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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Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS).
Why it matters
This review describes how an extra copy of the DYRK1A gene in Down syndrome affects brain development and is linked to cognitive impairment and Alzheimer's disease. In mouse models, normalizing DYRK1A improved synaptic plasticity and learning and memory, but this is early research and not yet a treatment for people.
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This study aims to comprehensively review the role of glial fibrillary acidic protein (GFAP) as a marker of astrocyte activation in Alzheimer's disease (AD).
Why it matters
This literature review concludes that GFAP is a sensitive biomarker of astrocyte activation from the preclinical phase of Alzheimer's, correlating with amyloid-beta accumulation and neuroinflammation, and may help predict conversion from mild cognitive impairment. It is a review of biomarkers for detection and monitoring, not evidence of a treatment, cure or prevention.
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Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear.
Why it matters
In cell and animal models, the stress hormone corticosterone raised Psen2 and deleting Psen2 prevented corticosterone-induced death of adult hippocampal neural stem cells, but the Psen2 N141I mutation did not worsen this death or behavioral deficits. The authors conclude that the Psen2 N141I mutation alone may not be sufficient to link chronic stress to Alzheimer's disease.
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Triggered by LPS and AGEs in food, inflammatory cytokines can enter the brain and stimulate microglial activation, inflammation, and oxidative damage.
Why it matters
This narrative review proposes that reducing dietary lipopolysaccharides, arachidonic acid, and advanced glycation end products could lower neuroinflammation and thereby reduce the risk of cognitive impairment and Alzheimer's disease. It presents a hypothesis based on mechanisms, not tested clinical outcomes, so it does not show that dietary changes treat, cure, or prevent Alzheimer's disease.
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Previous studies have shown that preeclampsia increases the risk of cerebrovascular and cardiovascular diseases, as well as cognitive impairments, up to evolving dementia in the future.
Why it matters
This work concerns whether markers of neuroinflammation and neurodegeneration in hypertensive disorders of pregnancy relate to later neurological problems. The text states it is not clear whether these markers correlate with long-term complications, so no treatment or prevention conclusion can be drawn.
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Immunotherapy is rapidly becoming one of the most promising directions in the modern approach to cancer treatment.
Why it matters
This review notes that immunotherapy is being tested in Alzheimer's disease but that immunotherapies are associated with neurotoxic side effects such as neuroinflammation, encephalitis, cognitive decline, and peripheral neuropathy. It reports no evidence that immunotherapy cures or prevents Alzheimer's disease.
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Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear.
Why it matters
In cell and animal models, the stress hormone corticosterone raised Psen2 and deleting Psen2 prevented corticosterone-induced death of adult hippocampal neural stem cells, but the Psen2 N141I mutation did not worsen this death or behavioral deficits. The authors conclude that the Psen2 N141I mutation alone may not be sufficient to link chronic stress to Alzheimer's disease.
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The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections.
Why it matters
This review discusses autophagy and mitophagy at the synapse and their links to neurodegenerative diseases including Alzheimer's. It summarizes research in cells and animal models and discusses diagnostic and therapeutic potential, but does not demonstrate any treatment, cure or prevention.
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Impaired glucose metabolism in adult Down Syndrome (DS) has been well-documented in vivo and information on the underlying biochemical defect i.e. aberrant glucose handling enzymes is already available.
Why it matters
In fetal Down syndrome brain tissue, levels of several carbohydrate-handling enzymes were comparable to controls. This laboratory finding concerns early development and provides no basis for treating, curing or preventing Alzheimer's disease.
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Down syndrome (DS) brains, from 19 gestational weeks to 50 years of age were studied by immunohistochemical methods with a polyclonal antibody against synthetic peptide comprising part of the Kunitz-type protease inhibitor (KPI) domain of Alzheimer disease amyloid precursor protein (APP), residues 301 to 323 of APP 770.
Why it matters
In brain tissue from people with Down syndrome, a Kunitz-type protease inhibitor part of the amyloid precursor protein was found at high levels in cerebral blood vessels from infancy onward, and this was reduced in those with Alzheimer-type dementia. The authors suggest this high vessel expression may be one factor predisposing to vascular disease and amyloid deposition in Down syndrome.
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27/100
La aprobación de lecanemab y donanemab para el tratamiento de la enfermedad de Alzheimer temprana plantea nuevos desafíos para la neurología vascular, principalmente por la aparición de anomalías en las imágenes relacionadas con el amiloide (ARIA).
Why it matters
The approval of lecanemab and donanemab for early Alzheimer's disease raises new challenges for vascular neurology, mainly because of ARIA, which can appear as brain edema or sulcal effusions (ARIA-E) and as microhemorrhages, superficial siderosis, or macrohemorrhages (ARIA-H). The authors note that APOE ε4 genotype and drug dose are main risk factors, that ARIA symptoms can be mistaken for acute cerebrovascular events, and that the coexistence of Alzheimer's disease, cerebral amyloid angiopathy, ARIA, and cerebrovascular disease requires reconsidering the use of anticoagulants and thrombolytics.
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Las enfermedades neurodegenerativas representan un importante problema de salud pública debido a su creciente prevalencia y al carácter progresivo e irreversible del daño neuronal que producen.
Why it matters
This systematic review of 38 studies found that plasma p-tau217 had the highest diagnostic performance for Alzheimer's disease, followed by p-tau181, GFAP, NfL and the Aβ42/Aβ40 ratio, and that combining markers improves detection. The review supports early diagnosis but notes that diagnosis is often made late and does not report a treatment or cure.
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Dysfunctional GAA results in widespread glycogen accumulation leading to muscle weakness, cardiovascular and breathing problems and premature death.
Why it matters
This study is about spinal microglia in a rat model of Pompe disease, not Alzheimer's disease. It reports that these microglia were not pro-inflammatory but acquired some disease-associated microglia characteristics, and provides no information on treating, curing or preventing Alzheimer's.
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Các bệnh lý như lao và Alzheimer đòi hỏi phát hiện sớm với độ nhạy cao để can thiệp kịp thời, tuy nhiên các kỹ thuật hiện nay như ELISA, PCR còn hạn chế về chi phí và độ nhạy. Những tiến bộ gần đây trong công nghệ nano cho thấy hạt nano vàng vỏ đồng kết hợp sinh phẩm tái tổ hợp (protein hoặc aptamer) có thể khuếch đại tín hiệu màu, mở ra triển vọng cho chẩn đoán sớm siêu nhạy. Bài tổng quan này phân tích cơ chế kỹ thuật xét nghiệm kháng nguyên bằng sự hình thành vỏ nano đồng trên hạt vàng, trong đó ion Cu²⁺ được khử bởi natri ascorbate trên bề mặt AuNPs với vai trò ổn định của polyethylenimine, tạo cấu trúc Au-Cu đa giác giúp tăng cường tín hiệu plasmon.
Why it matters
This review describes a gold nanoparticle-based test using recombinant proteins or aptamers that can detect p-tau231 or AβO42 in Alzheimer's disease with detection limits down to picogram/mL, visible to the naked eye. The method shows promise for low-cost, sensitive early diagnosis, but challenges remain regarding copper layer stability, cross-reactivity and standardization, and no treatment or cure is reported.
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Alzheimer disease (AD) is a multi-factorial neurodegenerative disease that is characterized by accumulation of amyloid-beta (Aβ), protein aggregation and progressive neuronal dysfunction.
Why it matters
Using molecular docking, several Ginkgo biloba phytocompounds showed good binding interactions with APP, neprilysin and alpha-synuclein, with amentoflavone binding relatively strongly to APP. This is an in-silico study only and provides no evidence of clinical benefit.
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Benzene-1,3-disulfonic acid exhibited strong binding to the Arg136-containing pocket with a top docking score of -5.93 kcal/mol and an estimated inhibition constant (Ki) of 44.6 µmol.
Why it matters
Using computer docking, a small molecule was found to bind to a site on ApoE, and it was predicted to have poor oral absorption and limited brain penetration but a favorable safety profile. This is an early, computer-based study, and the molecule has not been tested in animals or people.
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Recent progress of pharmacotherapy enabled anti-amyloid and anti-tau immunotherapy for Alzheimer disease.
Why it matters
This paper proposes a 'D-neuron protection / activation' therapy concept for neuropsychiatric illnesses including dementia, based on D-neuron findings in post-mortem schizophrenia brains. It suggests indirect biomarkers for evaluating D-neuron activity but reports no clinical trial or confirmed treatment effect.
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However, postmortem investigations indicate that the AD-typical progressive amnestic syndrome may also result from predominantly limbic non-AD neuropathology such as TDP-43 proteinopathy and argyrophilic grain disease.
Why it matters
In clinically diagnosed Alzheimer's disease, temporo-parietal gray matter and perfusion were more closely associated with cholinergic deficit than basal forebrain volumes, making them possible markers for cholinergic treatment response. The study also notes that the typical progressive amnestic syndrome may result from non-Alzheimer's limbic pathologies such as TDP-43 proteinopathy and argyrophilic grain disease.
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A 34-year-old man developed three generalised seizures over a period of 2 weeks.
Why it matters
This case report describes a 34-year-old man with recurrent seizures, progressive cognitive decline, parkinsonism and a calcified brain, raising the question of Fahr's disease. It is a single case and does not provide evidence about treating, curing or preventing Alzheimer's disease.
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The present study investigated the frequency and distribution of TUNEL-positive neurons in brains of dementia with Lewy bodies (DLB) in comparison with those in brains of Alzheimer's disease (AD), Down syndrome (DS) and non-demented elderly persons.
Why it matters
This post-mortem brain study found TUNEL-positive neurons, a marker of DNA fragmentation, in dementia with Lewy bodies, Alzheimer's disease and Down syndrome brains. It describes neuronal damage patterns only and does not test any treatment, cure or prevention.
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Some individuals with Down syndrome develop an Alzheimer-type dementia in the third and fourth decades of life.
Why it matters
In 21 patients with Down syndrome, this study found no difference in apolipoprotein E genotype distribution compared with the general population. It concluded that the epsilon 4 allele had no influence on the appearance of Alzheimer disease in these patients, so it reports no treatment, cure or prevention.
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Manganese-superoxide dismutase (Mn-SOD) was localized in the cerebral cortex and hippocampus of patients with Alzheimer-type senile dementia (ATD) by immunocytochemistry and the relationship of Mn-SOD with two major pathological features of ATD, i.e., senile plaques and neurofibrillar tangles (NFTs), was examined.
Why it matters
In brain tissue from patients with Alzheimer-type senile dementia, astrocytes in senile plaques showed strong immunoreactivity for manganese superoxide dismutase, while NFT-loaded neurons did not. This is a descriptive tissue study suggesting an association with plaque formation, not a treatment or cure.
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Using anti-SP28 (a polyclonal antibody to a 28 residue synthetic peptide homologous to the NH2-terminal region of Alzheimer amyloid beta-protein) to investigate the cerebral cortex of 8 Alzheimer and 6 Down patients and 13 nondemented individuals, we found that, besides senile plaques and congophilic vessels, extracellular deposits unrelated to degenerating neurites, tangle-bearing neurons or congophilic vessels were labelled.
Why it matters
Using an antibody to the amyloid beta-protein, this study found extracellular deposits in the cerebral cortex of all 8 Alzheimer patients, 4 of 6 Down syndrome patients, and 5 of 13 nondemented elderly individuals. These deposits did not react with Congo red or thioflavine S, suggesting they may be made of beta-protein or its precursors that lack the conformation of amyloid fibrils.
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Early hypoxic-ischemic brain lesions were examined regarding 26 autopsy cases which had severe asphyxia at birth and died within the first week.
Why it matters
This autopsy study describes early brain damage patterns in newborns who died after severe asphyxia at birth. It is about birth-related brain injury and does not address treating, curing, or preventing Alzheimer's disease.
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Alzheimer's disease (AD) manifests as a chronic neurodegenerative syndrome featuring cognitive impairment alongside characteristic neuropathological markers: amyloid-beta (Aβ) plaques and tau-associated neurofibrillary tangles.
Why it matters
Tannins extracted from Phyllanthus amarus suppressed Aβ aggregation, reduced neuroinflammation and restored cognitive function in AD-model mice. This is cellular and animal work, so it supports further research but does not yet provide a proven therapy for patients.
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.
- Tau forms in CSF as a reliable biomarker for progressive supranuclear palsy
- Heritability of brain morphology related to schizophrenia: a large-scale automated magnetic resonance imaging segmentation study
- Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles
- Diagnostic value of CSF biomarker profile in frontotemporal lobar degeneration
- Klotho overexpression improves amyloid-β clearance and cognition in the APP/PS1 mouse model of Alzheimer's disease
- Aldehyde-Mediated Neurotoxicity and Lutein Intervention: A Novel Therapeutic Strategy for Alzheimer's Disease
- LPS-induced Murine Neuroinflammation Model: Main Features and Suitability for Pre-clinical Assessment of Nutraceuticals
- Advanced Glycation End-Products Are Associated With the Presence and Severity of Paratonia in Early Stage Alzheimer Disease
- Vascular subcortical hyperintensities predict conversion to vascular and mixed dementia in MCI patients
- Analysis of glial acidic fibrillary protein in the human entorhinal cortex during aging and in Alzheimer's disease