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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cis-trans isomerization of proteins phosphorylated by proline-directed kinases is proposed to control numerous signaling molecules and is implicated in the pathogenesis of Alzheimer's and other diseases.
Why it matters
Antibodies that distinguish cis from trans forms of phosphorylated tau showed that the cis form appears early in the brains of people with mild cognitive impairment and accumulates in degenerated neurons. Unlike trans p-tau, the cis isomer cannot promote microtubule assembly and is more prone to aggregation, and the authors suggest isomer-specific antibodies or vaccines may have value for early diagnosis and treatment.
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This software program with application of SPM8 plus DARTEL to VBM provides a high performance for AD diagnosis by using MRI.
Why it matters
A new automated MRI analysis method detected atrophy in medial temporal structures and distinguished very mild, mild, and moderate-to-severe Alzheimer disease from healthy controls with accuracies of 91.6%, 95.8%, and 98.2%. This is a diagnostic tool only and does not treat, cure, or prevent the disease.
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Alzheimer's disease (AD) in younger patients is associated with a higher prevalence of atypical symptoms.
Why it matters
This study compared cognitive performance in people with early-onset versus late-onset Alzheimer's disease and found that early-onset disease is associated with a distinct profile. It is about describing differences in symptoms, not about treating, curing or preventing the disease.
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A family history of Alzheimer's disease (AD) increases one's risk of developing late-onset AD (LOAD), and a maternal family history of LOAD influences risk more than a paternal family history.
Why it matters
In non-demented, mild cognitive impairment, and late-onset Alzheimer's disease participants, a maternal family history of Alzheimer's disease was associated with Alzheimer's-typical biomarker changes on PET imaging and cerebrospinal fluid analysis. This suggests that family history, especially from the mother, may influence biomarker levels.
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Brain glucose metabolism is impaired in Alzheimer's disease (AD), the most common form of dementia.
Why it matters
In autopsied frontal cortex from nine Alzheimer's disease, 10 type 2 diabetes, eight T2DM-AD and seven control cases, this study found decreased levels and activities of components of the insulin-PI3K-AKT signalling pathway. It suggests impaired insulin signalling might contribute to neurodegeneration, but this is tissue-based work and not a treatment, cure or prevention.
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49/100
The sirtuin pathway, which is most notable for its association with the anti-ageing effects of calorie restriction, has received particular attention, and pharmacological or transgenic upregulation of the sirtuin pathway has shown promising results in laboratory models of ageing.
Why it matters
This 2011 review looks at the sirtuin pathway, which is best known for its link to the anti-ageing effects of calorie restriction. It reports that boosting the pathway with drugs or genetic changes "has shown promising results in laboratory models of ageing". It also explains that increasing α-secretase moves APP processing away from the route that makes the "presumptive toxic" amyloid-beta. These are lab findings and background biology, not evidence that any diet, supplement or drug helps people with Alzheimer's.
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Tau is the major microtubule associated protein (MAP) of a mature neuron.
Why it matters
This review describes how abnormally hyperphosphorylated tau in Alzheimer's disease brain sequesters normal tau and other microtubule-associated proteins and self-assembles into filaments. It is a summary of tau biology and pathology with no treatment, cure or prevention tested.
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Alzheimer's disease (AD), the most prominent cause of senile dementia, is clinically characterized by the extracellular deposition of beta-amyloid (Abeta) and the intracellular neurofibrillary tangles.
Why it matters
This review states that Alzheimer's disease arises from disturbed balance of amyloid-beta in the brain, where even a moderate drop in clearance leads to accumulation, and that microglia play major roles in taking up and breaking down amyloid-beta. It is a review of clearance mechanisms and reports no treatment, cure or prevention.
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There is accumulating evidence that soluble amyloid-beta (Abeta) oligomers, rather than amyloid fibrils, are the principal pathogenic species in Alzheimer disease (AD).
Why it matters
Using a new ELISA, higher levels of high-molecular-weight amyloid-β oligomers were detected in cerebrospinal fluid from 25 patients with Alzheimer's disease or mild cognitive impairment compared with 25 age-matched controls, and levels negatively correlated with Mini-Mental State Examination scores. The authors conclude these oligomers could be useful as a diagnostic marker and potential surrogate marker for disease severity, but no treatment was tested.
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In Alzheimer disease (AD), which is the most common cause of dementia, the underlying disease pathology most probably precedes the onset of cognitive symptoms by many years.
Why it matters
This 2010 review describes how PET brain scans can show glucose use, brain chemical systems, inflammation and amyloid deposits in living people with Alzheimer's, and says such scans are aiding early and differential diagnosis. It suggests amyloid imaging "could be useful as early diagnostic marker" and for choosing patients for anti-amyloid therapy, while glucose PET "could be a suitable" marker for tracking progression. It reports no new data, and the authors say multi-tracer PET is too burdensome and expensive to become routine clinical care soon.
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[(11)C]-Pittsburgh Compound B (PIB) PET is specific for fibrillar Abeta molecular pathology but not for pathologic diagnosis of comorbid Alzheimer disease in individuals with Parkinson disease dementia.
Why it matters
In three people with Parkinson disease dementia scanned within 15 months of death, amyloid PET (PIB) was elevated in two. At autopsy those two had abundant diffuse amyloid plaques but only sparse neuritic plaques, and all three met only "low-probability" Alzheimer criteria. The authors conclude that PIB PET is "specific for fibrillar Abeta molecular pathology but not for pathologic diagnosis of comorbid Alzheimer disease" in this group, which is a caution against reading a positive scan as an Alzheimer's diagnosis. This comes from three cases only.
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The aim of the study is to evaluate whether depression or apathy in patients with amnestic-mild cognitive impairment (MCI) increases the risk of progressing to Alzheimer's disease (AD).
Why it matters
Among 131 people with newly diagnosed amnestic mild cognitive impairment, those with apathy had an almost sevenfold higher risk of progressing to Alzheimer's disease, while depression was not associated with increased risk. The authors conclude that apathy, but not depression, predicts which patients with amnestic mild cognitive impairment will progress.
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The combination of neuropsychological tests and P300 measurements proved useful in improving reliability and increasing sensitivity to early cognitive decline or disease progression in AD patients.
Why it matters
In this one-year study, P300 latency became more prolonged in people with probable Alzheimer's disease and mild cognitive impairment even though their cognitive test scores did not significantly decline. This suggests P300 may be a sensitive measure of cognitive decline, but no treatment was tested.
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Microbleeds (MBs) are commonly observed in Alzheimer disease.
Why it matters
Among patients with Alzheimer disease, those with multiple microbleeds had worse scores on the Mini-Mental State Examination than those without microbleeds. This is an association study and does not test treating, curing, or preventing Alzheimer's disease.
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Degeneration of language regions in the dominant hemisphere can result in primary progressive aphasia (PPA), a clinical syndrome characterized by progressive deficits in speech and/or language function.
Why it matters
This study used automated MRI analysis to tell apart variants of primary progressive aphasia and normal controls with high accuracy. It is a diagnostic classification study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Estrogen-containing hormone therapy initiated during late postmenopause does not improve episodic memory (an important early symptom of Alzheimer's disease), and it increases dementia risk.
Why it matters
This review reports that estrogen-containing hormone therapy started in late postmenopause does not improve episodic memory and increases dementia risk. Whether estrogen exposure in midlife affects later Alzheimer's risk is still uncertain and is being studied in ongoing trials.
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In cerebral amyloid angiopathy (CAA), amyloid fibrils deposit in walls of arteries, arterioles and less frequently in veins and capillaries of the central nervous system, often resulting in secondary degenerative vascular changes.
Why it matters
This paper reviews the genetics and molecular pathogenesis of cerebral amyloid angiopathies, in which amyloid-beta and other proteins deposit in blood vessel walls. It does not report any treatment, cure or prevention for Alzheimer's disease.
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Alzheimer disease (AD) is associated with cognitive decline and increased incidence of seizures.
Why it matters
This review discusses evidence that seizures and abnormal excitatory neuronal activity may contribute to cognitive decline in Alzheimer disease, including findings in animal models. It raises the possibility that such activity is an upstream mechanism, but does not establish a treatment or cure.
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49/100
The epsilon4 allele of APOE is a well-characterized genetic risk factor for late-onset Alzheimer disease (LOAD).
Why it matters
In a Japanese case-control study using 260 genetic markers around the APOE gene, 36 markers were significantly associated with late-onset Alzheimer's disease. These markers lie in a region containing PVRL2, TOMM40, APOE and APOC1, suggesting that genes other than APOE in this region could also contribute to disease risk.
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49/100
Only Apolipoprotein E polymorphisms have been consistently associated with the risk of late-onset Alzheimer disease (LOAD), but they represent only a minority of the underlying genetic effect.
Why it matters
This genome-wide association study confirmed the known APOE link and found a new risk locus on chromosome 12, along with several other signals that were replicated. These results help to further define the genetic architecture of late-onset Alzheimer disease, but they do not by themselves provide a treatment or cure.
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Alzheimer's disease (AD) is the most common form of neurodegenerative disease associated with dementia in the elderly.
Why it matters
This review describes evidence of oxidative stress in Alzheimer's disease brains and mixed results from antioxidant studies, including only a marginal effect of vitamin E in one trial and no effect in another. It does not show that antioxidant therapy treats or prevents Alzheimer's disease.
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Among mild to moderate AD patients, enrolled in an actual clinical trial, these results suggest evidence based guidelines for using the MacCAT-CR understanding subscale to help guide judgments about whether a patient has the capacity to consent.
Why it matters
This study looked at how well a standardized assessment tool helped identify which people with mild to moderate Alzheimer disease could give their own informed consent for a clinical trial. It is about research procedures and consent, not about treating, curing or preventing Alzheimer disease.
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Although it has been suggested that variations in mean EEG frequency are greater in the former, the existence of meaningful differences remains controversial.
Why it matters
This study compared EEG findings in early Alzheimer's disease, dementia with Lewy bodies and Parkinson's disease with dementia over a 2-year follow-up, and reported that whether meaningful differences exist remains controversial. It provides no information on treating, curing or preventing Alzheimer's disease.
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Researchers evaluated twenty-one patients diagnosed with MCI using PET studies with (11)C-PIB and (18)F-fluoro-deoxy-glucose (FDG), cognitive assessments, and CSF sampling.
Why it matters
Uses PET imaging to look at amyloid deposits in patients with mild cognitive impairment.
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Prevention of Alzheimer disease (AD) is a national and global imperative.
Why it matters
This paper discusses challenges in designing trials for disease-modifying Alzheimer's therapies, including using biomarkers and risk factors to enrich prevention trials. It is a review of trial methodology and does not report any treatment result or show that any specific therapy works.
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 phenotypic change but not proliferation underlies glial responses in Alzheimer disease
- Anti-Amyloid Monoclonal Antibodies in Early Alzheimer Disease: Lecanemab and Donanemab
- Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing
- Neuroinflammatory Biomarkers in Alzheimer's Disease: From Pathophysiology to Clinical Implications
- Rates of decline in Alzheimer disease decrease with age
- Timing of Biomarker Changes in Sporadic Alzheimer's Disease in Estimated Years from Symptom Onset
- Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer's disease
- Alzheimer Europe Publication Highlights Inequalities in Access to Dementia Care and Treatment Across Europe
- Effects of Exercise on Cognition: The Finnish Alzheimer Disease Exercise Trial: A Randomized, Controlled Trial
- A global view of the genetic basis of Alzheimer disease