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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Insomnia in cognitively unimpaired adults at increased risk for AD is associated to poorer performance in some executive functions and volume changes in cortical and subcortical gray matter, including key areas involved in Alzheimer's disease, as well as decreased white matter diffusivity.
Why it matters
In cognitively unimpaired adults at increased Alzheimer risk, insomnia was linked to poorer performance on some executive tasks and to gray and white matter differences. This is a cross-sectional association and does not show that treating insomnia prevents Alzheimer disease.
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Changes in the properties of DTI may be the potential mechanism of WMH-related MCI, especially the right IFOF and the right ILF, which may become imaging markers for predicting WMH-related cognitive dysfunction.
Why it matters
This study found that damage to certain white matter tracts was linked to cognitive impairment in people with white matter hyperintensities, and a machine learning model recognised this with about 80% accuracy. It is about imaging markers of small vessel disease and does not test any treatment, cure or prevention.
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Immune cells residing in white adipose tissue have been highlighted as important factors contributing to the pathogenesis of metabolic diseases, but the molecular regulators that drive adipose tissue immune cell remodeling during obesity remain largely unknown.
Why it matters
This study describes a Trem2+ lipid-associated macrophage subset in fat tissue of mice and humans during obesity. It concerns metabolic disease and does not test any treatment, cure or prevention for Alzheimer's disease.
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD).
Why it matters
This genetic study found that a variant in the PLCG2 gene is linked to lower risk of Alzheimer's disease, dementia with Lewy bodies and frontotemporal dementia, and to longer life. It identifies a possible biological pathway but does not provide a treatment or cure.
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Patients with Alzheimer's Disease (AD) exhibit decreased retinal blood flow and vessel density (VD).
Why it matters
This small case-control study used eye scans to look for retinal blood vessel changes in people with early Alzheimer's disease or mild cognitive impairment. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Rare coding variants in TREM2, PLCG2, and ABI3 were recently associated with the susceptibility to Alzheimer's disease (AD) in Caucasians.
Why it matters
In 419 people with Alzheimer's and 486 controls from Argentina, rare variants in TREM2, PLCG2 and ABI3 showed frequencies and risk estimates similar to earlier European reports, and were significantly linked to Alzheimer's when combined with European data. Carriers mostly had Caucasian ancestry. The authors conclude these variants also influence risk in Argentina and may have a European origin.
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The ordered assembly of tau protein into abnormal filamentous inclusions underlies many human neurodegenerative diseases 1 .
Why it matters
Using electron cryo-microscopy on brain tissue from people with Pick's disease, a form of frontotemporal dementia, this study found that the tau filaments are built from 3R tau (residues Lys254–Phe378) folded differently from the tau filaments in Alzheimer's disease. The authors say this establishes that tau can take distinct, disease-specific folds in the human brain, a step toward understanding how these clumps form and spread. It is a structural study and does not test any treatment or diagnostic.
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61/100
Our results indicate that APOE ε4 is independently associated with a greater severity of LB pathology.
Why it matters
In this autopsy study, APOE ε4 was associated with greater severity of Lewy body pathology independently of Alzheimer disease pathology. It describes a risk relationship and does not provide a treatment, cure or prevention.
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61/100
Cerebrospinal fluid (CSF) core Alzheimer disease (AD) biomarkers have shown an excellent capacity for the in vivo detection of AD.
Why it matters
This study developed a two-step cerebrospinal fluid algorithm to help tell apart different subtypes of frontotemporal lobar degeneration by first ruling out Alzheimer's disease pathology. It is a diagnostic tool study and does not offer a treatment, cure, or prevention for Alzheimer's disease.
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From the population-based Rotterdam Study, 4,447 participants underwent dietary assessment and brain MRI scanning between 2005 and 2015.
Why it matters
This study found that better diet quality was related to larger brain tissue volumes in dementia-free older adults. It does not show that improving diet prevents dementia, and the findings are from an observational study of brain structure.
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The cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43) is a common histopathological hallmark of the amyotrophic lateral sclerosis and frontotemporal dementia disease spectrum (ALS/FTD).
Why it matters
TDP-43 aggregates were found to be enriched for nuclear pore and transport components, and mutant TDP-43 interfered with nuclear import and RNA export in neurons and patient-derived cells. This is laboratory and tissue work implicating transport defects in ALS/FTD, with no treatment tested.
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YKL-40 (also known as Chitinase 3-like 1) is a glycoprotein produced by inflammatory, cancer and stem cells.
Why it matters
This study analysed levels of the protein YKL-40 in brain and cerebrospinal fluid from people with different neurodegenerative dementias associated with inflammation. It is a characterization study and does not report a treatment, cure, or prevention for Alzheimer's disease.
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At 6 mo, the n-3 FA group displayed marked increases in DHA and EPA plasma concentrations (2.6- and 3.5-fold), as well as decreased methylation in 2 out of 4 CpG sites ( P r = -0.25, P = 0.045; and r = -0.26, P = 0.041, respectively), but not to changes in plasma DHA concentration, and were not related to apolipoprotein E-4 allele frequency.
Why it matters
This study looked at blood markers, not at memory or thinking, in patients taking omega-3 fatty acids. It found changes in DNA methylation in blood cells, which does not show any benefit for treating, curing, or preventing Alzheimer's disease.
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The combination of sAPPβ with YKL-40 and with NfL in CSF could be useful to increase the certainty of the diagnosis of FTLD-related syndromes in clinical practice.
Why it matters
In this cross-sectional study, people with frontotemporal lobar degeneration-related syndromes had lower CSF sAPPβ than controls and people with Alzheimer's disease, while NfL and YKL-40 were high in both disease groups. These are biomarker differences for diagnosis, not evidence of a treatment, cure, or prevention.
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Amyotrophic lateral sclerosis (ALS) is a rapidly progressing neurodegenerative disease that is characterized by motor neuron loss and that leads to paralysis and death 2-5 years after disease onset.
Why it matters
In TDP-43 transgenic mice, lowering ataxin-2 by genetic knockout or by antisense oligonucleotides reduced TDP-43 aggregation, improved motor function and markedly extended survival. This is animal work and does not yet show that the approach helps people with ALS or frontotemporal dementia.
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Our data reveal an association of APOE ε3/3- TOMM40 '523 haplotypes with cognitive decline in community-based older persons such that the S/S poly-T genotype is related to faster cognitive decline, primarily in the domains of episodic and semantic memory.
Why it matters
Among older people with the APOE ε3/3 genotype, a particular TOMM40 variant was associated with faster decline in global cognition and episodic memory. This is an observational finding about genetic risk and does not show any treatment or prevention.
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Neuronal intranuclear inclusion disease (NIID) is a slowly progressive neurodegenerative disease characterized by eosinophilic hyaline intranuclear inclusions in the central and peripheral nervous system, and also in the visceral organs.
Why it matters
This study describes 57 cases of adult-onset neuronal intranuclear inclusion disease, a neurodegenerative disease that can present with dementia, and suggests it may be more common and underdiagnosed than previously thought. It is about diagnosis and recognition of this condition, not about treating, curing, or preventing Alzheimer's disease.
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Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain.
Why it matters
In this first NINDS/NIBIB consensus panel, 7 neuropathologists used preliminary criteria to blindly review 25 brains with different tau diseases, including CTE and Alzheimer's, and agreed well (Cohen's kappa 0.67; 0.78 against the CTE diagnosis). The panel defined CTE's tell-tale lesion as abnormal tau in nerve and support cells clustered around small blood vessels deep in the brain's folds, and set a minimum tissue-sampling and staining scheme. The criteria apply only to brain tissue examined after death, are described as a "first step" toward validated criteria, and say nothing about treating or preventing Alzheimer's disease.
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Researchers developed an adeno-associated virus-based model to study tau propagation from the entorhinal cortex to the dentate gyrus.
Why it matters
Reports that depleting microglia and inhibiting exosome synthesis halted the spread of tau.
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T2DM may promote neurodegeneration independent of AD dementia diagnosis, and its effect may be driven by tau phosphorylation.
Why it matters
In this cross-sectional sample, type 2 diabetes was associated with thinner frontal and parietal cortex and higher CSF tau, but not with amyloid on PET or CSF amyloid levels. The study cannot establish cause and effect, and it does not show that treating diabetes prevents or cures Alzheimer's.
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The conservation of sleep across all animal species suggests that sleep serves a vital function.
Why it matters
In live mice, natural sleep or anesthesia was associated with a 60% increase in the space between brain cells, which increased the exchange of brain fluids and the rate of beta-amyloid clearance during sleep. The authors suggest the restorative function of sleep may come from enhanced removal of potentially neurotoxic waste that builds up while awake.
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Human apolipoprotein E has three isoforms: APOE2, APOE3 and APOE4.
Why it matters
In mice, the Alzheimer's risk gene form APOE4, or having no APOE at all, made the brain's blood-vessel barrier leaky through an inflammatory pathway involving a protein called cyclophilin A (CypA) in the cells around small vessels. The APOE2 and APOE3 forms did not do this. The authors report that this vessel damage came before damage to nerve cells, and that APOE3, but not APOE4, switched the pathway off. They suggest CypA as a possible treatment target, but this is animal research with no numbers in our record, and it does not show that blocking CypA helps people with or at risk of Alzheimer's.
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A locus on chromosome 9p21 has been associated with both disorders, and we aimed to identify the causal gene within this region.
Why it matters
In a Flanders-Belgian patient-control group, a genetic marker near C9orf72 was associated with frontotemporal lobar degeneration and ALS, and C9orf72 expression was about half as high in two carriers as in nine controls. This gene-identification work does not provide a treatment or cure.
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In our training set, people with Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies had lower CSF α-synuclein concentrations than patients with Alzheimer's disease and other neurological disorders.
Why it matters
This study found that lower cerebrospinal fluid alpha-synuclein concentrations, as measured by ELISA, separated people with synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy from those with other disorders. It does not test any treatment, cure or prevention for Alzheimer's disease, though it included people with Alzheimer's disease as a comparison group.
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TDP-43 is a predominantly nuclear RNA-binding protein that forms inclusion bodies in frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS).
Why it matters
In human brain tissue, this laboratory study mapped where the protein TDP-43 binds RNA. It found a preference for "long clusters of UG-rich sequences", and in brains from people with frontotemporal lobar degeneration (FTLD) the largest increases in binding were to two noncoding RNAs, MALAT1 and NEAT1. The authors report that TDP-43 binding "influenced alternative splicing" depending on where it bound, and they link the affected genes to neuronal development and neurological disease. The work concerns FTLD and ALS, not Alzheimer's disease, and it tests no treatment, test 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.
- White matter lesions: Spatial heterogeneity, links to risk factors, cognition, genetics, and atrophy
- Modulation of human neural stem cell differentiation in Alzheimer (APP23) transgenic mice by phenserine
- Simultaneous manipulation of multiple brain targets by green tea catechins: a potential neuroprotective strategy for Alzheimer and Parkinson diseases
- Synaptic biomarkers in CSF aid in diagnosis, correlate with cognition and predict progression in MCI and Alzheimer's disease
- Proteomic and functional analyses reveal a mitochondrial dysfunction in P301L tau transgenic mice
- Replacement of brain-resident myeloid cells does not alter cerebral amyloid-β deposition in mouse models of Alzheimer's disease
- Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation
- Blood-based analysis of different tau variants in patients with multiple traumatic injuries
- Apolipoprotein E controls the risk and age at onset of Parkinson disease
- Upregulation of SET expression by BACE1 and its implications in Down syndrome