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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Reduced bone mineral density and increased risk of falls are related with Alzheimer disease, and these increase likelihood of bone osteoporotic fractures causing serious complications such as disability, fear of falling, loss autonomy, decreased quality of life, and anticipated mortality in elderly patients.
Why it matters
This is a protocol for a planned 6-month randomized trial of a physical exercise program plus a Mediterranean diet in institutionalized patients with Alzheimer disease. It will assess effects on bone density, falls, balance, and gait, so no results on treating, curing, or preventing Alzheimer's disease are available yet.
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This observational study included 290 cognitively unimpaired (CU) participants with a family history (FH) of clinically diagnosed sporadic AD (age 49-73 years) from the Alzheimer's and Families (ALFA) study. [ 18 F]flutemetamol-PET standardized uptake value ratios, CSF β-amyloid 42/40 ratio, and phosphorylated tau were used as AD biomarkers.
Why it matters
In 290 cognitively unimpaired adults with a family history of sporadic Alzheimer's disease, this study examined whether being closer to a parent's age at onset was linked to Alzheimer's and nerve injury biomarkers in midlife. It is about risk and biomarker timing, not about treating, curing or preventing the disease.
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A large number of mouse models have been engineered, characterized and used to advance biomedical research in Alzheimer disease (AD).
Why it matters
This review discusses how preclinical mouse models have been engineered and used to advance Alzheimer disease research, from early toxin or lesion models to genetic models of familial disease. It describes research tools and does not report a treatment, cure or prevention for patients.
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In the last decades, an important role of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD) diagnosis has emerged.
Why it matters
This study assessed how accurately cerebrospinal fluid amyloid-beta 42, total tau and phosphorylated tau, measured by a chemiluminescent enzyme immunoassay, diagnose Alzheimer disease. It concerns diagnostic testing and does not evaluate any treatment, cure or prevention.
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Neuropathological studies indicate concomitant Alzheimer's disease (AD) pathology in patients with dementia with Lewy bodies (DLB).
Why it matters
This study measured cerebrospinal fluid Aβ42, total tau and tau phosphorylated at threonine 181 in 38 patients with probable dementia with Lewy bodies to see how often Alzheimer's biomarker profiles appear. It is a biomarker prevalence study, so it does not provide a treatment, cure or prevention.
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Magnetic resonance imaging (MRI) volumetric measures have become a standard tool for the detection of incipient Alzheimer's Disease (AD) dementia in mild cognitive impairment (MCI).
Why it matters
MRI volumetric measures of the hippocampus and entorhinal cortex predicted conversion to Alzheimer's dementia even at the mid-term, with better specificity and AUC as follow-up time increased. This concerns prediction and diagnosis, not treatment, cure or prevention.
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Plant iridoids such as catalpol and its 10-O-trans-p-coumaroyl derivative, geniposide, harpagoside, and loganin, and seco-iridoids, oleuropein and its aglycone and oleocanthal have been found to exhibit significant neuroprotective effect and the property of slowing down the process of neurogedeneration in AD and PD.
Why it matters
This review reports that certain plant iridoids and seco-iridoids have shown significant neuroprotective effects and the property of slowing neurodegeneration in Alzheimer's and Parkinson's diseases. It is a review of these compounds and does not establish that any of them treat, cure, or prevent Alzheimer's disease in people.
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The prevalence and incidence of dementia increase exponentially from the age of 65 onwards.
Why it matters
This review reports that dementia prevalence and incidence rise sharply from age 65 and will increase as populations age, while some recent studies suggest a slight drop in age- and sex-adjusted risk in some countries. It describes patterns over time and does not test any treatment or prevention.
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The concentration of 124 I-RmAb158-scFv8D3, as measured in vivo with PET, increased with age and corresponded well with the ex vivo autoradiography and Aβ immunohistochemistry results.
Why it matters
In Alzheimer transgenic mice, PET imaging with the Aβ protofibril-selective radioligand 124I-RmAb158-scFv8D3 detected lower signals in mice treated with the BACE-1 inhibitor NB-360 than in untreated animals, matching decreased Aβ levels measured after death. This shows the imaging method can follow disease progression and detect treatment effects in these mice, but it is an animal study and does not show a treatment or cure for people.
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This influential 2018 paper proposed defining Alzheimer's disease by what is happening biologically in the brain (amyloid plaques, tau tangles, and neuron loss, measured by scans or spinal fluid tests) instead of by memory symptoms alone.
Why it matters
This influential 2018 paper proposed defining Alzheimer's disease by what is happening biologically in the brain (amyloid plaques, tau tangles, and neuron loss, measured by scans or spinal fluid tests) instead of by memory symptoms alone. It explicitly said this 'AT(N)' framework was meant for research studies, not everyday clinical diagnosis.
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The vascular hypothesis of Alzheimer's disease (VHAD) was proposed 24 years ago from observations made in our laboratory using aging rats subjected to chronic brain hypoperfusion.
Why it matters
This paper argues that brain hypoperfusion may be involved in Alzheimer's disease and could serve as a biomarker for predicting progression from mild cognitive impairment to Alzheimer's. It discusses imaging for prediction and for assessing interventions, but does not report a treatment or cure.
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In CN subjects, study-wide significant (P -9 ) loci were identified for total tau near SRRM4 and C14orf79 and for hippocampal volume near MTUS1.
Why it matters
This study looked for genetic variants linked to Alzheimer's-related brain and fluid measures in people before dementia diagnosis. It is an early genetic association study and does not provide a treatment, cure, or prevention.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease that impairs memory and cognitive judgment.
Why it matters
This review reports that physical inactivity is a common preventable risk factor for Alzheimer's disease and that exercise is linked to reduced risk and to improved cognition and daily functioning in people with the disease. These findings come largely from prospective studies and do not prove that exercise prevents or cures Alzheimer's disease.
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Mitochondrial dysfunction is linked with the etiopathogenesis of Alzheimer disease and Parkinson disease.
Why it matters
This study found mitochondrial 5-methylcytosine at CpG and non-CpG sites in brain regions of control human postmortem brains and reported an altered mitochondrial DNA methylation pattern in Alzheimer's disease-related pathology and Parkinson disease. It describes an epigenetic observation and does not show that changing this pattern treats or prevents disease.
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Antidepressants have modest efficacy in late-life depression (LLD), perhaps because various neurobiologic processes compromise frontolimbic networks required for antidepressant response.
Why it matters
This paper proposes that amyloid accumulation may be an etiologic factor for frontolimbic compromise that predisposes some older adults to depression and treatment resistance. It presents a hypothesis and supporting findings, not a tested treatment, cure or prevention for Alzheimer's disease.
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Oxidative stress (OS) has been demonstrated to be involved in the pathogenesis of the two major types of dementia: Alzheimer's disease (AD) and vascular dementia (VaD).
Why it matters
This review states that oxidative stress is involved in the pathogenesis of both Alzheimer's disease and vascular dementia, and that research has looked at whether antioxidant therapy plays a role in prevention and treatment. It concludes that the role of the antioxidant defence system and stress responses is very complex and that more research is needed, so no antioxidant treatment is established.
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42/100
According to the ' amyloid cascade hypothesis of Alzheimer's disease ' first proposed about 16 years ago, the accumulation of Aβ peptides in the human central nervous system (CNS) is the primary influence driving Alzheimer's disease (AD) pathogenesis, and Aβ peptide accretion is the result of an imbalance between Aβ peptide production and clearance.
Why it matters
This commentary discusses the idea that amyloid and inflammatory signals from microbiome microbes might add to amyloid burden, and that clearance of amyloid may be impaired by deficits in TREM2. It is a perspective paper and reports no treatment, cure, or prevention.
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These data provide potential insights into the biology of CSF in AD and MCI progression and provide a novel tool for AD researchers and clinicians working to improve diagnostic accuracy, evaluation of treatment efficacy, and early diagnosis.
Why it matters
This project developed a multiplexed mass spectrometry-based approach for measuring candidate Alzheimer's disease biomarkers in cerebrospinal fluid, identifying several peptides with potential diagnostic or predictive utility. The work concerns biomarker measurement and qualification, not treating, curing, or preventing the disease.
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Analyses of cerebrospinal fluid (CSF) biomarkers (β-amyloid protein, total tau protein, and hyperphosphorylated tau protein) are part of the diagnostic criteria of Alzheimer disease.
Why it matters
This study examined how different sample handling procedures before analysis affect cerebrospinal fluid Alzheimer's biomarker concentrations. It is a laboratory methods study and does not test any treatment, cure, or prevention.
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This review traces evidence that age-related dementia (Alzheimer's disease) results from the destructive impact of the pulse on cerebral vasculature.
Why it matters
This review proposes that age-related dementia is caused by pulse-induced damage to small cerebral vessels, leading to silent microbleeds. It discusses implications for therapy but presents no new treatment or cure tested in patients.
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Recently, studies have provided convincing data that TYRO protein tyrosine kinase-binding protein (TYROBP), a key regulator in immune systems, is significantly upregulated in the brain of patients with Alzheimer's disease (AD).
Why it matters
This review notes that TYROBP is upregulated in the brains of people with Alzheimer's disease and acts as a signaling adaptor for receptors including TREM2. It states that the role of TYROBP in Alzheimer's disease remains unclear and reports no treatment, cure, or prevention.
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42/100
Two independent cohorts were used in this study.
Why it matters
This study examined brain structural changes linked to depressive symptoms in Alzheimer's disease patients and their relationship to cerebrospinal fluid Alzheimer's biomarkers in two cohorts. It is about understanding brain changes, not treating, curing, or preventing the disease.
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Late-onset Alzheimer's disease (LOAD), which is characterized by progressive deterioration in cognition, function, and behavior, is the most common cause of dementia and the sixth leading cause of all deaths, placing a considerable burden on Western societies.
Why it matters
This review summarizes what is known about genetic risk factors for late-onset Alzheimer's disease in Caribbean Hispanic and African American populations, groups that have been underrepresented in genetic studies. It does not report a treatment, cure, or prevention, and it calls for future research rather than presenting new findings.
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β-Site amyloid precursor protein cleaving enzyme1 (BACE1) is one of the key enzymes involved in the processing of the amyloid precursor protein (APP) and formation of amyloid β peptide (Aβ) species.
Why it matters
The study reports the discovery and preclinical characterization of AZD3839, a potent and selective inhibitor of human BACE1, which inhibited BACE1 activity in biochemical assays. This is preclinical drug development, not evidence from patients that the compound treats or prevents Alzheimer's disease.
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Alzheimer Disease (AD) is the most common neurodegenerative disorder worldwide, and account for 60% to 70% of all cases of progressive cognitive impairment in elderly patients.
Why it matters
This review discusses platelets and their relevance in Alzheimer disease, noting that amyloid precursor protein is expressed in non-neuronal tissues as well as the brain. It is a review of biology and does not report 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.
- Aβ-degrading enzymes: potential for treatment of Alzheimer disease
- Does Therapeutic Exercise Support Improvement in Cognitive Function and Instrumental Activities of Daily Living in Patients with Mild Alzheimer's Disease? A Randomized Controlled Trial
- The clinical efficacy of reminiscence therapy in patients with mild-to-moderate Alzheimer disease: Study protocol for a randomized parallel-design controlled trial
- Genetic associations with EEG signatures in mild cognitive impairment: insights into Alzheimer's disease pathophysiology
- Advancing Theranostics in Alzheimer Disease: FDA Approval of Amyloid- PET Drugs for Selection of Patients for Amyloid-ߖDirected Therapies and Other Labeling Updates
- EFNS guidelines for the diagnosis and management of Alzheimer's disease
- Amyloid-β assessed by florbetapir F 18 PET and 18-month cognitive decline: a multicenter study
- Safety, tolerability and efficacy of the glutaminyl cyclase inhibitor PQ912 in Alzheimer's disease: results of a randomized, double-blind, placebo-controlled phase 2a study
- Impaired default network functional connectivity in autosomal dominant Alzheimer disease
- Tau extent is associated with lower cognition in Down syndrome-related Alzheimer's disease