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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Fifty patients with liver cirrhosis underwent neurological, psychometric, electroencephalographic and biochemical examination as well as cranial magnetic resonance imaging (MRI) to study the incidence of pallidal lesions in cirrhotics and their correlation to liver function, as well as to neurological and mental state.
Why it matters
This study of liver cirrhosis patients found bilateral pallidal hyperintensities on T1-weighted MRI in 92% of cases, with signal intensity increasing as liver function declined and decreasing after liver transplantation. The lesions' cause remained unclear, and the findings concern liver disease rather than Alzheimer's disease treatment, cure or prevention.
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The relationship between Alzheimer's disease (AD) and expression of fetal proteins was examined by: (i) determining the phosphate content of tau prepared from fetal brains (F-tau); (ii) comparing F-tau, tau from normal adult human brains (N-tau) and tau from paired helical filaments in AD brains (PHF-tau) for phosphate content; and (iii) testing the reactivity of F-tau with five antibodies known to recognize PHF-tau.
Why it matters
This laboratory study found that fetal tau contains about 7 mol phosphate per mol protein, comparable to the phosphate content of PHF-tau from Alzheimer brains and 3-4 times higher than normal adult tau. It is basic biochemistry from 1993 about tau phosphorylation, not a treatment, cure or prevention finding.
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Kainic acid lesions of rat striatum caused an elevation of amyloid precursor protein (APP) immunoreactivity in neurons and neurites, some of which were then phagocytosed by reactive microglia/macrophages.
Why it matters
In this rat model, damaged neurons produced more amyloid precursor protein, which was then taken up by reactive microglia and macrophages, but this did not result in Alzheimer-type amyloid deposits. Because it is an animal study, it does not directly show what happens in human Alzheimer's disease.
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39/100
The amyloid beta protein and the amyloid beta-protein precursor (APP) are major constituents of senile plaques and cerebrovascular deposits in patients with Alzheimer disease and Down syndrome.
Why it matters
This study found that in normal and Alzheimer's disease brain, both the 105-kDa and 120-kDa amyloid precursor protein forms contain the Kunitz protease inhibitor domain, and that KPI- forms represent less than 14% of total brain APP. It is a basic biochemical finding about APP in brain tissue and does not test any treatment, cure or prevention.
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The amyloid precursor protein (APP) is thought to be processed aberrantly to yield the major constituent of the amyloid plaques observed in the brains of patients with Alzheimer disease and Down syndrome.
Why it matters
This study showed that the amyloid precursor protein gene is expressed in mouse oocytes, preimplantation embryos and later embryonic stages, with changes in the ratios of its splicing forms and a 10-fold increase in APP clone abundance between two stages. It is a basic developmental study in mice and does not test or propose any treatment, cure or prevention for Alzheimer's disease.
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In Alzheimer's disease, in Down syndrome and in normal aging, scattered deposits of amyloid fibril precursors occur in both cerebral cortex and subcortical grey structures.
Why it matters
In brains from Alzheimer and Down syndrome patients, abnormal presynaptic terminals were found near early amyloid deposits. It is unclear whether the deposits come before or after the terminal changes, and no treatment is tested.
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Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology.
Why it matters
This autopsy study compared brain proteins in people with Alzheimer's disease and adults with Down syndrome, finding a more marked astrocytic reaction in Down syndrome. It is a tissue study and does not test any treatment, cure or prevention.
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Prosodic contours in the verbal output of 30 patients with Idiopathic Parkinson's disease were contrasted to those of fifteen age-, sex-, and educationally matched normal subjects.
Why it matters
In 30 patients with Parkinson's disease, prosody problems related to motor control rather than loss of linguistic knowledge. This is a characterization study and reports no treatment, cure, or prevention.
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The Alzheimer type II astrocyte change is the distinctive morphologic alteration in brain of humans and experimental animals succumbing to hepatic encephalopathy (HE).
Why it matters
This study examined astrocyte changes in a rat model of hepatic encephalopathy, including the Alzheimer type II astrocyte change. It concerns liver-related brain dysfunction, not Alzheimer's disease, and reports no treatment, cure or prevention.
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38/100
The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease.
Why it matters
This laboratory and post-mortem brain study found that a fragment of amyloid precursor protein, APP-CTFβ, accumulates at excitatory synapses and may contribute to early synaptic alterations in Alzheimer's disease. It identifies a possible mechanism, not a treatment, cure or prevention.
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IFNAR1 plays a crucial role in brain and mitochondrial homeostasis, loss of which results in neurodegeneration and neuropathology resembling PDD.
Why it matters
In mice lacking IFNAR1 in neurons or astrocytes, brain energy metabolism was disrupted and Parkinsonian dementia-like features developed. This is animal research on Parkinson's disease, so it does not provide a treatment or prevention for Alzheimer's disease.
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The blood-brain barrier (BBB) displays a highly organized and complex structure, which is important for maintaining brain homeostasis and protecting the brain from foreign molecules or pathogens.
Why it matters
This review describes transport pathways across the blood-brain barrier, including receptor-mediated transcytosis, and how they might be targeted to deliver drugs or antibodies into the brain. It focuses on LRP1, a key mediator of amyloid beta clearance in Alzheimer's disease, and TfR1, already used as a target for antibody delivery into the brain, as well as P-gp and PCSK9.
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SynCav1 exerted robust neuroprotective effects on cognition.
Why it matters
In this early laboratory work, a treatment called SynCav1 protected thinking and brain cells in models of TDP-43-related damage. These findings are preliminary and support further research into SynCav1 as a possible treatment for TDP-43-related neurodegeneration, but they do not yet show benefit in people.
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High Resolution Image Download MS PowerPoint Slide Abnormal accumulation of tau fibrillar aggregates is a hallmark of tauopathies, including Alzheimer’s disease.
Why it matters
In laboratory experiments, a cinnamon bud extract and cinnamaldehyde inhibited tau aggregate maturation, promoted nonfibrillar off-pathway species and produced aggregates with reduced cytotoxicity and lower seeding capacity. These are in vitro findings, so no conclusion can be drawn about treating or preventing Alzheimer's disease in people.
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38/100
Our data suggests that microglial reactivity may play a role in hippocampal atrophy; potentially contributing to the increasingly recognized interaction between vascular and neurodegenerative pathology.
Why it matters
In 77 patients with cerebral small vessel disease, greater baseline microglial reactivity was associated with hippocampal atrophy over one year but not with global brain atrophy, and there were no significant associations with cognitive impairment. Blood-brain barrier permeability was not associated with atrophy or cognitive impairment, and the authors suggest microglial reactivity may play a role in hippocampal atrophy.
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38/100
Alcohol use disorder (AUD) is linked with changes in brain structure and function, with robust evidence for neurodegenerative changes, including synaptic loss in preclinical models.
Why it matters
This is the first in vivo evidence linking synaptic density to alcohol use, showing that alcohol use disorder and alcohol consumption are associated with lower SV2A expression. The authors say this may guide future research into relapse and dementia risk in people with alcohol use disorder, but no treatment or prevention is tested here.
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Fifteen cases were identified, spanning argyrophilic grain disease, primary age-related tauopathy, corticobasal degeneration, genetic frontotemporal dementia, and progressive supranuclear palsy.
Why it matters
In this brain bank series of 15 cases, only 47% showed agreement between clinical and pathological diagnosis, showing how hard these diseases are to diagnose in life. The study provides tissue and clinical data for research, but does not test any treatment, cure or prevention.
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APP‐mediated signaling plays a key role in regulating sleep, maintaining BBB integrity, and preserving memory in AD.
Why it matters
In Alzheimer's disease mouse models, expressing a membrane-tethered APP intracellular domain rescued sleep and cognitive impairments, prevented blood-brain barrier leakage, and promoted astrocyte redistribution. This is an animal study showing that APP-mediated signaling plays a role in sleep, blood-brain barrier integrity and memory, but it does not establish a treatment for people.
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Progressive aggregation of TAR DNA-binding protein 43 (TDP-43) is a hallmark of numerous neurodegenerative diseases, including amyotrophic lateral sclerosis, frontotemporal dementia, Alzheimer's disease, and limbic predominant age-related TDP-43 encephalopathy (LATE).
Why it matters
This laboratory study found that lipid bilayers containing anionic phosphatidylserine and cardiolipin accelerated TDP-43 aggregation, and that TDP-43 fibrils damaged cell endosomes, impaired autophagy and triggered an unfolded protein response in rat dopaminergic cells. These are in-vitro findings and no treatment, cure or prevention for Alzheimer's disease is tested.
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38/100
Primary and secondary tauopathies are major causes of dementia characterized by the abnormal accumulation of microtubule-associated protein tau.
Why it matters
This review describes emerging evidence that tau accumulation and glial-driven inflammation promote the activation and recruitment of effector T cells into the tauopathy brain. It suggests that blocking or reshaping T cell responses shows promise for reducing neurodegeneration, but this is a review of early evidence, not a tested treatment.
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Median serum levels of tau variants were increased in patients with multiple traumatic injuries at day 0 compared with controls (t-tau: 43 [IQR, 21-95] vs 3 [IQR, 3-5] pg/mL; BD-tau: 78 [IQR, 30-343] vs 2 [IQR, 2-3] pg/mL; p-tau231: 61 [IQR, 21-79] vs 2 [IQR, 1-3] pg/mL; all, P < .001).
Why it matters
In 214 serum samples, levels of tau variants (t-tau, BD-tau and p-tau231) were much higher on the day of injury in patients with multiple traumatic injuries than in controls. This study is about trauma, not Alzheimer's disease, and it does not test any treatment, prevention or cure for Alzheimer's disease.
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Neuronal cytoplasmic aggregation and nuclear depletion of the TAR DNA-binding protein 43 (TDP-43) is the most characteristic pathology of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), causing toxicity through cytoplasmic gain and nuclear loss of function mechanisms.
Why it matters
The small molecule JRMS reduced TDP-43 aggregation and promoted its nuclear localization in cell lines, neurons, brain slices, and an in vivo model. These findings identify JRMS as a promising therapeutic strategy, but it has not yet been tested in humans.
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Participants were 68.7±9.3 years old; 70% were female; 8% identified as Black, 89% White, as 3% other racial group; and 14% identified as Hispanic.
Why it matters
This study found that higher inflammation was linked to more white matter hyperintensities, and more neighborhood tree canopy was linked to fewer, with tree canopy appearing to offset some of the effect of inflammation. It is cross-sectional and does not test a treatment, cure, or prevention.
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In DS, PSMD changed approximately 10‐15 years before the onset of AD symptoms and linearly increased with AD clinical stages, AD pathology, and SVD metrics.
Why it matters
This cross-sectional study found that a diffusion imaging marker of white matter damage increased along the Alzheimer's continuum in people with Down syndrome and changed about 10-15 years before symptoms. It suggests the marker may help detect early white matter changes, but it does not test any treatment, cure or prevention.
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The assay demonstrated robust quantification of BD-Tau in CSF, plasma, and serum with measured concentrations ranging from 3 to 20 pg/mL across 15 paired plasma and serum samples.
Why it matters
This study describes the analytical qualification of the BD-Tau Xplorer kit on an automated platform, showing accurate and reproducible measurement of BD-Tau in cerebrospinal fluid, plasma and serum, with an exploratory assessment showing better discrimination of Alzheimer's disease versus controls than a comparison assay. The authors state that further validation in larger and more differentiated cohorts is needed before its value as a marker for prognosis and monitoring can be established, and no treatment or cure is reported.
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.
- Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment
- Tannic acid is a natural β-secretase inhibitor that prevents cognitive impairment and mitigates Alzheimer-like pathology in transgenic mice
- Synaptic Activity Regulates Interstitial Fluid Amyloid-β Levels In Vivo
- Promoting Sleep Oscillations and Their Functional Coupling by Transcranial Stimulation Enhances Memory Consolidation in Mild Cognitive Impairment
- The peripheral benzodiazepine receptor (Translocator protein 18kDa) in microglia: from pathology to imaging
- Abeta species removal after abeta42 immunization
- Microglia at sites of atrophy restrict the progression of retinal degeneration via galectin-3 and Trem2
- ADF/Cofilin-actin rods in neurodegenerative diseases
- Effect of Dextromethorphan-Quinidine on Agitation in Patients With Alzheimer Disease Dementia: A Randomized Clinical Trial
- External Validation of Joint Propagation Model‐Based Tau PET CenTauR units