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534 studies tagged down, dated 1975-09-01 to 2026-10-30. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Differential endothelial cell remodeling in Down syndrome and APP duplication drives distinct blood brain barrier dysfunction 2026-10-30
- Memory and Plasma pTau217 Refine Prognosis in Down Syndrome 2026-10-02
- Tau extent is associated with lower cognition in Down syndrome-related Alzheimer's disease 2026-10-01
Studies
534 studies carry this tag.
Date range
1975 to 2026
Top journals
- Proceedings of the National Academy of Sciences of the United States of America 21
- Alzheimer s & Dementia 20
- Alzheimer's & dementia : the journal of the Alzheimer's Association 15
- Neurology 14
- Neuroscience letters 14
239 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Ninety-six individuals with Down syndrome over age 35 years were evaluated and followed up for evidence of nontreatable dementia.
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The aim of this study was to test whether there is an excess of dementia of Alzheimer type (DAT) cases in Down syndrome (DS) relatives.
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The Alzheimer amyloid protein precursor (APP) has previously been localized to human chromosome 21q11.2-q21.
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Sixty-eight human fibroblast cell strains were assayed for radioresistant DNA synthesis (RDS), which is defined here as the absence of a steep component of inhibition of DNA synthesis in a dose-response curve when rate of DNA synthesis is plotted against radiation doses from 0 to 20 Gy or more.
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Postmortem morphometric analyses of Bielschowsky stained sections from brains of 70 mentally retarded people without Down syndrome, age 65 and over when they died, indicated Alzheimer-type neuropathology in 22 cases (31%) and a majority with at least presence of some Alzheimer-type lesions.
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We have reported recently the sublocalization of an Alzheimer Disease-associated gene that encodes for cerebrovascular beta-amyloid protein (BAP).
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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.
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The dendritic atrophy seen in childhood continued into adulthood, with a marked decrease in dendritic branching, dendritic length, and spine frequency in elderly adults with the Down syndrome.
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Alzheimer's disease is a neurodegenerative disorder characterized by global cognitive decline.
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The gene encoding the beta-amyloid precursor protein has been assigned to human chromosome 21, as has a gene responsible for at least some cases of familial Alzheimer disease.
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The human ETS2 gene, a member of the ETS gene family, with sequence homology with the retroviral ets sequence of the avian erythroblastosis retrovirus E26 is located on chromosome 21.
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Mouse trisomy 16 has been proposed as an animal model of Down syndrome (DS), since this chromosome contains homologues of several loci from the q22 band of human chromosome 21.
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ALZ-50 is a monoclonal antibody that recognizes a protein of apparent molecular mass 68 kilodaltons (A68).
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Digital and palmar dermatoglyphics were examined in 29 men and 27 women with dementia of the Alzheimer type (DAT) and 112 age-, sex-, and racial group-matched controls.
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The neuropathology of Down syndrome (DS) at middle age is compared with that of Alzheimer disease (AD) at that age, through a review of the published literature and from the author's personal observations on brains from a series of patients of different ages with DS.
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The cause(s) of Alzheimer disease (AD) remain unknown.
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Hereditary cerebral hemorrhage with amyloidosis in Dutch patients is an autosomal dominant form of vascular amyloidosis restricted to the leptomeninges and cerebral cortex.
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Deposits of amyloid fibers are found in large numbers in the walls of blood vessels and in neuritic plaques in the brains of patients with Alzheimer disease and adults with Down syndrome.
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The presence of abundant intraneuronal amyloid in the form of neurofibrillary tangles (NFT) in the brains of Guamanian parkinsonism-dementia patients and the absence of extraneuronal amyloid in the form of vascular amyloid deposits or senile plaques permit the purification of NFT without contamination with extraneuronal amyloid.
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The human amyloid beta protein is the major constituent of the brain amyloid plaques found in Alzheimer disease.
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This study sought to test the hypothesis that adults with Down Syndrome may age faster than the general population by comparing the rate of increase in their mortality with age with that of the general population by the method originally described by Gompertz.
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Clinical and neuropathologic evidence points to the development of Alzheimer's disease (AD) in seven Down's syndrome patients above age 40.
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We have purified and characterized the cerebral amyloid protein that forms the plaque core in Alzheimer disease and in aged individuals with Down syndrome.
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Down syndrome is caused by trisomy of chromosome 21 and is comprised of a constellation of abnormalities including neuropathological features that closely resemble those characterizing the neurodegeneration of Alzheimer disease.
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56/100
One hundred brains of patients with Down's syndrome (DS) who died in institutions for chronic care were examined for clinicopathological correlation of Alzheimer's disease.
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47/100
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The activity of the pyruvate dehydrogenase complex (PDHC) was reduced in affected areas of brain from patients with Huntington disease (caudate, putamen) and Alzheimer disease (frontal cortex) where choline acetyltransferase (CAT) activity was low.
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Because of their initially low levels of mental functioning, Down syndrome persons' clinical symptoms frequently go undetected until the disease is advanced and deterioration severe.
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The clinical features of 11 families containing 73 individuals with dominantly inherited cerebellar ataxia of late onset are described.
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In patients with Down syndrome, senile plaques and neurofibrillary tangles accumulate in the cortex at an earlier age than in persons of normal karyotype.
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The degree of neurofibrillary tangle formation, granulovascuolar degeneration, and nerve cell loss was quantified in serial sections of the hippocampal formation from the brains of 5 adults dying with Down syndrome (monogolism).
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Alzheimer disease was transmitted in a pattern consistent with an autosomal dominant trait in three families.
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A brief description is given of neurofibrillary changes of the paired helical filament type in a variety of chronic neurological diseases.
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37/100
Progressive electroencephalographic disorganization and decreased voltage amplitude in the late components of the averaged visual evoked potentials were recorded in the last two years of life of a patient with Down disease and Alzheimer degeneration.
From across this tag
10 of the 527 studies in this tag, 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.
- Dementia in Down syndrome. Untangling the threads
- Detection of an Alzheimer disease pattern of cerebral metabolism in Down syndrome
- Enhancing protein O-GlcNAcylation in down syndrome mice mitigates memory dysfunctions through the rescue of mitochondrial bioenergetics, stress responses and pathological markers
- Autoimmune thyroiditis associated with mild "subclinical" hypothyroidism in adults with Down syndrome: a comparison of patients with and without manifestations of Alzheimer disease
- The striatum is an early, accurate indicator of amyloid burden using [11C]PiB in Down syndrome: Comparison of two radiotracers
- Discrepancies in assessing intellectual disability levels in adults with Down syndrome: Implications for dementia diagnosis
- Aging in Down Syndrome and the Development of Alzheimer's Disease Neuropathology
- Quantitative analysis of senile plaques in Alzheimer disease: observation of log-normal size distribution and molecular epidemiology of differences associated with apolipoprotein E genotype and trisomy 21 (Down syndrome)
- Therapeutic approaches in the improvement of cognitive performance in Down syndrome: past, present, and future
- Serum Beta-Synuclein Is Higher in Down Syndrome and Precedes Rise of pTau181