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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Trans-active response DNA-binding protein-43 (TDP-43) is the major pathological protein in motor neuron disease and TDP-43 pathology has been described in the brains of up to 50% of patients with Alzheimer disease (AD).
Why it matters
Mice expressing cytosolic TDP-43 in the hippocampus showed marked neuronal loss and atrophy, and those with the ΔNLS form survived only to about 24 months regardless of APP/PSEN1 background. This animal model may help researchers study hippocampal sclerosis of aging and TDP-43 pathology seen alongside Alzheimer's disease, but it does not yet offer a treatment.
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Aβ treatment inhibited microglial activity and phagocytosis, but SMOC2 disruption enhanced these functions (p < 0.05).
Why it matters
In this laboratory study, disrupting SMOC2 enhanced microglial activity and phagocytosis while reducing amyloid beta levels, and SMOC2 appears to act through the TGF-β1/NF-κB pathway. These findings offer insight into Alzheimer's mechanisms but are preliminary and do not show a treatment for people.
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Neurogranin levels were significantly reduced in MTLE-HS patients as compared to FLE patients and healthy controls but were not correlated with any of the clinical and cognitive variables.
Why it matters
In this preliminary study of people with focal epilepsy, neurogranin levels were reduced in patients with treatment resistance, suggesting the protein may serve as a biomarker for monitoring seizure activity. The study is about epilepsy, not Alzheimer's disease, and does not test any treatment for Alzheimer's.
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The anterior thalamic nuclei are important for cognition, and memory in particular.
Why it matters
In post-mortem tissue, the anteroventral thalamic nucleus was smaller in people with Down syndrome and had a marked reduction in neurons immunoreactive for calcium-binding proteins. This descriptive brain tissue study does not test any treatment, cure or prevention for Alzheimer's disease.
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The apolipoprotein E4 (APOE4) variant is the strongest genetic risk factor for Alzheimer disease (AD), while the APOE2 allele is protective.
Why it matters
In human induced pluripotent stem cell-derived astrocytes, APOE4 caused dysregulated cholesterol and lipid homeostasis, increased inflammatory signaling, and reduced amyloid-beta uptake, while APOE2 showed opposing effects. These cell-based findings reveal a disease-relevant phenotype for APOE4 astrocytes, but no treatment is tested.
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These results suggest palm11-PrRP31 is a promising agent for the treatment of neurodegenerative disorders.
Why it matters
In APP/PS1 mice, a lipidized prolactin-releasing peptide analog was tested for effects on amyloid plaques and inflammation in the cerebellum. This is an animal study and does not show that the treatment works in people with Alzheimer's disease.
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The average lifespan of individuals with Down syndrome has approximately doubled over the past three decades to 55-60 years.
Why it matters
In this autopsy case of a woman with Down syndrome and Alzheimer-type dementia, amyloid precursor protein immunoreactivity was absent from senile plaques even though amyloid beta was present in plaque cores and diffuse plaques. The authors suggest the timing of these immunoreactive changes may relate to the disease process, but this is a single case and no treatment is tested.
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Our work suggests an anti-inflammatory effect of quercetin in the CA1 hippocampal region of aged triple transgenic Alzheimer's disease mice.
Why it matters
In aged triple transgenic Alzheimer's disease mice, quercetin treatment reduced markers of inflammation and amyloid aggregates in one hippocampal region. This is animal research only and does not show that quercetin treats, cures, or prevents Alzheimer's disease in people.
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The humble success of current therapeutic strategies along with the lack of basic knowledge of the brain disease mechanisms calls for alternatives that benefit patients in the present moment.
Why it matters
This paper discusses deep brain stimulation as a possible strategy to restore brain activity and cognitive function, noting that amyloid and tau-targeted therapies have shown only moderate success. It is a discussion of a potential approach, not a completed trial showing that deep brain stimulation treats or prevents Alzheimer's disease.
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Down syndrome (DS) is an aneuploidy syndrome that is caused by trisomy for human chromosome 21 resulting in a characteristic cognitive and behavioral phenotype, which includes executive functioning and adaptive behavior difficulties possibly due to prefrontal cortex (PFC) deficits.
Why it matters
In 69 young adults with Down syndrome, certain variants of the COMT and DAT1 genes were associated with better performance on executive function tasks. This concerns genetic influences on cognition in Down syndrome, not any treatment, cure or prevention of Alzheimer's disease.
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Isoprostanes are a recently discovered group of prostaglandin isomers.
Why it matters
This review describes isoprostanes as markers of oxidative stress that are increased in several conditions including Alzheimer disease and Down syndrome. Measuring a marker does not treat or prevent the disease, and the paper reports no intervention or outcome.
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Human trisomy 21 is the most frequent live-born human aneuploidy and causes a constellation of disease phenotypes classified as Down syndrome, which include heart defects, myeloproliferative disorder, cognitive disabilities and Alzheimer-type neurodegeneration.
Why it matters
This paper describes how mouse chromosome engineering can help identify genes involved in Down syndrome features, including Alzheimer-type neurodegeneration. It is a research approach and reports no treatment, cure or prevention for Alzheimer's disease.
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CSF phospho-tau (p-tau(181)) levels have shown good diagnostic utility in differential diagnosis of Alzheimer disease (AD).
Why it matters
In 46 neurological patients without neurodegenerative disease, spinal fluid phosphorylated tau levels did not depend on age, cognitive status or gender. This supports the marker's use in diagnosis but offers nothing for treatment or prevention.
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These observations: (i) support the hypothesis of transneuronal spread of neurofibrillary changes from the DR to its interconnected cortical brain areas; and (ii) indicate that the supratrochlear subnucleus of the DR is affected by neurofibrillary changes before the transentorhinal cortex during the disease process underlying AD.
Why it matters
In 118 brains, neurofibrillary changes were found in the dorsal raphe nucleus of all cases with cortical changes and in more than one fifth of those without. This supports the idea that tau changes may begin in this brain region before spreading, but it is an autopsy observation and not a treatment.
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Reduced telomere length has recently been reported in T lymphocytes of individuals with trisomy 21 Down syndrome (DS) and dementia.
Why it matters
This study found shorter telomeres in T lymphocytes from older men with fragile X premutation alleles, including those with fragile X-associated tremor/ataxia syndrome and dementia. It suggests telomere shortening may be a biomarker, but it is a small study and does not show a treatment or cure for Alzheimer's disease.
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It was first demonstrated that the differentiation and functioning of cultured brain cells requires not only ALA, but also the very long polyunsaturated omega-3 (DHA) and omega-6 carbon chains.
Why it matters
This paper reports that cultured brain cells need very long omega-3 and omega-6 chains as well as ALA, and that poorer glycaemic control is linked to lower performance on tests such as memory. These are laboratory and observational findings and do not show that any nutrient supplement prevents or treats Alzheimer's disease.
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There is a need for improvement of the diagnosis of vascular dementia (VaD).
Why it matters
This review discusses candidate cerebrospinal fluid markers that reflect blood-brain barrier damage, demyelination, neuronal degeneration and axonal degeneration in vascular dementia. It notes none of these markers is specific to subcortical vascular dementia, but together with standard workup they may aid diagnosis.
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Down Syndrome (DS) is the most common of the chromosomal disorders and manifests abnormalities in several organ systems.
Why it matters
This case report describes a 49-year-old person with Down syndrome whose triplegia, respiratory failure and death were attributed to severe degenerative cervical spine disease. It concerns cervical spine abnormalities, not the treatment, cure or prevention of Alzheimer's disease.
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An increased risk of Alzheimer disease (AD) has been reported in young mothers of Down syndrome (DS) probands.
Why it matters
This study examined apolipoprotein E epsilon 4 frequencies in mothers and fathers of children with Down syndrome and the meiotic origin of non-disjunction. The authors conclude the simplest interpretation is that the previously reported associations are due to random statistical variation rather than a real effect of the epsilon 4 allele, though they say the issue deserves further study.
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Transgenic mice expressing the oncogenic protein-serine/threonine kinase Mos at high levels in the brain display progressive neuronal degeneration and gliosis.
Why it matters
Mice with a gene that raises protein phosphorylation in the brain showed nerve degeneration, gliosis, and altered tau phosphorylation similar but not identical to Alzheimer's disease. This is animal research from 1996 and does not show any treatment, cure, or prevention.
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The main purpose of this study was to investigate differences regarding endogenous opioids in post-mortem frontal cortex of adult patients with Down syndrome (DS), patients with Alzheimer disease (AD) and neurologically healthy persons, respectively, using specific radioimmunoassays.
Why it matters
Levels of leu-enkephalin and dynorphin A were increased in the frontal cortex of people with Down syndrome and people with Alzheimer's disease compared with controls. The authors suggest a relationship with cognitive impairment, but this is post-mortem tissue analysis and no treatment was tested.
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S100 beta protein, a member of a Ca(2+)-binding protein family present primarily in the nervous system, affects the survival and differentiation of both neurons and glia cells.
Why it matters
In this mouse study, raising S100 beta protein two- or seven-fold above normal did not change APP mRNA levels, and neither control nor transgenic aged mice showed abnormal amyloid deposits in plaques. The authors note this does not rule out focal changes in APP transcription or effects on APP protein processing, so it leaves the role of S100 beta in Alzheimer's disease unresolved.
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In addition to clinical and neuropathological similarities between Alzheimer's disease and Down syndrome there are genetic and biochemical data which suggest common disease mechanism.
Why it matters
In this in-vitro assay, cells from people with Alzheimer-type dementia showed a large drop in mitotic index when glutamine was added, suggesting glutamine sensitivity or a problem in the glutamine/glutamate pathway may be involved in the disease. The authors state these findings would need to be confirmed before they could inform preventive strategies.
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Individuals with Down syndrome develop neuropathologic and in some cases clinical evidence of Alzheimer disease after age 40.
Why it matters
In CT scans of 18 people with Down syndrome, a measure of mesial temporal-lobe atrophy correlated with severity of cognitive impairment and predicted dementia status with accuracy greater than 75%. This is a small imaging study about detecting dementia, not treating, curing or preventing it.
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A pilot study was performed to test the ability of MR to evaluate the brain lucencies shown by CT in Alzheimer disease patients and in normal control subjects.
Why it matters
This small 1986 pilot study found that MRI was more sensitive than CT for detecting brain signal changes, with patches of increased signal intensity seen in seven of eight Alzheimer disease patients and in eight of nine normal subjects over 45. These are imaging observations only and provide no 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.
- Tau proteins in the temporal and frontal cortices in patients with vascular dementia
- Automated Speech Analysis to Differentiate Frontal and Right Anterior Temporal Lobe Atrophy in Frontotemporal Dementia
- TREM2 interacts with TDP-43 and mediates microglial neuroprotection against TDP-43-related neurodegeneration
- Genetic Analysis of Retinal Cell Types in Neuropsychiatric Disorders
- Hippocampal and amygdala volumes in children and adults with childhood maltreatment-related posttraumatic stress disorder: a meta-analysis
- Gain-of-function Modulation of TREM2 and its Impact on Amyloid-β and Tau Pathologies in Alzheimer's Disease: A Systematic Review and Meta-analysis of Animal Studies
- γ-Secretase exosites as targets for substrate-selective lowering of Aβ generation
- Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration
- The increase in TDP-43 and neurogranin blood levels at different stages of cognitive impairment in the elderly people: A cross-sectional study
- Donepezil significantly improves abilities in daily lives of female Down syndrome patients with severe cognitive impairment: a 24-week randomized, double-blind, placebo-controlled trial