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.
-
Spatial transcriptomics (ST) represents a revolutionary approach in molecular biology, providing unprecedented insights into the spatial organization of gene expression within tissues.
Why it matters
This review describes spatial transcriptomics technologies and computational tools, including their use in studying neuronal vulnerability in Alzheimer's disease. It is a methods review and does not report any treatment, cure, or prevention findings.
-
We observed that mice lacking IR in GFAP astrocytes (GFAP IR KO mice) develop mood disturbances and maintained intact cognition, while at the same time show greater pathology when cross-bred with APP/PS1 mice, a model of familial Alzheimer´s disease (AD).
Why it matters
Mice lacking insulin or IGF-I receptors in astrocytes showed different patterns of mood, cognition, and Alzheimer-like pathology. This is animal work showing cell-specific and context-dependent roles, and it does not provide a treatment, cure, or prevention for Alzheimer's disease.
-
Tau pathology is a major age-related event in Down syndrome with Alzheimer’s disease (DS-AD).
Why it matters
This study examined how two tau PET tracers and one amyloid ligand bind in post-mortem brain tissue from adults with Down syndrome and Alzheimer's disease. It assesses tracer binding properties for biomarker development and does not test any treatment, cure or prevention.
-
34/100
Proinflammatory cytokine macrophage migration inhibitory factor (MIF) is a multifunctional cytokine and has been found involved in many neurological diseases such as Alzheimer disease (AD), epilepsy, and multiple sclerosis.
Why it matters
This study describes where and when the protein MIF appears in the developing mouse hippocampus and how blocking it affects cell growth in the lab. It is early animal and cell work and does not test any treatment, cure, or prevention in people.
-
Besides the typical cognitive decline, patients with Alzheimer's disease (AD) develop disorders of the respiratory system, such as sleep apnea, shortness of breath, and arrhythmias.
Why it matters
Rats given streptozotocin into the brain, a model of Alzheimer-like changes, were studied for their breathing responses to high carbon dioxide and low oxygen while awake and asleep. This is animal research and does not establish any treatment for people.
-
Down syndrome (DS) is the most common genetically defined cause of intellectual disability and accounts for over 50% of the cases of Alzheimer-type dementia in persons younger than 50 years of age.
Why it matters
This review discusses the glutamatergic hypothesis for Down syndrome and the potential use of the NMDA receptor antagonist memantine to improve hippocampus-dependent memory deficits. It describes early preclinical and clinical work and does not establish that memantine treats or prevents Alzheimer's disease.
-
A double blind, placebo-controlled phase II study revealed that the antihistamine, Dimebon® (dimebolin, latrepirdine) improved cognition in Alzheimer disease (AD) patients compared to placebo controls.
Why it matters
In 3xTg-AD mice, dimebon reduced hippocampal APP/Aβ by immunohistochemistry but did not change full-length APP, soluble Aβ, oligomers, BACE1 or GFAP, and actually increased the number of APP/Aβ plaques; it also did not alter tau. A phase III trial of dimebon had already failed to show significant differences from placebo, so this does not support dimebon as an effective treatment.
-
Detection of cerebrospinal fluid (CSF) biomarker deviations improve prediction of progression from mild cognitive impairment (MCI) to dementia.
Why it matters
This study followed patients with mild cognitive impairment for 24 months and found that progression from very mild to more pronounced MCI was not associated with deviations in spinal fluid biomarkers. The authors had expected to find such deviations, but the results did not support that expectation.
-
BACE2 is homologous to BACE1, a beta-secretase that is involved in the amyloidogenic pathway of amyloid precursor protein (APP), and maps to the Down syndrome critical region of chromosome 21.
Why it matters
In a transgenic mouse model, BACE2 overexpression was not involved in the amyloidogenic pathway, cognitive dysfunction, or cholinergic degeneration, though the mice showed increased anxiety-like behaviour. These are animal results and do not support BACE2 as a target for treating or preventing Alzheimer's disease.
-
We investigated a possible role in Alzheimer's disease (AD) for FKBP12, a peptidyl-prolyl cis-trans isomerase known to be important in protein assembly, folding and transportation by using Western blotting and microscopic analyses in postmortem brain tissues from elderly controls and the patients with AD.
Why it matters
The protein FKBP12 was found in neurofibrillary tangles and other tau-related structures in Alzheimer disease brains, and its overall expression was lower than in controls. This suggests FKBP12 may be involved in tau metabolism, but the study was done on postmortem tissue and did not test any treatment.
-
S100beta is a soluble protein released by glial cells mainly under the activation of the 5-HT1A receptor.
Why it matters
This animal and mouse study found daily rhythms in S100beta protein expression that differed between males and females. It concerns a biomarker of brain damage and raises questions about these rhythms, with no direct implications for treating, curing, or preventing Alzheimer's disease.
-
YKL-39 is a Glyco_18 domain containing chitinase-like protein which is currently recognized as a biomarker for the activation of chondrocytes and the progress of the osteoarthritis in human.
Why it matters
This laboratory study examined how TGF-beta and IL-4 stimulate expression of the osteoarthritis marker YKL-39 in differentiating macrophages. It is about osteoarthritis biology, not Alzheimer's disease, so it has no direct implications for treating, curing or preventing Alzheimer's.
-
Cerebrospinal fluid (CSF) total Tau levels vary widely in neurodegenerative disorders, thus being not useful in their discrimination over Alzheimer disease.
Why it matters
This study found that the ratio of truncated to extended tau forms in cerebrospinal fluid was significantly decreased in people with progressive supranuclear palsy compared with controls and people with Alzheimer's disease. It suggests a possible marker to distinguish progressive supranuclear palsy, but it does not test a treatment, cure, or prevention for Alzheimer's disease.
-
The objective of this study was to investigate the levels of tau protein in neurosyphilis.
Why it matters
This study found that total tau protein in spinal fluid was increased in people with neurosyphilis, similar to people with Alzheimer's disease. It is a small study about diagnosis and does not test any treatment for Alzheimer's.
-
Down syndrome (DS) patients suffer from mental retardation, but also display enhanced beta-APP production and develop cortical amyloid plaques at an early age.
Why it matters
In brain tissue from adults with Down syndrome and in cells from people with Down syndrome, the Notch pathway was more active, and the study found that the proteins APP and Notch1 can interact and affect each other's target genes. This is laboratory work on tissue and cells, so it does not show whether targeting Notch would treat or prevent Alzheimer's disease.
-
Hyperphosphorylated microtubule-associated protein tau is the major protein component of neurofibrillary tangles in the brain of patients with Alzheimer's disease (AD).
Why it matters
In rats, melatonin was tested for its ability to prevent tau hyperphosphorylation induced by isoproterenol. This is an animal study of a prevention approach, and the text states there is currently no effective cure to arrest this hyperphosphorylation.
-
Aceruloplasminemia is an interesting disease, the study of which helps elucidate how iron-induced oxidative stress is involved in neuronal cell death.
Why it matters
In five patients with aceruloplasminemia, a disease of iron overload, deformed astrocytes and globular structures were found in the brain and linked to iron deposition and oxidative stress. This is a study of a rare iron metabolism disorder, not Alzheimer's disease, so it does not directly inform Alzheimer's treatment or prevention.
-
Early-onset cataract and Alzheimer's disease occur with high frequency in Down syndrome (trisomy 21), the most common chromosome duplication in human live births.
Why it matters
Mice carrying a complete copy of the wild-type human amyloid precursor protein gene showed fiber cell membrane defects in the lens and increased age-related lens degeneration. The authors suggest this supports a link between Alzheimer pathophysiology and cataract formation, but this is an animal study and does not test a treatment or cure for Alzheimer's disease.
-
Frequency of two mutations associated with ASA pseudodeficiency in the Croatian population is slightly below the range reported for other populations.
Why it matters
Frequencies of two arylsulfatase A pseudodeficiency mutations were estimated in healthy Croatian subjects and in people with Alzheimer-type dementia and Down syndrome, and arylsulfatase A activity was slightly but not significantly decreased in the dementia and Down syndrome groups. The study reports no significant effect and no treatment, cure or prevention.
-
34/100
Down syndrome (trisomy 21) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration.
Why it matters
This review discusses how developmental brain abnormalities in Down syndrome, together with aberrant expression of genes on chromosome 21 including APP, SOD1, and S100 beta, may predispose certain brain regions and nerve cell types to age-dependent Alzheimer-type neurodegeneration. It presents a model involving cholinergic, serotonergic, and catecholaminergic transmission shifting toward a pro-apoptotic state, but offers no treatment or prevention.
-
Forced overexpression of wild-type Alzheimer amyloid precursor protein (APP) causes postmitotic neurons to degenerate.
Why it matters
In cultured human postmitotic neurons, overexpression of wild-type amyloid precursor protein activated caspase-3 and caused degeneration. This was a cell study, so it does not show that blocking caspase-3 would treat or prevent Alzheimer's disease in people.
-
The decrease in the number of neurons free of neurofibrillary changes, neurons with neurofibrillary degeneration, and the total volume of beta-amyloid (A beta) deposits in the amygdala of people with Down syndrome and in late stages of Alzheimer disease were estimated by using morphometry and regression analysis.
Why it matters
This brain tissue study found that loss of neurons was linked to decreased beta-amyloid deposits in the amygdala and that amyloid could disappear about 2.2 years after neuron loss, suggesting the brain can clear amyloid. This is laboratory work on tissue and does not show a treatment or cure.
-
In Down syndrome (DS), enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration of Alzheimer-type.
Why it matters
In brain tissue from 9 adults with Down syndrome and Alzheimer-like lesions, 9 with Alzheimer disease and 9 controls, NAIP-like immunoreactivity was significantly decreased in some cortical regions in the Down syndrome and Alzheimer disease groups. The authors state the mode of NAIP action is unknown, and this is tissue research, not a treatment or cure.
-
Human carbonyl reductase (CBR) belongs to a group of NADPH-dependent enzymes called aldo-keto reductases.
Why it matters
This laboratory study mapped the carbonyl reductase gene near the SOD1 gene on chromosome 21 and found it was overactive in cells with trisomy 21, which could affect free radicals. The authors suggest this gene is a candidate for contributing to Down syndrome and Alzheimer's disease pathology, but this is a cell-based finding with no direct treatment implication.
-
To investigate the roles imposed on astrocytes for glutamate metabolism, a specific inhibitor of glutamine synthetase (GS), methionine sulfoximine (MSO), was repeatedly administered to rats and histopathological changes were correlated with glycogen accumulation and the immunocytochemistry of GS and glial fibrillary acidic protein (GFAP).
Why it matters
In rats, repeated doses of a chemical that blocks glutamine synthetase caused astrocytes to swell and glycogen to build up in certain brain regions, along with changes in GS and GFAP. This is an animal study from 1989 and does not test any treatment, cure or prevention of Alzheimer's disease in people.
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.
- Soluble TAM receptors sAXL and sTyro3 predict structural and functional protection in Alzheimer's disease
- Neuropathological analysis of pathological forms of astroglia in Wilson's disease
- Bayesian Genome-wide TWAS Method to Leverage both cis- and trans-eQTL Information through Summary Statistics
- Clinical, imaging and blood biomarker outcomes in a Phase 3 clinical trial of tau aggregation inhibitor hydromethylthionine mesylate in mild cognitive impairment and mild to moderate dementia due to Alzheimer's disease
- Cerebrospinal fluid soluble TREM2 in aging and Alzheimer's disease
- CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease
- Aperiodic EEG signatures: unveiling the interplay between APOE ε4 and mild cognitive impairment subtypes
- Gut Microbiota Composition Is Related to AD Pathology
- P3‐402: Detection of PCC functional connectivity characteristics in subcortical vascular mild cognitive impairment: A resting‐state fMRI study
- Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner