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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Neuroinflammation is considered one of the cardinal features of Alzheimer's disease (AD).
Why it matters
This review describes how the peripheral immune system can play a detrimental or beneficial role in brain inflammation and how several groups have targeted it as a possible therapeutic approach for Alzheimer's disease. These are investigated targets, not established treatments, and the review reports no proven cure or prevention.
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Research into the function of microglia has dramatically accelerated during the last few years, largely due to recent genetic findings implicating microglia in virtually every neurodegenerative disorder.
Why it matters
This review notes that most Alzheimer's disease risk loci found through genome-wide association studies lie in or near genes expressed most highly in microglia, and that nearly every microglial function has been proposed to influence disease progression. It does not report a treatment, cure or prevention for Alzheimer's disease.
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Two thirds of all persons with late-onset Alzheimer's disease (AD) are women.
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Ten participants with AD (5 male and 5 female; mean [SD] age, 72.7 [6.3] years; 10 [100%] β-amyloid positive) were compared with 11 participants who were cognitively normal (5 male and 6 female; mean [SD] age, 72.9 [8.7] years; 11 [100%] β-amyloid negative).
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We expect to demonstrate that personalized TMS intervention has a measurable positive impact in cognition, emotion, daily living activities and brain connectivity, thus representing a potential treatment for Alzheimer's disease.
Why it matters
This is a proposal for a planned randomized trial of personalized transcranial magnetic stimulation in 54 patients with Alzheimer's disease. The authors expect it may improve cognition, emotion, daily activities, and brain connectivity, but no results are available yet.
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The majority of patients with Parkinson's Disease develop Dementia (PDD) in late stages of the disease and have widespread neocortical distribution of alpha-synuclein pathology at autopsy, compared with PD without dementia, in which neocortical synuclein pathology is less prevalent.
Why it matters
This review reports that in Lewy body disorders, alpha-synuclein pathology is often accompanied by amyloid plaque and tau tangle pathology characteristic of Alzheimer's disease. It suggests that this combination of pathologies may contribute to cognitive impairment and a shorter interval to dementia.
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Alzheimer disease (AD), a progressive and neurodegenerative disease, is the most common form of dementia with high incidence in elderly people.
Why it matters
This review describes how mutations in APP, PSEN1, and PSEN2 cause early-onset inherited Alzheimer disease and how APOE epsilon4 and more than 20 other gene regions contribute to late-onset risk. It summarizes genetic knowledge and does not report a treatment or cure.
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Prospective studies are needed to validate current findings.
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Alzheimer disease (AD) is a frequent and devastating neurodegenerative disease in humans, but still no curative treatment has been developed.
Why it matters
This review notes that no curative treatment has been developed and that the precise disease mechanisms remain unknown, while astrocyte changes are seen in human AD brains and in vitro and animal models. It presents astrocytes as research targets, not as a proven therapy.
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These observations provide cellular evidence to support the hypothesis that dendritic spine plasticity is a mechanism of cognitive resilience that protects older individuals with AD pathology from developing dementia.
Why it matters
This study compared dendritic spines in the prefrontal cortex of people who had Alzheimer's pathology with and without dementia. It found that spine density was reduced in those with dementia, suggesting structural features may relate to cognitive resilience, but it is a small post-mortem study and does not test a treatment or cure.
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48/100
Young onset Alzheimer's disease (YOAD) is defined as symptom onset before the age of 65 years and is particularly associated with phenotypic heterogeneity.
Why it matters
Eyetracking metrics correlated with standard visual cognitive tests in young onset Alzheimer's disease, and a machine learning approach discriminated patients from controls with about 95% accuracy. This is a potential diagnostic tool and does not treat, cure, or prevent Alzheimer's disease.
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With promising results in recent treatment trials for Alzheimer's disease (AD), it becomes increasingly important to distinguish AD at early stages from other causes for cognitive impairment.
Why it matters
In 158 patients with mild cognitive impairment or dementia from various causes, this study tested whether neuropsychological testing combined with machine learning could identify those with possible Alzheimer disease. It is a diagnostic study and does not test any treatment or prevention.
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Alzheimer's disease (AD) is strongly associated with microglia-induced neuroinflammation.
Why it matters
In transgenic Alzheimer's mouse models, microglia clustered around amyloid plaques became hyperreactive when the animals had systemic inflammation, and these plaque-associated microglia showed a proinflammatory gene profile. This is animal work, so it does not yet show whether the same hyperreactivity happens in people or whether it can be targeted to treat Alzheimer's disease.
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Alzheimer's disease (AD) is a complex disorder and the most common form of neurodegenerative dementia.
Why it matters
This review discusses the role of inflammatory molecules such as chemokines and cytokines in the progression and diagnosis of Alzheimer's disease. It does not report a specific treatment, cure, or prevention for Alzheimer's disease.
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Neuropsychiatric symptoms (NPS) are common in Alzheimer disease (AD) and vascular dementia (VaD), and are distressful to patients and caregivers.
Why it matters
Comparing patients with Alzheimer disease, vascular dementia and mixed dementia, those with vascular dementia had significantly more agitation, and differences in neuropsychiatric symptoms were likely related to the underlying pathology. The authors conclude these differences need further study because they have implications for treatment, but no treatment itself was tested.
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APOE4 genotype is the strongest genetic risk factor for Alzheimer's disease.
Why it matters
This review states that APOE4 is the strongest genetic risk factor for Alzheimer's disease and that ApoE isoforms have differential effects on amyloid beta metabolism. It summarizes possible mechanisms by which ApoE contributes to disease but reports no treatment, cure or prevention.
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Quantitative Susceptibility Mapping (QSM) MRI at 7 Tesla and 11-Carbon Pittsburgh-Compound-B PET were used for investigating the relationship between brain iron and Amyloid beta (Aβ) plaque-load in a context of increased risk for Alzheimer's disease (AD), as reflected by the Apolipoprotein E ε4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects.
Why it matters
In this imaging study, higher brain iron was associated with higher amyloid plaque load and with APOE-e4 carrier status in people with mild cognitive impairment. The authors say this confirms earlier reports of an association between increased brain iron burden and risk for neurocognitive dysfunction due to Alzheimer's disease.
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Pseudotemporal measurements from baseline PET data explained 87% ( P Pseudotemporal analysis of baseline PET images is capable of predicting the regional pattern of longitudinal Aβ accumulation in AD at a group level.
Why it matters
This study found that analysis of baseline amyloid PET images could predict the regional pattern of later amyloid accumulation at a group level. The authors suggest this approach could identify brain regions with high amyloid accumulation rates, which may be of interest for antiamyloid clinical trials.
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Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline, such as cardiometabolic diseases.
Why it matters
Using data from over 500,000 middle- and older-aged UK Biobank adults, this study tested whether the APOE e4 genetic risk factor for dementia had a larger association with cognitive ability at older ages or in people with cardiometabolic diseases. Carriers of the e4 allele may be more vulnerable to conditions that are independent risk factors for cognitive decline.
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APOE2 is associated with less cognitive decline during aging.
Why it matters
In a review of National Alzheimer's Coordinating Center records, the APOE2 gene variant was associated with less cognitive decline during aging, including in people with little amyloid and after adjusting for other Alzheimer's-related brain changes. In mice carrying human APOE genes, APOE2 animals kept better memory with age even though they showed similar or greater synaptic loss, inflammation and oxidative stress. Memory instead tracked how much apoE protein the animals had (highest with APOE2) and how much cholesterol was in the brain (lowest with APOE2), but these are associations, and the study does not show that changing either one protects memory.
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High SMD is a harbinger of greater rates of clinical progression in preclinical AD.
Why it matters
In this study of 58 cognitively normal older adults with high amyloid burden, those with high subjective memory decline did not show significantly greater episodic memory decline, but they did progress to mild cognitive impairment or Alzheimer's dementia at higher rates. It suggests subjective memory decline may be an early warning sign, but it does not test a treatment or cure.
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Amyloid (senile) plaques, one of the two pathologic hallmarks of Alzheimer disease (AD), are associated with dystrophic neurites and glial responses, both astrocytic and microglial.
Why it matters
In brain tissue from people with Alzheimer disease, dystrophic neurites, reactive astrocytes, and activated microglia around plaques increased with longer symptom duration, suggesting plaques become more toxic over the clinical course. This is a tissue study and does not test any treatment, cure, or prevention.
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48/100
Extant data from in vivo animal models and postmortem studies indicate that Alzheimer's disease (AD) pathology is associated with reduction of the brain antioxidant glutathione (GSH), yet direct clinical evidence has been lacking.
Why it matters
Brain levels of the antioxidant glutathione were lower in people with mild cognitive impairment and Alzheimer's disease, and measuring these levels with magnetic resonance spectroscopy may help identify these conditions. This points to glutathione as a possible biomarker, though the study does not show that changing glutathione levels affects the disease.
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48/100
The mechanisms that contribute to selective vulnerability of the magnocellular basal forebrain cholinergic neurons in neurodegenerative diseases, such as Alzheimer's disease, are not fully understood.
Why it matters
This study examined whether amyloid-beta builds up inside cholinergic neurons in the basal forebrain of young, aged, and Alzheimer's brains. It is a descriptive analysis of brain tissue and does not test any treatment, cure, or prevention.
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This review highlights a great heterogeneity in RCTs design of drugs for A/A in AD and some key methodological issues such as definition of A/A, choice of outcome measures and caregiver participation that could be addressed by an expert consensus to optimize future trials design.
Why it matters
This review of 18 trials found that 7 of 10 completed trials of drugs for agitation and aggression in Alzheimer's disease showed no greater benefit than placebo. It highlights problems with trial design and outcome measurement rather than offering a 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.
- A Spanish grammaticality judgment task for neurodegenerative diseases: inflectional, transitivity, and word order comprehension in PPA and Alzheimer's Disease
- The Alzheimer's Disease Assessment Scale-Cognitive-Plus (ADAS-Cog-Plus): an expansion of the ADAS-Cog to improve responsiveness in MCI
- Association of MRI Indices of Glymphatic System With Amyloid Deposition and Cognition in Mild Cognitive Impairment and Alzheimer Disease
- Mixed Pathologies and Cognitive Outcomes in Persons Considered for Anti-Amyloid Treatment Eligibility Assessment: A Community-Based Study
- Vascular pathology in Alzheimer disease: correlation of cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis with cognitive decline
- Double blind study of melatonin effects on the sleep-wake rhythm, cognitive and non-cognitive functions in Alzheimer type dementia
- Data-driven discovery of probable Alzheimer's disease and related dementia subphenotypes using electronic health records
- A cross-sectional study in healthy elderly subjects aimed at development of an algorithm to increase identification of Alzheimer pathology for the purpose of clinical trial participation
- Salivary biomarkers for the molecular diagnosis of dementia with Lewy bodies
- An open-label trial of Korean red ginseng as an adjuvant treatment for cognitive impairment in patients with Alzheimer's disease