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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Multiple studies in humans and animals have demonstrated the profound impact that exercise can have on the immune system.
Why it matters
This debate article asks whether exercise itself can weaken immune function and raise infection risk, and it notes that this idea has recently been challenged because athletes also face anxiety, sleep disruption, travel, exposure and nutritional deficits. It does not address treating, curing or preventing Alzheimer's disease.
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Our results demonstrate that tau, not amyloid, was associated with a depression diagnosis.
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A promising new therapeutic target for the treatment of Alzheimer's disease (AD) is the circadian system.
Why it matters
In mouse microglia, blocking REV-ERB proteins increased amyloid-beta clearance, and this reduced amyloid plaque deposition in the 5XFAD mouse model. This is animal research on a potential target and has not been shown to help people.
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Parkinson's disease (PD) and frontotemporal dementia/amyotrophic lateral sclerosis (FTD/ALS) are insidious and incurable neurodegenerative diseases that represent a significant burden to affected individuals, caregivers, and an ageing population.
Why it matters
This review argues that lysosomal failure is a primary mechanism in Parkinson's disease and frontotemporal dementia/amyotrophic lateral sclerosis and provides rationale for targeting lysosomes in future therapeutics. It is about other neurodegenerative diseases and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Diabetes mellitus is one of the major risk factors for cognitive dysfunction.
Why it matters
This review discusses glucagon-like peptide-1 as a possible link between metabolic and brain impairment in neurodegenerative diseases. It reports no treatment, cure, or prevention for Alzheimer's disease.
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The mechanisms of action of the dietary components of the Mediterranean diet are reviewed in prevention of cardiovascular disease, stroke, age-associated cognitive decline and Alzheimer disease.
Why it matters
This review describes how components of the Mediterranean diet, including omega-3 fatty acids and plant polyphenols, may help prevent stroke, age-related cognitive decline and Alzheimer's disease. It notes that polyphenols modulate tau phosphorylation and beta-amyloid aggregation in animal models, so the human benefit is not established as a treatment or cure.
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This neurodegenerative disorder is associated with neuronal death and gliosis heavily impacting the cerebral cortex.
Why it matters
This study used single-nuclei RNA sequencing to examine brain cell changes in people with different genetic forms of Alzheimer's disease. It is a laboratory analysis of brain tissue and does not test any treatment, so it cannot yet say whether these findings will help patients.
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Current brain spheroids or organoids derived from human induced pluripotent stem cells (hiPSCs) still lack a microglia component, the resident immune cells in the brain.
Why it matters
This study engineered brain region-specific organoids from human induced pluripotent stem cells incorporated with isogenic microglia-like cells that expressed microglial markers and phagocytosed iron oxides. It is a laboratory model development and does not show any treatment, cure or prevention for Alzheimer's disease.
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47/100
Microglia affect Alzheimer's disease (AD) pathogenesis in opposing manners, by protecting against amyloid accumulation in early phases of the disease and promoting neuropathology in advanced stages.
Why it matters
This mouse study used microscopy to compare microglial interactions with amyloid plaques across APOE genotypes and sexes. It is animal work and does not report any treatment, cure, or prevention for Alzheimer's disease.
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47/100
These findings demonstrate that chronic InRapa administration is able to exert a neuroprotective effect on Ts65Dn hippocampus by reducing AD pathological hallmarks and by restoring protein homeostasis, thus ultimately resulting in improved cognition.
Why it matters
In a mouse model of Down syndrome, 12 weeks of intranasal rapamycin rescued cognition and reduced amyloid precursor protein levels, its processing, and tau hyperphosphorylation. These are animal results only, and the treatment has not been tested in people.
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Among participants with normal cognition, higher aortic PWV related to lower frontal lobe CBF (β=-0.43; P=0.04) and higher CVR in the whole brain (β=0.11; P=0.02), frontal lobes (β=0.12; P<0.05), temporal lobes (β=0.11; P=0.02), and occipital lobes (β=0.14; P=0.01).
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Chronic neuroinflammation is a hallmark of the onset and progression of brain proteinopathies such as Alzheimer disease (AD) and it is suspected to participate in the neurodegenerative process.
Why it matters
In a mouse model with both amyloid and tau pathology, lacking the NRF2 gene worsened inflammation and shortened survival, while the drug dimethyl fumarate reduced glial and inflammatory markers and improved cognition and motor problems. This is preclinical animal work and does not show that dimethyl fumarate treats, cures, or prevents Alzheimer's disease in people.
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Among 124 876 cases and controls, genome-wide conjunction analyses of ALS, FTD, PD, AD, CBD, and PSP revealed significant genetic overlap between ALS and FTD at known ALS loci: rs13302855 and rs3849942 (nearest gene, C9orf72; P = .03 for rs13302855 and P = .005 for rs3849942) and rs4239633 (nearest gene, UNC13A; P = .03).
Why it matters
This genetic analysis found significant genetic overlap between amyotrophic lateral sclerosis and frontotemporal dementia, and between ALS and progressive supranuclear palsy. It concerns shared genetic risk between diseases and does not test any treatment, cure, or prevention for Alzheimer disease.
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People with Down syndrome (DS) are at high risk for developing Alzheimer disease (AD).
Why it matters
This review describes metabolic and vascular imaging findings in Down syndrome, including reductions in glucose metabolism and signs of inflammation, that appear linked to cognitive decline and Alzheimer's disease. The authors note a gap in vascular imaging knowledge and suggest future longitudinal studies, but no treatment, cure, or prevention is tested.
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Alzheimer's disease (AD) is the most common form of dementia and one of the major causes of disability and dependency in older people.
Why it matters
This study compared the gut bacteria of transgenic Alzheimer's model mice with normal mice at different ages and found shifts in bacterial composition over the lifespan. This is animal research and does not yet show whether changing gut bacteria would treat or prevent Alzheimer's disease in people.
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The derivation of microglia from human stem cells provides systems for understanding microglial biology and enables functional studies of disease-causing mutations.
Why it matters
Using microglia grown from human stem cells, this study found that TREM2 mutations causing frontotemporal dementia-like syndrome and Nasu-Hakola disease produce an immature TREM2 protein that does not mature properly. It is laboratory cell work on rare genetic diseases and does not show a treatment, cure or prevention for Alzheimer's.
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In the central nervous system (CNS), microglia are innate immune mononuclear phagocytes (CNS MPs) that can phagocytose infectious particles, apoptotic cells, neurons, and pathological protein aggregates, such as Aβ in Alzheimer's disease (AD).
Why it matters
This work developed and validated flow cytometry assays to compare phagocytosis in two types of brain immune cells, including uptake of amyloid-beta fibrils. It is a methods and cell-characterization study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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47/100
It is clear that innate immune system status is altered in numerous neurodegenerative diseases.
Why it matters
This study examined behavior and cognition in Trem2 knockout mice under basal conditions and after immune stimulation with lipopolysaccharide. It is an animal study of TREM2 function and does not show a treatment, cure or prevention for Alzheimer's disease.
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Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia.
Why it matters
This review argues that sustained reduced blood flow to the brain may cause white matter damage, a feature shared by Alzheimer's disease and small vessel disease. It proposes that refined rodent models of chronic cerebral hypoperfusion are needed to test candidate drugs and lifestyle factors before human trials.
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Neuroinflammation is one of the main mechanisms involved in the progression of several neurodegenerative diseases, such as Parkinson, Alzheimer, multiple sclerosis, amyotrophic lateral sclerosis and others.
Why it matters
This review states that flavonoids such as quercetin, genistein, hesperetin and epigallocatechin-3-gallate can reduce inflammatory responses in neurodegenerative disease models. It is a summary of laboratory and model findings, not evidence that flavonoids treat or prevent Alzheimer's disease in people.
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Amyotrophic lateral sclerosis (ALS) is a degenerative disorder that is characterized by loss of motor neurons and shows clinical, pathological, and genetic overlap with frontotemporal dementia (FTD).
Why it matters
This review highlights the contribution of microglia to ALS/FTD pathogenesis and discusses the connection between autoimmunity and the C9orf72 gene, the most commonly mutated gene in ALS/FTD. It concerns ALS and frontotemporal dementia and does not report a treatment or cure for Alzheimer's disease.
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Accumulating studies suggest that overnutrition-associated obesity may lead to development of type 2 diabetes mellitus and metabolic syndromes (MetS).
Why it matters
In obese mice fed a high-fat diet, recombinant human FGF21 improved cognitive dysfunction and anxiety-like behavior through metabolic regulation and reduced inflammation. This is animal research, and the authors suggest FGF21 might be a molecular target for a disease-course-modifying strategy, which is not yet established for people.
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The term "aging-related tau astrogliopathy" (ARTAG) describes pathological accumulation of abnormally phosphorylated tau protein in astrocytes.
Why it matters
In this study of 628 postmortem brains, aging-related tau astrogliopathy (ARTAG) was associated with age at death, male sex, frontotemporal lobar degeneration tauopathy, brain atrophy, ventricular enlargement, and Alzheimer's disease-related variables. This describes patterns of tau pathology in astrocytes and proposes a reference map, but it does not report a treatment, cure, or prevention.
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Affect sharing and prosocial motivation are integral parts of empathy that are conceptually and mechanistically distinct.
Why it matters
This study used a neurodegenerative disease lesion model with 275 participants to examine the neural correlates of affect sharing and prosocial motivation, two aspects of empathy. It is observational, so it cannot show that any treatment would prevent or cure Alzheimer's disease or other neurodegenerative diseases.
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Computational docking and scoring techniques have revolutionized structural bioinformatics by providing unprecedented insights on key aspects of ligand-receptor interaction.
Why it matters
This paper describes computational docking tools using BACE1 as a case study for structure-based drug design. It is a methods discussion and does not report any treatment, cure, or prevention for Alzheimer's disease.
From across this topic
10 of the 4,748 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.
- Proteomic Profiling of Extracellular Vesicles Derived from Cerebrospinal Fluid of Alzheimer's Disease Patients: A Pilot Study
- Does neuroinflammation drive the relationship between tau hyperphosphorylation and dementia development following traumatic brain injury?
- The striatum is an early, accurate indicator of amyloid burden using [11C]PiB in Down syndrome: Comparison of two radiotracers
- Concurrence of TDP-43, tau and alpha-synuclein pathology in brains of Alzheimer's disease and dementia with Lewy bodies
- Effects of APOE on brain white matter microstructure in healthy adults
- Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR) activity via a PRAS40-mediated mechanism
- Clinical effects of Abeta immunization (AN1792) in patients with AD in an interrupted trial
- Accelerated in vitro fibril formation by a mutant alpha-synuclein linked to early-onset Parkinson disease
- P301S mutant human tau transgenic mice manifest early symptoms of human tauopathies with dementia and altered sensorimotor gating
- Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo