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 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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We have investigated the extent and pattern of immunostaining for the TAR DNA-binding protein, TDP-43, in 37 patients with frontotemporal lobar degeneration with ubiquitin (UBQ) pathology (FTLD-U).
Why it matters
In brain tissue from 37 people with frontotemporal lobar degeneration with ubiquitin pathology (FTLD-U), this study confirmed that the protein TDP-43 is part of the abnormal inclusions in the cortex and hippocampus, and that the three inclusion patterns the authors had earlier described with ubiquitin staining look the same with TDP-43 staining. Similar TDP-43 inclusions were seen in motor neurones of a few patients with FTD or FTD plus motor neurone disease, and were common in spinal cord motor neurones in motor neurone disease alone. The study describes tissue findings in FTLD and MND, not Alzheimer's disease, and reports no test, treatment or prevention.
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20 (45%) patients developed a neurological disorder after a mean of 11.5 years from the reported onset of RBD and a mean follow-up of 5.1 years from the diagnosis of idiopathic RBD at our sleep centre.
Why it matters
Among 44 patients diagnosed with idiopathic REM sleep behaviour disorder, 20 (45%) later developed a neurological disorder such as Parkinson's disease, dementia with Lewy bodies or mild cognitive impairment. This suggests RBD can appear before these disorders, which may help identify people early, but it does not show how to treat, cure or prevent them.
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Frontotemporal lobar degeneration, corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP) have overlapping clinical features.
Why it matters
In 127 autopsy-confirmed cases of frontotemporal lobar degeneration, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD), the clinical pictures overlapped. Some presentations still pointed to the underlying disease: every PSP-like or CBD-like case had tau-positive pathology, and every case of frontotemporal dementia with motor neuron disease was tau-negative with motor neuron degeneration. Frontal-variant FTD was split almost evenly between tau-positive and tau-negative disease, and PSP or CBD accounted for almost 70% of the 13 progressive non-fluent aphasia cases. This is a retrospective autopsy series about diagnosis, not treatment.
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These cross-sectional data provide evidence that tHcy is a risk factor for white matter damage.
Why it matters
In 259 people from a community study in northern Manhattan, those with higher blood homocysteine had more white matter damage on brain scans (a scan finding the authors note "may be a risk factor" for both stroke and dementia). The link held after accounting for sociodemographics and vascular risk factors. The authors call homocysteine "a risk factor for white matter damage", but this was a single snapshot, so it cannot show cause and effect, and it did not measure dementia or test any treatment.
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Arterial stiffness is a growing epidemic associated with increased risk of cardiovascular events, dementia, and death.
Why it matters
Arterial stiffness is described as a growing condition linked to increased risk of cardiovascular events, dementia, and death. The review discusses lifestyle changes and therapies that reduce arterial stiffness, which might help lower these risks.
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The epsilon4 allele of APOE is a risk factor for Alzheimer disease (AD).
Why it matters
In a large group of Alzheimer patients and controls, carrying the APOE epsilon4 allele was strongly linked to lower CSF levels of amyloid-beta42. This suggests APOE may be involved in how amyloid-beta is handled, but it does not show that measuring or changing this alters disease.
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Deterioration in Alzheimer disease appears to be driven by neuritic plaques and neurofibrillary tangles at different stages of the disease.
Why it matters
In this autopsy series, neuritic plaques were found in all patients with Alzheimer's disease and distinguished normal controls from mild cases, while tangles increased with dementia severity. It examines brain pathology and its relation to disease stage, not any treatment or cure.
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In a previous study of normal elderly male twins, the heritability of quantitative white matter hyperintensity (WMH) volume has been estimated to be high (0.73).
Why it matters
This study estimated how much of the variation in white matter hyperintensity volume on brain scans is inherited, using a family-based sample. It is about genetic influence on a brain scan marker, not about treating, curing or preventing Alzheimer's disease.
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Type 2 diabetes is associated with hippocampal and amygdalar atrophy, regardless of vascular pathology.
Why it matters
In 506 adults aged 60–90 without dementia, people with type 2 diabetes had more shrinkage of the hippocampus and amygdala on MRI. This was not explained by worse carotid atherosclerosis, white matter lesions or brain infarcts. Among people without diabetes, higher insulin resistance went with more amygdala shrinkage. The authors say this "could suggest" diabetes directly affects Alzheimer-type brain changes, but the study measured MRI atrophy, not Alzheimer pathology or dementia, and it shows an association, not cause and effect.
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Inflammation in Alzheimer's disease (AD) patients is characterized by increased cytokines and activated microglia.
Why it matters
In an Alzheimer mouse model, dietary curcumin reduced oxidized proteins, an inflammatory cytokine and, at low dose, amyloid plaque burden. This is early animal work and does not show that curcumin treats or prevents Alzheimer's disease in people.
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Temporal pole hyperintensity is a radiologic marker of CADASIL.
Why it matters
This study found that MRI hyperintensities in the temporal white matter and external capsule-insula region were significantly higher in patients with CADASIL than in patients with sporadic leukoaraiosis. It concerns an inherited small vessel disease and reports nothing about treating, curing or preventing Alzheimer's disease.
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The defining neuropathological characteristics of Alzheimer's disease are abundant filamentous tau lesions and deposits of fibrillar amyloid beta peptides.
Why it matters
This 2001 review groups corticobasal degeneration, progressive supranuclear palsy, Pick's disease and the inherited FTDP-17 as "neurodegenerative tauopathies", diseases with tau tangles but no amyloid deposits, and argues that tau gene mutations in FTDP-17 and tau risk variants in PSP and CBD tie tau abnormalities "directly to the etiology and pathogenesis" of these diseases. It notes that relatives sharing an FTDP-17 mutation "often exhibit diverse" syndromes, which suggests other genetic or epigenetic factors also shape the illness, and it says the proposed mechanisms "remain to be tested and validated." It is a review with no new patient data. It does not show that tau causes Alzheimer's disease, and it reports no treatment.
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Tau proteins belong to the family of microtubule-associated proteins.
Why it matters
This 2000 review explains that tau, a protein that helps build the microtubule "tracks" inside nerve cells, comes from one gene on chromosome 17 in six adult-brain forms, and that it is the main component of the tangles found in Alzheimer's disease and other "tauopathies". The authors suggest that abnormal phosphorylation "might be" a key step in tau clumping, that each tauopathy may have its own pattern of tau forms and brain distribution, and they report that the spread of tau lesions through the neocortex tracks the severity of dementia. These are descriptions of brain pathology and associations, not evidence about any test, treatment or way to prevent the disease.
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Patients with anti-Ta (also called anti-Ma2) antibodies were young men with testicular tumours (100%), frequent hypothalamic involvement (70%) and a poor neurological outcome.
Why it matters
This study describes neurological symptoms, immunological findings and tumour associations in 50 patients with paraneoplastic limbic encephalitis, a condition related to cancer. It is not about Alzheimer's disease and reports no treatment, cure or prevention for it.
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The amyloid precursor protein (APP) plays a crucial role in the pathogenesis of Alzheimer's disease.
Why it matters
Reducing the cholesterol level of living hippocampal neurons by 70% completely inhibited the formation of amyloid-β, without affecting a non-amyloid form of the precursor protein, and this was fully reversible by adding cholesterol back. The authors say cholesterol is required for amyloid-β formation, implying a link between cholesterol, amyloid-β and Alzheimer's disease.
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The pathogenesis of human immunodeficiency virus (HIV)-associated dementia is unclear, and the underlying pathological substrate has been a matter of debate.
Why it matters
This study of brain tissue from 51 AIDS patients examined the link between HIV-associated dementia and markers for HIV-1, macrophages and microglia. It concerns HIV-associated dementia, not Alzheimer's disease, and reports no treatment, cure or prevention for Alzheimer's.
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Trisomy 21 or Down syndrome (DS) is the most frequent genetic cause of mental retardation, affecting one in 800 live born human beings.
Why it matters
In mice carrying extra copies of genes that correspond to part of human chromosome 21 (21q21-22.3, including the Down syndrome "critical region"), the Ts65Dn model, animals performed worse on "a complex learning task requiring the integration of visual and spatial information". The authors say the reproducibility of this deficit indicates that extra dosage of "a gene or genes in this region" contributes, and that the human versions "may contribute to cognitive deficits in DS". These mice "do not show early-onset of Alzheimer disease pathology", so this is a Down syndrome learning model, not an Alzheimer's model, and it reports no treatment.
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Normal processing of the amyloid beta protein precursor (beta APP) results in secretion of a soluble 4-kilodalton protein essentially identical to the amyloid beta protein (A beta) that forms insoluble fibrillar deposits in Alzheimer's disease.
Why it matters
In cells expressing amyloid precursor protein with APP717 mutations linked to familial Alzheimer's disease, the share of longer amyloid beta (such as Aβ1-42) rose 1.5- to 1.9-fold. The authors suggest these mutations may cause Alzheimer's by increasing long amyloid beta, which forms fibrils more rapidly.
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Gerstmann-Sträussler syndrome is a rare familial neurodegenerative condition that is vertically transmitted, in an apparently autosomal dominant way.
Why it matters
This study linked a variant in the prion protein gene to Gerstmann-Sträussler syndrome, a rare inherited neurodegenerative condition. It concerns the genetics of that syndrome, not the treatment, cure, or prevention of Alzheimer's disease.
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54/100
When cases of senile dementia were compared to controls (matched with respect to the cause of death) the activity of CAT (the potential index of cholinergic neurons) appears to be reduced in the cerebral cortex.
Why it matters
This study found reduced activity of a cholinergic enzyme in the cerebral cortex of people with senile dementia compared to controls. It is an early observational study and does not provide information on treating, curing, or preventing Alzheimer's disease.
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Late-onset unexplained epilepsy (LOUE) represents a substantial proportion of epilepsies with onset after 50 years and often manifests as temporal lobe epilepsy (LO-TLE).
Why it matters
This Italian cross-sectional cohort study compared the cognitive and cerebrospinal fluid profile of patients with late-onset temporal lobe epilepsy with healthy controls and patients with mild cognitive impairment due to Alzheimer's disease, finding that only a subset showed Alzheimer's-related biomarkers. It points to biological heterogeneity and non-Alzheimer mechanisms, with no treatment, cure, or prevention tested.
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Amyloid-related imaging abnormalities (ARIA) are the principal safety concern limiting anti-amyloid therapies for Alzheimer's disease, yet their biology remains unclear.
Why it matters
This small case-control study of three patients with amyloid-related imaging abnormalities (ARIA) found that ARIA was associated with coordinated reprogramming of CD8+ T cells. The authors say these findings identify a peripheral immune signature with implications for biomarker development and risk mitigation, pending validation in larger cohorts.
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Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau.
Why it matters
This longitudinal study found that modifiable risk factors such as higher blood pressure, hyperlipidemia, ischemic heart disease, smoking and lower education were linked to increasing white matter hyperintensities, while the APOE ε4 allele was linked to faster amyloid-β and tau accumulation. It suggests that modifiable risks for future dementia mainly affect vascular brain pathology, though lower BMI was tied to tau and diabetes to amyloid-β.
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Of 293 participants screened, 130 were randomized, and 109 (83.8%) completed the study.
Why it matters
In this phase 2 trial, 130 participants with mild-to-moderate dementia with Lewy bodies were randomized, and zervimesine was found to be safe and well tolerated, with favorable trends on exploratory endpoints. The authors state these results provide a rationale for testing zervimesine in larger studies, so efficacy for treating the disease is not yet established.
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53/100
Diagnosing Alzheimer's disease (AD) in adults with Down syndrome (DS), a population with a high genetically determined risk of AD, remains challenging.
Why it matters
In 2329 samples from people with Down syndrome and controls, plasma p-tau217 detected amyloid positivity and predicted clinical progression with high accuracy. This is an observational diagnostic study and does not test any treatment, cure, or prevention.
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.
- TREM2 Insufficiency Protects against Pulmonary Fibrosis by Inhibiting M2 Macrophage Polarization
- Low cerebral blood flow is associated with lower memory function in metabolic syndrome
- {gamma}-Secretase Substrate Concentration Modulates the Abeta42/Abeta40 Ratio: IMPLICATIONS FOR ALZHEIMER DISEASE
- Gut microbiome, cognitive function and brain structure: a multi-omics integration analysis
- Limbic-predominant age-related TDP-43 encephalopathy in the oldest old: a population-based study
- Porphyromonas gingivalis disrupts hippocampal circadian clock via PI3K/AKT pathway, exacerbating Alzheimer‐like pathology
- Transmission and spreading of tauopathy in transgenic mouse brain
- Astrocytosis and axonal proliferation in the hippocampus of S100b transgenic mice
- Expression of the amyloid precursor protein gene in mouse oocytes and embryos
- The Hidden Global Health Crisis of Omega-3 Deficiency