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.
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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.
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A study on long-term astrocytic responses (from 1 day to 20 months after lesioning in 4-month-old rats, and from 1 day to 6 months in 20-month-old rats) to diverse unilateral damage of the nucleus basalis (nbM) by injection of 40 nmol of ibotenic acid, or 50 or 100 nmols of quisqualic acid was performed using a histochemical method (immunoreactivity against the glial fibrillary acidic protein GFAP).
Why it matters
In rats with nucleus basalis lesions, reactive astrocytes were found in local, proximal and remote brain regions and persisted for many months. This is an animal study from 2000 and does not test any treatment, cure or prevention.
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The patients were at stage V of sexual development.
Why it matters
This small study of 13 young women with Down syndrome found normal ovarian and uterine structure and mostly normal hormone levels, with some hormones elevated compared to controls. It provides no information about treating, curing or preventing Alzheimer's disease.
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[3H]inositol(1,4,5)-trisphosphate (IP3) binding studies have shown decreased [3H]IP3 binding to brain tissue in several neurodegenerative diseases, including Alzheimer's and Huntington's diseases.
Why it matters
This rat study found that a neurotoxin caused loss of IP3-receptor protein in the brain, and it cites earlier findings of reduced IP3-receptor protein in Alzheimer brains. It is basic animal and tissue work and does not test any treatment, cure, or prevention of Alzheimer's disease.
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Neuropeptide Y (NPY)-containing neurons are depleted in the cortices of individuals with Alzheimer disease (AD), yet spared in the striatum of patients with Huntington chorea.
Why it matters
In cultured cortical neurons from a mouse model of Down syndrome, the number and shape of neuropeptide Y neurons were abnormal and could be normalized by contact with normal glial cells. This is a cell-culture study and provides no treatment, cure or prevention for Alzheimer's disease.
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Neuropsychologic tests were performed in subjects with Down syndrome in order to assess the effect of a 90-day treatment with L-acetyl-carnitine (LAC).
Why it matters
In this small study, 90 days of treatment with L-acetyl-carnitine was associated with improved visual memory and attention in people with Down syndrome, but not in people with mental deficiency from other causes. The authors suggest a possible link to cholinergic transmission, but this does not demonstrate any treatment, cure or prevention for Alzheimer's disease.
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Recent reports suggest that cultivated nonneuronal cells from individuals with Alzheimer disease (AD) and other specific hereditary neurodegenerative disorders show hypersensitivity to DNA-damaging agents such as x-rays and radiomimetic chemicals.
Why it matters
Cells from people with familial Alzheimer disease did not show significant hypersensitivity to x-irradiation compared with controls, so the proposed DNA-repair defect hypothesis was not supported. This laboratory study offers 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.
- 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