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 4,948 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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The 5' untranslated region (UTR) of the APP gene, encompassing 147 base pairs between the transcriptional (+1) and the translational start site, was examined for its role in APP expression.
Why it matters
This laboratory study identified a nuclear factor-binding domain in the 5' untranslated region of the amyloid precursor protein gene and found that eliminating factor binding reduced expression from the APP promoter. It is basic gene-regulation research and reports no treatment, cure or prevention for Alzheimer's disease.
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Down syndrome (DS) is a chromosomal abnormality (trisomy 21) associated with mental retardation and Alzheimer-like dementia, characteristic change of the individual's phenotype and premature ageing.
Why it matters
This study found signs of oxidative damage in blood from children with Down syndrome, along with lower coenzyme Q10 levels inside their cells. The authors link oxidative imbalance to the clinical features of Down syndrome, but no treatment or prevention was tested.
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Researchers since the 1990s have predominantly focused on the amyloid hypothesis and the formation of amyloid fibrils as the culprit behind AD when we began working on soluble Abeta (sAbeta).
Why it matters
This paper reports that N-terminal truncated peptides are the major components of soluble and insoluble amyloid beta in Alzheimer disease, that soluble amyloid beta species belong to the 42 form, and that soluble amyloid beta 42 is present in Down syndrome brains in prenatal and early postnatal development. It describes research findings about amyloid beta forms and reports no treatment or cure.
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Frontotemporal dementia regards a group of presenile progressive neurodegenerative form of dementias which includes Pick's disease, corticobasal degeneration, frontotemporal dementia with motor neuron disease, frontal lobe degeneration, dementia-parkinsonism-amyotrophy complex, familial non-specific dementia mapping to chromosome 3, non-Alzheimer degenerative dementia lacking distinctive histological features as well as a number other infrequent syndromes with dementia and focal neurological signs.
Why it matters
This study describes where metallothionein-I-II is found in the brains of people with frontotemporal dementia and its relationship to GFAP in astrocytes. It concerns frontotemporal dementia, not Alzheimer's disease, and does not test any treatment, cure, or prevention.
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31/100
Mutations in the human prion protein gene (PRNP) are responsible for hereditary diseases called transmissible spongiform encephalopathies (TSE) and a polymorphic site at codon 129 determines sensitivity to infectious forms of these maladies.
Why it matters
This study established conditions for detecting prion protein gene variants, including codon 129, using denaturing HPLC. It is a laboratory method for genetic screening and reports no treatment, cure or prevention for Alzheimer's disease.
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In persons with Down syndrome, soluble Abeta peptides, which result from the processing of the amyloid precursor protein, appear in the brain decades before the extracellular deposition of neuritic plaques.
Why it matters
This paper proposes that soluble Abeta peptides, especially Abeta1-42, form tight complexes with the alpha7 nicotinic acetylcholine receptor and may mediate progressive worsening of adaptive functions in Down syndrome. It is a hypothesis paper and does not show a treatment or cure.
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31/100
Inositol monophosphatase (IMPase), a cytoplasmic enzyme that hydrolyses inositol monophosphates to produce inositol is also found in the cerebrospinal fluid (CSF).
Why it matters
Inositol monophosphatase activity in cerebrospinal fluid was unchanged in Down syndrome, Alzheimer-type dementia and multi-infarct dementia compared with age-matched normal subjects. The study found no evidence that altered inositol levels in these conditions are explained by changes in this enzyme's activity, and it tests no treatment.
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Changes in the metabolic activity within the brain of patients suffering from Alzheimer's disease (AD) were investigated and compared with biochemical alterations in the hippocampus induced by fimbria/fornix transection in the rat.
Why it matters
In rats with a cut to the septo-hippocampal pathway, the hippocampus showed loss of cholinergic markers, raised glucose transporter binding and PFK activity, astrogliosis, and lower mitochondrial enzyme activity, some of which resembled changes in Alzheimer's disease brain. This is an animal model of metabolic events and does not test any treatment, cure or prevention.
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The occurrence of +1 frameshifted proteins, such as amyloid precursor protein (APP+1) and ubiquitin-B (UBB+1) in Down syndrome (DS) has been linked to the onset of Alzheimer's disease (AD).
Why it matters
This review describes how +1 frameshifted proteins such as APP+1 and UBB+1 accumulate in the neuropathological hallmarks of Down syndrome and Alzheimer's disease and may harm neuronal function, caused by a process the authors call molecular misreading. It is a discussion of a proposed disease mechanism and does not report or test any treatment, cure, or prevention.
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Alzheimer type II astrocytosis is the pathological hallmark of hepatic encephalopathy.
Why it matters
In cerebellar tissue from 15 patients with cirrhosis and hepatic encephalopathy, Bergmann glial cells did not show altered GFAP immunoreactivity compared with controls. This concerns a liver-related brain condition and does not address treating, curing or preventing Alzheimer disease.
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Paired helical filaments (PHF), which constitute neurofibrillary tangles (NFT) and neuritic plaque (NP) neurites, serve as a useful marker for Alzheimer disease (AD).
Why it matters
This study produced a monospecific antiserum that reacts only with neurofibrillary tangles and neuritic plaque neurites in Alzheimer's disease brain tissue, and also with tangles in Down syndrome and some other conditions. The antiserum is a laboratory tool intended to help study the nature and origin of filamentous protein abnormalities in Alzheimer's disease and related disorders, not a treatment or cure.
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We have evaluated serum alpha 1-antichymotrypsin content in dementia of the Alzheimer type (DAT).
Why it matters
This study found that serum alpha 1-antichymotrypsin was significantly higher in people with dementia of the Alzheimer type than in controls, while alpha 1-antitrypsin and inter-alpha-trypsin inhibitor levels did not differ. The authors suggest this measurement may be useful as a diagnostic marker, not as a treatment, cure or prevention.
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The pathological activation of AD microglia significantly amplifies endogenous aging characteristics.
Why it matters
In mice, Alzheimer's pathology accelerated the accumulation of late-stage disease-associated microglia and amplified aging-related lipid and lysosomal programs, with a collapse of microglial proteostasis. TREM2 acted as a key switch for this compensatory program, suggesting a possible target, but this is animal and cell-based work only.
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HIIT alone and in combination with CBD treatment significantly improved cognitive impairment induced by AD.
Why it matters
In a rat model of Alzheimer's disease, high-intensity interval training alone and combined with cannabidiol improved cognitive impairment and reduced BACE1 while increasing nestin, but neither treatment changed miRNA-124 levels. These are animal findings and do not establish a treatment for people.
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30/100
Vascular dementia (VaD), a primary cognitive disorder caused by cerebrovascular pathology, features significant white matter damage from chronic cerebral hypoperfusion strongly correlated with cognitive decline.
Why it matters
This review discusses how damage to myelin and interactions between oligodendrocytes and microglia contribute to vascular dementia. It outlines mechanisms and possible communication pathways but reports no treatment tested in patients.
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Tauopathies are a group of neurodegenerative disorders, including Alzheimer's disease, frontotemporal dementia, and progressive supranuclear palsy, characterized by the pathological accumulation of tau protein.
Why it matters
In aged tauopathy mice, delivering artificial microRNAs into the prefrontal cortex after symptoms began led to long-term improvements in memory, neuronal firing and reduced pathological tau at synapses. This is animal research, so it is not yet known whether this approach would work or be safe in people.
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hONE-NPCs expressed proteins such as Ki67, Nestin, GFAP, and b-III Tubulin, which are associated with cellular proliferation and the neuronal progenitor lineage.
Why it matters
Cells taken from the noses of people with Alzheimer's disease and progressive supranuclear palsy released different amounts of trophic factors than cells from healthy controls, and showed decreased proliferation. This is early laboratory research on cells and does not show a treatment or cure.
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White matter hyperintensities (WMHs) are a common finding on magnetic resonance (MR) images in older individuals, appearing as high-signal intensity regions on fluid-attenuated inversion recovery (FLAIR) imaging.
Why it matters
This study tested a machine learning method for measuring white matter hyperintensities, a marker linked to higher dementia and stroke risk, and found that adding attention blocks improved segmentation accuracy. Better measurement tools may help research and clinical assessment of this risk marker, but the study does not test any treatment or prevention for Alzheimer's disease.
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Levodopa/carbidopa is the cornerstone treatment for Parkinson's disease (PD), but in patients with dysphagia, there are limited options for the routes of administration.
Why it matters
In one patient with Lewy body dementia and swallowing difficulty, crushed levodopa/carbidopa given under the tongue improved parkinsonian symptoms within two hours. This is a single case report about giving an existing Parkinson's drug by a different route, not a treatment or cure for Alzheimer's disease.
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Presenilin 1 (PSEN1) mutations are the leading cause of early-onset Alzheimer disease (EOAD).
Why it matters
In an early-onset Alzheimer's cell model, the PSEN1 M139I mutation raised Aβ42/40 and microRNA-34a while lowering NOTCH-1, and blocking microRNA-34a reversed these effects. This is in-vitro work only, so it identifies a possible mechanism but no treatment for patients.
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Down syndrome (DS), characterised by compromised brain development and intellectual challenges, often manifests Alzheimer's disease (AD) -like symptoms.
Why it matters
This bibliometric analysis of 5,082 papers maps research trends on Down syndrome neuropathogenesis, noting Alzheimer's-related genes and proteins as a pervasive theme. It is a survey of publications and provides no treatment, cure or prevention findings.
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Regulator of calcineurin 1 (RCAN1) is related to the expression of human neurologic disorders such as Down syndrome, Alzheimer disease, and chromosome 21q deletion syndrome.
Why it matters
In mice with RCAN1 mutations, fecal corticosterone levels were normal in knockouts, and the authors found no evidence that corticosterone plays a causal role in the cognitive or anxiety behaviors seen in these mice. This is animal work and does not test any Alzheimer's treatment or prevention.
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Recent evidences indicate that polymorphisms within the promoter region of the vascular endothelial growth factor (VEGF) gene may elevate the risk for Alzheimer's disease (AD).
Why it matters
Two variants in the VEGF gene were not significantly more common in 93 Tunisian Alzheimer's patients than in 113 controls. A signal was seen only in the subgroup carrying the ApoE ε4 variant, so no clear genetic risk factor or treatment target was established.
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Plasma homocysteine value proved to be lower in 7 of the 30 and higher in 6 of the 30 patients studied than the reference range.
Why it matters
In 30 patients with Down syndrome, plasma homocysteine was lower than the reference range in 7 and higher in 6, and there was no significant alteration in antioxidant activity level. No statistically significant correlation was found between antioxidant activity and N-acetyl-beta-D-glucosaminidase values.
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A neuropathological study of Alzheimer type I (Alz I) and Alzheimer type II (Alz II) as well as Opalski (Opl) cells was performed serially on brain tissue from nine autopsied Wilson's disease (WD) cases.
Why it matters
This study examined abnormal astroglia cells in brain tissue from people with Wilson's disease, not Alzheimer disease. It describes the origin of these cells but provides no information about treating, curing or preventing Alzheimer disease.
From across this topic
10 of the 4,930 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.
- Colocalization of tau and alpha-synuclein epitopes in Lewy bodies
- Automated Anatomical Labeling of Activations in SPM Using a Macroscopic Anatomical Parcellation of the MNI MRI Single-Subject Brain
- Neuropsychological dysfunction and neuroimaging abnormalities in neurologically intact adults with sickle cell anemia
- Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents
- Movement Disorders Society Scientific Issues Committee report: SIC Task Force appraisal of clinical diagnostic criteria for Parkinsonian disorders
- ALS/FTD-Linked Mutation in FUS Suppresses Intra-axonal Protein Synthesis and Drives Disease Without Nuclear Loss-of-Function of FUS
- Down's syndrome, neuroinflammation, and Alzheimer neuropathogenesis
- The two faces of protein misfolding: gain- and loss-of-function in neurodegenerative diseases
- Tau is a candidate gene for chromosome 17 frontotemporal dementia
- Characteristics of two distinct clinical phenotypes in pathologically proven progressive supranuclear palsy: Richardson's syndrome and PSP-parkinsonism