in Alzheimer disease: implications for assessment
- Age-dependent axonal degeneration in an Alzheimer mouse model
- Association of Plasma and Cerebrospinal Fluid Alzheimer Disease Biomarkers With Race and the Role of Genetic Ancestry, Vascular Comorbidities, and Neighborhood Factors
- Cerebrolysin in Alzheimer's disease: a randomized, double-blind, placebo-controlled trial with a neurotrophic agent