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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Adults with DS have a significantly increased brain concentration of myo-inositol, and this is associated with reduced cognitive ability.
Why it matters
This case-control study found higher hippocampal myo-inositol concentration in adults with Down syndrome than controls, and within that group higher myo-inositol was linked to lower cognitive ability. It reports an association only and does not test any treatment.
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The authors identified 40 PCA cases.
Why it matters
This review of 40 cases describes posterior cortical atrophy as a dementia syndrome with prominent occipitoparietal pathology, and seven autopsied cases had Alzheimer's pathology with higher tangle densities in visual brain areas than typical Alzheimer's disease. It is a descriptive case series and does not report a treatment, cure, or prevention.
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Twenty patients with AD and 25 CN subjects had MRI scans and clinical evaluations twice approximately 1.9 years apart.
Why it matters
In 20 patients with Alzheimer disease, the entorhinal cortex shrank faster per year than the hippocampus, consistent with the view that Alzheimer pathology begins in the entorhinal cortex. This is a small imaging study of brain atrophy rates and does not test any treatment, cure, or prevention.
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53/100
Lesions in the hippocampus (HC), the entorhinal cortex (EC), and the prefrontal cortex (PFC) are associated with impairment of episodic memory; reduced HC volume is linked to memory declines in dementia; and decline in EC volume predicts progression from mild cognitive impairment to dementia.
Why it matters
In healthy adults, greater annual rate of shrinkage in the entorhinal cortex predicted poorer memory performance over 5 years, while hippocampal and prefrontal cortex volumes did not. The authors suggest even mild age-related shrinkage of the entorhinal cortex may be a sensitive predictor of memory decline, but this is not a treatment finding.
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Converging evidence suggests that the accumulation of cerebral amyloid beta-protein (Abeta) in Alzheimer's disease (AD) reflects an imbalance between the production and degradation of this self-aggregating peptide.
Why it matters
In APP transgenic mice, transgenic overexpression of insulin-degrading enzyme or neprilysin reduced brain amyloid-beta levels, prevented or retarded amyloid plaque formation, and rescued premature lethality. This was an animal study, so it is not yet known whether upregulating these proteases would be effective or safe in people with Alzheimer's disease.
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Frontotemporal dementia (FTD) is a pathologically heterogeneous group of presenile neurodegenerative disorders, with or without the deposition of hyperphosphorylated tau protein in affected brain regions.
Why it matters
This case-control study measured total tau, phosphorylated tau 181, and amyloid-beta1-42 in cerebrospinal fluid of patients with frontotemporal dementia, including cases due to tau mutations. It is about fluid markers in frontotemporal dementia, not about treating, curing, or preventing Alzheimer's disease.
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Why it matters
Reports that astrocytes from adult mice degrade amyloid-beta in vitro and in situ.
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A working group supported by the Office of Rare Diseases of the National Institutes of Health formulated neuropathologic criteria for corticobasal degeneration (CBD) that were subsequently validated by an independent group of neuropathologists.
Why it matters
These 2002 criteria, written by a working group supported by the NIH Office of Rare Diseases and "subsequently validated by an independent group of neuropathologists", define corticobasal degeneration (CBD) by what is found in brain tissue, not by symptoms, because CBD "can have diverse clinical presentations". The diagnosis rests on tau-positive lesions in nerve cells and glia of the cortex and striatum, "especially astrocytic plaques and thread-like lesions", with nerve-cell loss in focal cortical regions and the substantia nigra, and Alzheimer-type and Lewy body pathology must be assessed "to rule out other causes of dementia and Parkinsonism". The summary says the criteria separate CBD well from other tauopathies except frontotemporal dementia and Parkinsonism linked to chromosome 17, which needs "additional clinical or molecular genetic information"; it gives no accuracy figures and says nothing about treatment.
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The identification of mutations in the Tau gene in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has made it possible to express human tau protein with pathogenic mutations in transgenic animals.
Why it matters
In this mouse model, animals with a human P301S tau mutation developed tau filaments and loss of motor neurons, resembling features of human tau disorders. Because it is an animal study, it does not show that any treatment works in people or that Alzheimer's disease can be prevented.
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Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), also known as "Nasu-Hakola disease," is a globally distributed recessively inherited disease leading to death during the 5th decade of life and is characterized by early-onset progressive dementia and bone cysts.
Why it matters
This 2002 study identified TREM2 as the second gene behind Nasu-Hakola disease (PLOSL), a recessively inherited condition with bone cysts and early-onset progressive dementia, in patients who had no mutations in the first known gene, TYROBP. Because TREM2 and TYROBP form one receptor signalling complex on immune cells, the authors conclude that faults in either part produce the same disease. It does not study Alzheimer's disease or test any treatment, and the record does not report how many patients were studied.
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To identify genes influencing age at onset (AAO) in two common neurodegenerative diseases, a genomic screen was performed for AAO in families with Alzheimer disease (AD; n=449) and Parkinson disease (PD; n=174).
Why it matters
This genomic screen found that age at onset in Alzheimer disease and Parkinson disease is partly genetically controlled, with evidence for a common gene on chromosome 10q. It identifies genetic influences on when disease starts but does not provide any treatment, cure, or prevention.
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53/100
We identified 13 patients with a clinical diagnosis of PD who experienced dementia at least 4 years after parkinsonism onset (mean, 10.5 years) and subsequently underwent postmortem examination.
Why it matters
This study examined the brain pathology of 13 patients with Parkinson disease who developed dementia at least four years after parkinsonism onset, including some who lost the levodopa response. It describes neuropathologic findings and does not test a treatment for Alzheimer's disease.
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Alzheimer's disease and Parkinson's disease are associated with the cerebral accumulation of beta-amyloid and alpha-synuclein, respectively.
Why it matters
Mice expressing both human beta-amyloid and alpha-synuclein had worse learning, memory and motor deficits and more alpha-synuclein inclusions than mice with alpha-synuclein alone, and beta-amyloid promoted alpha-synuclein aggregation in cell-free and cell culture systems. This is animal and laboratory work suggesting beta-amyloid may worsen Lewy body disease, not a tested treatment.
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Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL; MIM 221770), also known as Nasu-Hakola disease, is a recessively inherited disease characterized by a combination of psychotic symptoms rapidly progressing to presenile dementia and bone cysts restricted to wrists and ankles.
Why it matters
In Nasu-Hakola disease (PLOSL), a rare inherited condition of "psychotic symptoms rapidly progressing to presenile dementia and bone cysts restricted to wrists and ankles", this study found loss-of-function mutations in the TYROBP (DAP12) gene: "one large deletion in all Finnish PLOSL alleles and another mutation in a Japanese patient". TYROBP was known as a signalling protein in immune NK cells, yet patients carrying two non-working copies showed "no abnormalities in NK cell function". The paper is about this rare disease only. It does not study Alzheimer's disease and does not test any treatment.
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Ageing of the brain leads to impairments in cognitive and motor skills, and is the major risk factor for several common neurological disorders such as Alzheimer disease (AD) and Parkinson disease (PD).
Why it matters
This study examined gene expression in the ageing mouse brain, noting features such as atrophy of pyramidal neurons, synaptic atrophy, cytoskeletal abnormalities and reactive astrocytes and microglia shared across mammalian species. It concerns normal brain ageing in mice and does not report a treatment, cure or prevention for Alzheimer's disease.
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Alpha-synuclein forms the major component of Lewy bodies and Lewy neurites, the defining neuropathological characteristics of Parkinson's disease and dementia with Lewy bodies.
Why it matters
This study found that the protein alpha-synuclein is the main building block of the filamentous clumps seen in multiple system atrophy, as well as in Parkinson's disease and dementia with Lewy bodies. This links these conditions as related alpha-synuclein disorders, but it does not test any treatment or cure.
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Ordered assembly of the amyloid-beta protein (A beta) into amyloid fibrils is a critical step in Alzheimer's disease (AD).
Why it matters
This study found that A beta is present in a detergent-insoluble membrane compartment in vivo and that secreted A beta levels are not elevated except in rare mutation-caused Alzheimer's disease. It describes where A beta is located but does not provide a treatment, cure, or prevention.
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Serotonin (5-HT) neuron and neurotransmitter loss in normal aging and neuropsychiatric diseases of late life may contribute to behavioral changes commonly observed in the elderly population.
Why it matters
This review suggests that age-related changes in serotonin neurons may make older people more likely to develop depression, and that combined problems with acetylcholine and serotonin function may contribute to cognitive impairment in Alzheimer's disease. It does not report a treatment, cure, or prevention, and the findings are presented as evidence and suggestions rather than confirmed results.
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Missense mutations in two related genes, termed presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees.
Why it matters
Transgenic mice coexpressing mutant presenilin 1 and mutant amyloid precursor protein developed amyloid deposits much earlier than mice expressing only the amyloid precursor protein mutation. This was an animal study, so it does not directly show how to treat or prevent Alzheimer's disease in humans.
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Overexpression of the familial Alzheimer's disease gene Presenilin 2 (PS2) in nerve growth factor-differentiated PC12 cells increased apoptosis induced by trophic factor withdrawal or beta-amyloid.
Why it matters
In PC12 cells, overexpression of presenilin 2 increased apoptosis, and a familial Alzheimer's disease mutation in PS2 produced a molecule with enhanced basal apoptotic activity. This is a cell study, so it does not show any treatment, cure, or prevention for Alzheimer's disease in people.
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Frontal sections of the temporal lobe including the transentorhinal/entorhinal region, amygdala, and/or hippocampus from human adult brains are studied for cytoskeleton changes using immunostaining with the antibodies AT8 and Alz-50 and selective silver impregnation methods for neurofibrillary changes of the Alzheimer type.
Why it matters
This study describes the sequence of cytoskeleton changes that occur as neurofibrillary tangles form in specific brain regions. It identifies layer pre-alpha in the transentorhinal/entorhinal region as containing some of the first nerve cells in the brain to develop these changes, offering a way to study early events in individual neurons.
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Amyloid beta-peptide (A beta) deposition in senile plaques and cerebral vessels is a neuropathological feature of Alzheimer disease (AD).
Why it matters
In autopsied brains of people who had late-onset Alzheimer's disease, those carrying one or two APOE4 alleles had more amyloid deposits in both plaques and blood vessels than people with two copies of APOE3. The authors describe this as "a distinct neuropathological phenotype", but the record reports no sample size or effect figures. It shows an association in people who already had the disease, and it does not test any treatment or prevention.
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The most common temporal lobe pathology is Ammons Horn sclerosis (AHS), and several different imaging techniques have been utilized to detect this with varying success.
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53/100
We have used restriction isotyping (restriction enzyme isoform genotyping) for rapid typing of common apolipoprotein E isoforms (E2, E3, E4).
Why it matters
This paper describes a method for rapid typing of apolipoprotein E isoforms (E2, E3, E4) using gene amplification and restriction enzyme digestion. It is a laboratory technique paper and does not directly address treating, curing, or preventing Alzheimer's disease.
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To examine the possibility that senile dementia may be associated with a loss of noradrenergic neurons that innervate the cerebral cortex, we used a Quantimet 720 image analyzer to estimate the number of neurons in the nucleus locus ceruleus in elderly patients with the clinical diagnosis of senile dementia.
Why it matters
This study found a loss of about 80% of locus ceruleus neurons in a subgroup of patients with senile dementia of the Alzheimer type. It describes a brain change associated with the disease, but does not test any treatment, cure or prevention.
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.
- Cognitive defects are reversible in inducible mice expressing pro-aggregant full-length human Tau
- In vivo quantification of hippocampal subfields using 4.7 T fast spin echo imaging
- The importance of neuritic plaques and tangles to the development and evolution of AD
- TREM2 drives microglia response to amyloid-β via SYK-dependent and -independent pathways
- Large-scale CSF proteome profiling identifies biomarkers for accurate diagnosis of frontotemporal dementia
- VCP/p97 is essential for maturation of ubiquitin-containing autophagosomes and this function is impaired by mutations that cause IBMPFD
- TREM2 brain transcript-specific studies in AD and TREM2 mutation carriers
- High‐frequency oscillations >250 Hz in people with Down syndrome and associated Alzheimer's disease dementia
- MRI volumes of the hippocampus and amygdala in adults with Down's syndrome with and without dementia
- Myo-inositol as a spectroscopic marker of neuroinflammation in frontotemporal lobar degeneration