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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47/100
The [(11)C]PIB uptake of the patients with AD did not increase significantly during follow-up when compared with that of the controls.
Why it matters
In patients with Alzheimer's disease, Pittsburgh compound B uptake did not increase significantly over two years compared with controls, despite progressive brain volume loss and declining cognitive performance. This suggests no or only little increase in amyloid tracer uptake during Alzheimer's disease progression over this period.
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Alzheimer's disease (AD) is an age-related dementia, characterized by amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss in the brain.
Why it matters
In mouse models of Alzheimer's disease, oral delivery of the C5a receptor antagonist PMX205 decreased pathology and improved behavioral performance. This is animal research and does not yet show that the treatment would work in people.
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Cerebrovascular disease and Alzheimer disease are common diseases of aging and frequently coexist in the same brain.
Why it matters
This review discusses evidence that brain infarction influences the course of Alzheimer's disease and that beta-amyloid can impair blood vessel function, including through cerebral amyloid angiopathy. It is a review of vascular mechanisms and does not report any treatment, cure or prevention.
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CSF T-tau and P-tau as well as the APOE epsilon4/epsilon4 genotype are robust predictors of AD and are also associated with a more rapid progression from MCI to AD.
Why it matters
In this study of 47 Alzheimer's, 58 mild cognitive impairment and 35 control participants, high CSF total tau or phosphorylated tau together with the APOE epsilon4/epsilon4 genotype predicted faster progression from mild cognitive impairment to Alzheimer's. It is about predicting progression, not about treating, curing or preventing the disease.
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These findings suggest that either microglial activation is limited to later stages of severe AD or [11C](R)-PK11195 is too insensitive to detect the level of microglial activation associated with mild to moderate AD.
Why it matters
Using PET imaging in a small number of subjects, probable Alzheimer's patients showed greater amyloid tracer retention than controls, while those with mild cognitive impairment ranged from control-like to Alzheimer-like levels. The study examined the relationship between amyloid deposition and microglial activation but did not test any treatment.
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Insoluble protein aggregates have been linked to Alzheimer's disease (AD) and frontotemporal dementia (FTD).
Why it matters
This review summarizes what has been learned about Alzheimer's disease and frontotemporal dementia from transgenic mice and invertebrate species such as flies and worms. It describes how these animal models have identified soluble oligomeric species and new drug targets, and suggests that early preclinical diagnosis may be within reach with advanced imaging.
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Inflammation is associated with Abeta pathology in Alzheimer's disease (AD) and transgenic AD models.
Why it matters
This study in Tg2576 Alzheimer mice found that exercise altered the immune profile toward a response coinciding with improved cognitive performance and decreased amyloid. This is animal research and does not yet show whether exercise would treat or prevent Alzheimer's disease in people.
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In subjects with aMCI poor global cognitive performance at baseline, the worsening on executive functions and on functional status but not the worsening on memory functions are independently associated with the conversion to dementia of Alzheimer type at 1 year, follow-up.
Why it matters
In this one-year follow-up, poor global cognitive performance at baseline, worsening executive function, and worsening functional status were independently associated with conversion from amnestic mild cognitive impairment to Alzheimer-type dementia, but worsening memory was not. This indicates that non-memory decline may matter for predicting conversion.
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A comparison of a randomized clinical trial of donepezil in AD patients and this observational study indicates that if appropriate methodological and statistical precautions are undertaken, then results from randomized clinical trials can be predictive with AD patients in clinical practice.
Why it matters
In an observational study, Alzheimer disease patients treated with donepezil declined less on the Mini-Mental State Exam over one year than those who received no anti-Alzheimer drugs, similar to results from a randomized trial. This supports that donepezil's trial benefits may apply in clinical practice, but it is not a cure.
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These findings suggest a functional disconnection between the hippocampus and other brain regions in patients with Alzheimer disease.
Why it matters
In a very small study of 8 patients with probable Alzheimer's disease and 8 healthy volunteers, patients showed markedly reduced functional connectivity between the hippocampus and other brain regions, including an absence of connectivity with the frontal lobes. This describes a functional disconnection in the disease but does not show how to treat or cure it.
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Growing evidence supports a strong and likely causal association between cardiovascular disease (CVD), and its risk factors, with incidence of cognitive decline and Alzheimer's disease.
Why it matters
This review reports that cardiovascular disease and its risk factors, such as hypertension and diabetes, are linked to higher risk of cognitive decline and Alzheimer's disease. It suggests that addressing cardiovascular risk factors may be a promising avenue for prevention research.
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The varied ways in which mutations in presenilins (PSEN1 and PSEN2) affect amyloid b precursor protein (APP) processing in causing early-onset familial Alzheimer disease (FAD) are complex and not yet properly understood.
Why it matters
For nine clinical presenilin mutations, all significantly increased the ratio of amyloid beta 42 to 40 in vitro, and the mean age of onset correlated with increased Abeta42 and decreased Abeta40. This is laboratory and tissue analysis of mutation effects and does not offer a treatment or cure.
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Biometals play an important role in Alzheimer disease, and recent reports have described the development of potential therapeutic agents based on modulation of metal bioavailability.
Why it matters
In cell culture, the metal ligand clioquinol with copper or zinc reduced secreted amyloid-beta by about 85-90%, apparently by up-regulating metalloprotease activity. This is laboratory research, so it does not show that clioquinol treats Alzheimer's disease in people.
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Genetic variations in promoter sequences that alter gene expression play a prominent role in increasing susceptibility to complex diseases.
Why it matters
This genetic study found rare APP promoter mutations in people with Alzheimer disease that roughly doubled APP transcriptional activity in vitro, similar to the effect of an extra APP copy in Down syndrome. It provides evidence of a genetic risk mechanism and reports no treatment or cure.
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As a safe and effective medicine, akatinol memantine, which has a similar effect as donepezil for AD, can remarkably improve the cognition, behavior, and mood of AD patients.
Why it matters
In this 100-patient trial, akatinol memantine and donepezil both improved cognition and daily life measures in mild to moderate Alzheimer's disease over 16 weeks. This shows symptom improvement with both drugs, not a cure or prevention of the disease.
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Hippocampal atrophy is a marker of Alzheimer disease (AD).
Why it matters
In 103 clinically diagnosed Alzheimer's patients and 73 controls, both aging and Alzheimer's disease were independently associated with smaller hippocampal volume, and both young and old Alzheimer's patients had hippocampal atrophy abnormal for their age. This supports hippocampal volume as a marker of Alzheimer's across ages and suggests age-dependent criteria are needed, but it does not address treatment or prevention.
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We review the clinical, radiologic, and neuropathologic features of the hereditary and sporadic forms of cerebral amyloid angiopathy (CAA) associated with vascular deposition of the beta-amyloid peptide.
Why it matters
This review describes hereditary and sporadic forms of cerebral amyloid angiopathy caused by vascular deposition of beta-amyloid peptide, including mutations in the amyloid precursor protein that cause bleeding, white matter lesions, and cognitive impairment. It is a descriptive review of these vascular conditions and does not report any treatment, cure, or prevention.
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There is concern that AIDS dementia complex (ADC) may be complicated by Alzheimer disease (AD).
Why it matters
This study found that people with AIDS dementia complex had decreased cerebrospinal fluid amyloid-beta 42 and increased total tau and phosphorylated tau, similar to Alzheimer disease. It suggests a possible AD-like process in that condition but does not show any treatment, cure, or prevention.
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ABCA1, a cholesterol transporter expressed in the brain, has been shown recently to be required to maintain normal apoE levels and lipidation in the central nervous system.
Why it matters
In two Alzheimer mouse models, removing the cholesterol transporter ABCA1 sharply lowered soluble apoE in the brain but left Abeta levels unchanged and did not reduce amyloid deposits; in the Tg-SwDI/B model, amyloid in both brain tissue and blood vessels increased. A larger share of apoE was instead held in the insoluble fraction, which the authors suggest means ABCA1's effects on apoE amount and lipidation shape amyloid build-up. These are animal findings and do not point to a treatment.
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We investigated consecutive patients with dementia.
Why it matters
This study explored the range of psychiatric and behavioral symptoms in patients with Alzheimer's disease compared with those who have cortical or subcortical vascular dementia. Understanding these differences may help doctors recognize which type of dementia a patient has, but it does not test any treatment.
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APOE-epsilon4 is associated with small vessel arteriolosclerosis, microinfarcts of the deep nuclei, neuritic senile plaque density, and amyloid angiopathy in patients with autopsy-proven Alzheimer disease (AD).
Why it matters
In brains from people who met criteria for intermediate to high likelihood of Alzheimer's disease, APOE epsilon4 was not associated with gross cerebrovascular pathology but was associated with greater small vessel arteriolosclerosis and with microinfarcts in the deep nuclei. This postmortem study links APOE epsilon4 to some vascular findings but does not show a treatment or prevention.
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From a prospective Memory Clinic cohort including consecutively referred patients, age 60 years or above, and with MMSE score 20 or above, 36 patients with AD and 30 with MCI were included in this study.
Why it matters
This study examined the relationship between unawareness of memory problems (anosognosia) and behavioral symptoms, executive test performance, and frontal cortex blood flow in 36 patients with Alzheimer's disease and 30 with mild cognitive impairment. It describes a clinical feature of the disease and does not test any treatment, cure, or prevention.
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Interest in characterizing the role of impaired insulin actions in Alzheimer's disease (AD) and vascular dementia is growing exponentially.
Why it matters
This review of animal models suggests Alzheimer's disease may be caused in part by insulin resistance in the brain, but no single animal model fully represented the disease. It did not resolve whether this insulin resistance is a local brain process or a complication of peripheral insulin resistance.
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Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline.
Why it matters
In a large prospective study, higher dietary intake of niacin was associated with a lower risk of incident Alzheimer's disease and a slower rate of cognitive decline. Niacin intake from foods was also inversely associated with Alzheimer's disease.
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47/100
A 1-minute semantic fluency test can assist in early detection of dementia in the memory clinic setting.
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.
- Alzheimer's disease
- Alzheimer-like amyloid and tau alterations associated with cognitive deficit in temporal lobe epilepsy
- Oxidative Stress as a Central Mechanistic Bridge Between Alzheimer’s and Vascular Pathologies in Mixed Dementia: Emerging Evidence and Therapeutic Perspectives
- Apolipoprotein E and Alzheimer disease: an update on genetic and functional analyses
- Clinical features and APOE genotype of pathologically proven early-onset Alzheimer disease
- Both Targeted Mass Spectrometry and Flow Sorting Analysis Methods Detected the Decreased Serum Apolipoprotein E Level in Alzheimer's Disease Patients
- Early and protective microglial activation in Alzheimer's disease: a prospective study using 18F-DPA-714 PET imaging
- Prevalence of Diagnosed Arthritis - United States, 2019-2021
- PART is part of Alzheimer disease
- Comparative Prognostic Performance of Hippocampal Volume and Plasma Biomarkers in Amyloid-Negative Subjective Cognitive Decline: A Four-Year Follow-up