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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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.
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Numerous intraneuronal neurofibrillary tangles and senile (neuritic) plaques are the two characteristic lesions in Alzheimer disease (AD) and adult Down syndrome (DS).
Why it matters
Spindle microtubule reassembly after colcemid exposure differed between Alzheimer's disease cells and controls, with controls showing intact microtubules earlier, while results from Down syndrome cells were inconsistent. The authors say it is unclear how Alzheimer's microtubules differ or whether this relates to neurofibrillary tangles, and that the difference could only form the basis of a diagnostic test if verified.
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This study compared the relationships of the development of both Alzheimer I & II cells to reactive astrogliosis and also their distributional patterns in the demyelinated and non-demyelinated lesions in 6 cases of Wilson's disease by the use of PAP immunohistochemical technique for glial fibrillary acidic protein (GFAP).
Why it matters
This small study of 6 Wilson's disease cases examined two types of astrocyte changes (Alzheimer I and II cells) and their relationship to reactive astrogliosis. It describes cell patterns in Wilson's disease tissue and does not test any treatment, prevention, or cure for Alzheimer's disease.
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The review further discusses AI-driven nanomedicine optimization and advanced human-relevant models, including brain-on-a-chip systems and three-dimensional (3D) bioprinting, as tools to improve translational prediction.
Why it matters
This review discusses pharmacological modulation of cGAS-STING-NLRP3 signaling by nano-immunomodulators in Alzheimer's and Parkinson's disease, along with AI-driven optimization and advanced models. It notes that AI approaches currently support candidate selection and mechanistic prediction rather than clinical validation, and outlines major challenges for clinical advancement, so no treatment or cure is established.
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Η νευρωνική εκφύλιση και δυσλειτουργία αποτελούν χαρακτηριστικά γνωρίσματα των νευροεκφυλιστικών ασθενειών. Σημαντική πρόκληση είναι η ανάπτυξη αξιόπιστων διαγνωστικών εργαλείων που θα επιτρέπουν την έγκαιρη διάγνωση των νόσων αυτών. Πρώτος στόχος της παρούσας διδακτορικής διατριβής είναι ο ποσοτικός προσδιορισμός επιλεγμένων πρωτεϊνικών βιοδεικτών στο εγκεφαλονωτιαίο υγρό (ΕΝΥ) και στο αίμα, με σκοπό την υποστήριξη της διαφορικής διάγνωσης διαφόρων νευροεκφυλιστικών ασθενειών. Εφαρμόστηκαν μονοπλεκτικές δοκιμασίες για τον εντοπισμό του uPAR σε ασθενείς με σποραδική νόσο Creutzfeldt-Jakob, καθώς και των TAU, α-synuclein (α-syn), YKL-40 σε ασθενείς με συνουκλεϊνοπάθειες. Η έλλειψη ευαισθησίας και ειδικότητας των μονοπλεκτικών δοκιμασιών οδήγησε στην αξιοποίηση της πολυπλεκτικής πλατφόρμας SIMOA τεσσάρων βιοδεικτών (GFAP, NfL, TAU, UCH-L1), σε δύο διαφορετικές κλινικές κοόρτες. Στους ασθενείς με νόσο Alzheimer (AD) και μετωποκροταφική άνοια (FTD), ο βιοδείκτης με την καλύτερη διαγνωστική απόδοση ήταν ο UCH-L1 στο ΕΝΥ, με τιμές διαχωρισμού στα >1260 pg/mL για AD και >1052 pg/mL για FTD. Η NfL στο ΕΝΥ έδειξε καλή διαγνωστική ακρίβεια για τη διάκριση ασθενών με AD και FTD από υγιείς μάρτυρες, με τιμή διαχωρισμού >688,8 pg/mL και >463,9 pg/mL, αντίστοιχα. Η TAU στο ΕΝΥ εμφάνισε τη δεύτερη καλύτερη απόδοση μετά το UCH-L1 για τη διάκριση των AD από μάρτυρες, με τιμή διαχωρισμού >137,0 pg/mL, ενώ έδειξε καλή ακρίβεια και στη διάκριση των AD από τους FTD. Επίσης, καλή διαγνωστική ικανότητα παρατηρήθηκε στη διάκριση FTD από μάρτυρες με τιμή διαχωρισμού >111,3 pg/mL. Τέλος, η GFAP στο ΕΝΥ παρουσίασε μετρίου βαθμού ακρίβεια στη διάκριση AD από ομάδα μαρτύρων με τιμή διαχωρισμού >5942 pg/mL. Στη Σκλήρυνση κατά πλάκας (MS) και στο Kλινικά μεμονωμένο σύνδρομο (CIS), η NfL ορού και ΕΝΥ έδειξε μέτρια διαγνωστική ακρίβεια στη διάκριση των MS από τους μάρτυρες, με τιμές διαχωρισμού >5,909 pg/mL και >453,4 pg/mL, αντίστοιχα. Η GFAP ορού παρουσίασε μέτρια διακριτική ικανότητα με τιμή διαχωρισμού >48,08 pg/mL στους MS έναντι των υγιών. Ενώ τέλος η TAU ήταν ο βιοδείκτης με την καλύτερη απόδοση στη διάκριση MS / CIS από τους μάρτυρες, με τιμή διαχωρισμού στον ορό >0,5823 / >0,5950 pg/mL, αντίστοιχα, ενώ στο ΕΝΥ <76,47 / <75,26 pg/mL, αντίστοιχα. Δεύτερος στόχος της μελέτης, είναι η διερεύνηση του ρόλου των νευρωνικών εξωσωμάτων στην παθογένεση και εξάπλωση των νευροεκφυλιστικών ασθενειών (με έμφαση στη νόσο Prion). Για τον σκοπό αυτό αξιοποιήθηκε παθολογικό μοντέλο μυός RML, το οπ
Why it matters
This doctoral thesis quantified protein biomarkers in cerebrospinal fluid and blood to support differential diagnosis of neurodegenerative diseases, finding that UCH-L1 had the best diagnostic performance for distinguishing Alzheimer's disease and frontotemporal dementia from controls, followed by NfL and TAU. The work is about diagnostic tools and does not report a treatment, prevention or cure for Alzheimer's disease.
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At the end of the last century, it was realized that not only damage to the gray matter of the brain causes cognitive decline, but also damage to the white matter can lead to a decrease in cognitive abilities of high severity, up to dementia.
Why it matters
This review compares cerebral small vessel disease and multiple sclerosis, noting that both are white matter diseases that can predict cognitive impairment and that they share features such as inflammation and vascular factors. It does not report any treatment, cure, or prevention.
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Here we present the cases of two individuals with language and behavioral symptoms indicative of the early clinical manifestations of both Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD).
Why it matters
Two individuals with language and behavioral symptoms suggesting both Alzheimer's disease and frontotemporal lobar degeneration had neuroimaging indicating primary tauopathy without amyloid deposition. The authors suggest these cases may represent a previously unrecognized syndrome, based on only two cases.
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In humans, GART [phosphoribosylglycinamide formyltransferase (EC 2.1.2.2) / phosphoribosylglycinamide synthetase (EC 6.3.4.13) / phosphoribosylaminoimidazole synthetase (EC 6.3.3.1)] is a trifunctional protein which catalyzes the second, third, and fifth reactions of the ten step de novo purine synthesis (DNPS) pathway.
Why it matters
This study characterized a HeLa cell model of de novo purine synthesis deficiency caused by loss of GART. It is basic cell biology with no direct testing of any treatment, cure or prevention for Alzheimer's disease.
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29/100
Recent data have allowed speculating that amyloid Aβ induces apoptosis via opening type-1 VDAC in cell membranes of hypo-metabolic neurons, a process most likely running over life time--as leaves fall from trees in the tropics--and ending in Alzheimer's disease whenever critical brain regions are affected.
Why it matters
This paper proposes a model in which amyloid Aβ opens type-1 VDAC in cell membranes of hypo-metabolic neurons, leading to apoptosis and eventually Alzheimer's disease. This is a speculative model that differs from the amyloid cascade theory and reports no treatment or cure.
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Subcortical vascular mild cognitive impairment (svMCI) is known to be a prodromal stage of subcortical vascular dementia (SVaD) (1-3) who may also developed to mixed Alzheimer's disease (AD) (4).
Why it matters
This small study of 26 patients with subcortical vascular mild cognitive impairment and 28 healthy controls used resting-state functional MRI to examine brain connectivity. The findings are preliminary and do not establish any treatment, cure, or prevention for Alzheimer's disease.
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In Transmissible Spongiform Encephalopathies (TSEs) and Alzheimer disease (AD) both misfolding and aggregation of specific proteins represent key features.
Why it matters
In mice infected with prions, the drug CHF5074 did not prolong survival when given into the brain, but did extend median survival by 21 days in mice infected in the abdomen. This is an animal study of prion disease, not Alzheimer's disease, so it does not establish any treatment or prevention benefit for people with Alzheimer's.
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Down syndrome, as a phenotypic result of trisomy 21, is a complex condition with a set of over 30 phenotypic features, which manifest themselves with varying frequencies among affected individuals.
Why it matters
This paper discusses how understanding the molecular biology of chromosome 21 genes could help explain features of Down syndrome, including early-onset Alzheimer's degeneration. It is a discussion of research strategy and does not test any treatment, cure or prevention.
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Tau-like protein levels from 40 Down syndrome (DS) persons (31-70 years old), 40 non-DS age-matched normal controls, 18 non-DS mentally retarded (MR) persons (26-91 years old), 25 probable Alzheimer disease (AD) patients (55-99 years old) and 24 non-demented elderly controls (54-79 years old) were measured using a sandwich enzyme linked immunosorbent assay.
Why it matters
Tau-like protein levels were significantly higher in 40 people with Down syndrome than in normal controls, mentally retarded persons, probable Alzheimer's disease patients, or non-demented elderly controls, and were detected in 22 of the 40. No relationship was found between these levels and age, gender, or apolipoprotein E phenotypes in any group.
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Patients with Down syndrome (human trisomy 21) develop neuropathological and cholinergic functional defects characteristic of Alzheimer's disease, which has been attributed to the location of the Alzheimer beta-amyloid precursor protein on chromosome 21.
Why it matters
In this mouse study, brain tissue grafts from trisomy 16 mice survived up to a year without developing beta-amyloid deposits or neurodegeneration, but both graft types showed neuroinflammatory responses. These are animal findings and do not establish any treatment, cure or prevention for Alzheimer's disease.
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However, bed rest results in many alterations which are disadavantageous.
Why it matters
This study concerns the effects of long-term bed rest on antioxidant defence and lipid peroxidation in men, not Alzheimer's disease. It provides no information relevant to treating, curing or preventing Alzheimer's disease.
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Thirty-four unique-sequence microclones were isolated from a previously described microdissection library of human chromosome 21 and were regionally mapped using a cell hybrid mapping panel which consists of six cell hybrids and divides chromosome 21 into eight regions.
Why it matters
This study isolated and mapped DNA clones from chromosome 21, finding that unique-sequence clones were unevenly distributed along the chromosome. It is a basic genetics resource that may support future research but does not test any treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer disease (AD) pathology affects the transentorhinal/entorhinal region early but whether entorhinal cortex (EC) astrocytes are causal drivers or therapeutic targets remains unresolved.
Why it matters
This review examines evidence on entorhinal cortex astrocytes in early Alzheimer's disease and concludes that whether they are causal drivers or therapeutic targets remains unresolved. It prioritizes candidate astrocyte modules for future study, but the most direct functional evidence comes from rodents and is described as circuit plausibility rather than proof in humans.
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Advanced Glycation End Products (AGEs) are reactive compounds formed through the non-enzymatic glycation of proteins, lipids, or nucleic acids due to exposure to reducing sugars.
Why it matters
In human iPSC-derived brain organoids, advanced glycation end-products activated microglia, increased amyloid-beta aggregates, and impaired neurodevelopment. These are laboratory findings in a model system, so they do not yet show any way to treat, cure, or prevent Alzheimer's disease in people.
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Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation.
Why it matters
This is a computational analysis of existing human brain data that identifies SYK kinase as a possible drug target and lists candidate inhibitors, so it does not test any treatment in patients. No clinical benefit, cure or prevention is shown.
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No entanto, os resultados dos estudos clínicos apresentam divergências entre si, além de limitações metodológicas, pequeno tamanho amostral e variabilidade na definição dos desfechos.
Why it matters
This review found that clinical studies of vitamin E and other antioxidants for dementia in Down syndrome disagree with each other and have methodological limitations, small sample sizes and inconsistent outcome definitions. The authors conclude the data are still preliminary and that robust randomized trials are lacking.
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.
- Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death
- Upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in Alzheimer's disease through inactivating the PI3K/Akt signaling pathway
- Electroacupuncture Improves M2 Microglia Polarization and Glia Anti-inflammation of Hippocampus in Alzheimer's Disease
- miR128 up-regulation correlates with impaired amyloid β(1-42) degradation in monocytes from patients with sporadic Alzheimer's disease
- Multimodal fusion model for diagnosing mild cognitive impairment in unilateral middle cerebral artery steno-occlusive disease
- Rehmannioside A improves cognitive impairment and alleviates ferroptosis via activating PI3K/AKT/Nrf2 and SLC7A11/GPX4 signaling pathway after ischemia
- Interplay between astrocyte reactivity and APOE ε4 status is associated with accelerated pTau-related tau pathology in Alzheimer's disease
- Neuropathology of frontotemporal lobar degeneration-tau (FTLD-tau)
- Cerebrospinal fluid proteins predict longitudinal hippocampal degeneration in early-stage dementia of the Alzheimer type
- Silent yet impaired: Hidden memory processing deficits in asymptomatic individuals with moderate‐to‐severe white matter hyperintensities