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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Hyperphosphorylation of microtubule-associated protein tau is one of the major pathological events in Alzheimer's disease (AD) and other related neurodegenerative diseases, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17).
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Neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and frontotemporal dementias (FTD), are considered distinct entities, however, there is increasing evidence of an overlap from the clinical, pathological and genetic points of view.
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40/100
The early stages of Alzheimer's disease are characterised by impaired synaptic plasticity and synapse loss.
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Little is known about how changes in DNA methylation mediate risk for human diseases including dementia.
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Intracerebral-ventricular (ICV) injection of streptozotocin (STZ) induces an insulin-resistant brain state that may underlie the neural pathogenesis of sporadic Alzheimer disease (AD).
Why it matters
In a streptozotocin-induced rat model of Alzheimer-like changes, geniposide improved learning and memory deficits, reduced tau phosphorylation and decreased apoptosis via the GSK3β pathway. This is animal research only, so it does not show that geniposide treats, cures or prevents Alzheimer disease in people.
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Altered synaptic function is considered one of the first features of Alzheimer disease (AD).
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40/100
Our findings support the theory that alterations in hippocampal glutamate levels potentially account for structural deficits in the hippocampus observed in schizophrenia neuroimaging studies.
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DNAX-activating protein of 12 kD (DAP12) is an immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptor protein found in myeloid cells and natural killer cells, and it couples to various receptors that mediate either cellular activation or inhibition.
Why it matters
This laboratory study in macrophages showed that a physical interaction between DOK3 and DAP12 is needed to inhibit lipopolysaccharide signaling. It is basic cell research and does not show a treatment or cure for Alzheimer's disease.
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Traumatic brain injury (TBI) results in significant disability due to cognitive deficits particularly in attention, learning and memory, and higher-order executive functions.
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Alzheimer's disease (AD) is the most common type of age-related dementia.
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Our case studies highlight that not all athletes with history of repeated concussions and neurological symptomology present neuropathological changes of CTE.
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40/100
The RCAN1 gene encodes three different protein isoforms: RCAN1-4, RCAN1-1L, and RCAN1-1S. RCAN1-1L is the RCAN1 isoform predominantly expressed in human brains.
Why it matters
This review proposes that prolonged high levels of the RCAN1-1 protein may promote neurodegeneration in Alzheimer disease and Down syndrome. It suggests that studying RCAN1 overexpression in models may help understand mechanisms, but it does not report a treatment or cure.
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A hallmark of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide in the brain.
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Methylation is a post-translational modification that can affect numerous features of proteins, notably cellular localization, turnover, activity, and molecular interactions.
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The E4 allele of the ApoE gene has consistently been shown to be related to an increased risk of Alzheimer's disease (AD).
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Interaction between Aβ and the receptor for advanced glycation end products (RAGE) has been implicated in neuronal degeneration associated with this disease.
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Our observations provide a necessary and timely insight into cellular mechanisms that underlie the initial pathological events that lead to synaptic dysfunction in Alzheimer's disease.
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Acute injections of Aβ oligomers had no effect on p-tau epitopes but did result in elevation of phosphorylated/activated GSK3 (pGSK3).
Why it matters
In a mouse model of tauopathy, chronic infusion of amyloid beta oligomers into the hippocampus caused 3- to 4-fold elevations in several p-tau isoforms with no changes in total tau levels, while acute injections had no effect on p-tau epitopes. The authors suggest that even brief elevations in amyloid beta production may have enduring impact on the risk for tauopathy, though this is animal research.
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40/100
Neurofibrillary lesions of abnormal Tau are hallmarks of Alzheimer disease and frontotemporal dementias.
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Childhood maltreatment or abuse is a major risk factor for mood, anxiety, substance abuse, psychotic, and personality disorders, and it is associated with reduced adult hippocampal volume, particularly on the left side.
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In these, at least one cardinal symptom or sign of PSP later emerges, associated with smaller midbrain volume and increased pons/midbrain ratio.
Why it matters
Three autopsy-proven cases of progressive supranuclear palsy initially presented as behavioral variant frontotemporal dementia, with PSP symptoms emerging up to 5 years later. This highlights diagnostic challenges and does not address treating, curing, or preventing Alzheimer's disease.
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Florbetapir PET can be used to detect increased cerebral-to-cerebellar fibrillar Aβ burden in a Down syndrome patient with Alzheimer disease, even in the presence of frequent amyloid angiopathy and diffuse plaques in the cerebellum.
Why it matters
In one 55-year-old man with Down syndrome and Alzheimer disease, a florbetapir PET scan taken 14 days before he died showed heavy amyloid in cortical, striatal and thalamic regions, "similar to that reported for patients with late-onset Alzheimer disease," and this matched his autopsy. The scan did not pick up the frequent amyloid deposits his autopsy found in the cerebellum. This is a single case. It suggests the scan can work in Down syndrome but does not measure how accurate it is, and it tests no treatment.
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The genetic origin of the three common variants of the human apolipoprotein E (apoE) protein, known as E2, E3 and E4, was understood in 1981, and since the mid 1980s these are probably the most-studied protein variants in human races.
Why it matters
This review describes the genetics of the APOE variants E2, E3, and E4 and reports a rare fourth variant, E3r, found in a few families. It is background genetics and does not report a treatment or cure.
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40/100
The emerging histomorphologic features of our CTE cohort may specify histologic criteria for CTE diagnosis, may identify emerging histologic variants of CTE and may facilitate more objective surveillance and accurate identification of sentinel CTE cases.
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Tauopathies are neurodegenerative disorders characterized by the accumulation of abnormal tau protein leading to cognitive and/or motor dysfunction.
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.
- Typical and atypical pathology in primary progressive aphasia variants
- Putting proteins in their place: palmitoylation in Huntington disease and other neuropsychiatric diseases
- Clinicopathological and imaging correlates of progressive aphasia and apraxia of speech
- Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis
- High-definition Transcranial Direct Current Stimulation Improves Cognitive Function in Patients with Cerebral Small Vessel Disease: An Open-label Pilot Study Informed by Cross-sectional Analysis
- Role of the low-density lipoprotein receptor-related protein in beta-amyloid metabolism and Alzheimer disease
- Neuropathological perspectives on neuroinflammation and tau molecular imaging in frontotemporal lobar degeneration
- A head-to-head comparison of multiple amyloid PET radiotracers for Down syndrome clinical trials
- Aggregation of detergent-insoluble tau is involved in neuronal loss but not in synaptic loss
- Coenzyme Q10 and oxidative imbalance in Down syndrome: biochemical and clinical aspects