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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Trem2 is an orphan, DAP12 associated receptor constitutively expressed in vivo by subsets of microglia in the healthy adult murine CNS and in vitro by subsets of oligodendrocytes in neonatal mixed glial cultures.
Why it matters
This study describes when and where TREM2 and DAP12 are expressed in the developing mouse brain and discusses Nasu-Hakola disease. It is early animal work and does not show that any treatment prevents or cures Alzheimer's disease.
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Down-regulation of protein phosphatase 2A (PP2A) is thought to play a critical role in tau hyperphosphorylation in Alzheimer's disease (AD).
Why it matters
This study found that a phosphorylated form of PP2A accumulates in neurons with early tangles or tangles in Alzheimer's disease. It is observational tissue work and does not test any treatment or show that targeting PP2A would help patients.
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40/100
Intraneuronal accumulation of phosphorylated Tau protein is a molecular pathology found in many forms of dementia, including Alzheimer disease.
Why it matters
This laboratory study examined how BAG-1 associates with the Hsc70.Tau complex and regulates proteasomal degradation of Tau protein. It is basic molecular research and does not test any treatment, cure, or prevention in people.
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Cholecystokinin (CCK) involvement in depression-like disorders is poorly documented.
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The involvement of regulatory T cells (Treg) in autoimmune-disease development has been demonstrated.
Why it matters
This study found a higher frequency of regulatory T cells in elderly people and increased suppressive activity in patients with Alzheimer's and Parkinson's disease, which are accompanied by neuroinflammation. It describes immune changes but does not report a treatment, cure, or prevention for Alzheimer's disease.
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Pituitary adenylate cyclase-activating polypeptide (PACAP, ADCYAP1: adenylate cyclase-activating polypeptide 1), a neuropeptide with neurotransmission modulating activity, is a promising schizophrenia candidate gene.
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Data on behavioral changes after thalamic lesion are sparse and largely based on isolated reports of patients with thalamic strokes.
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The findings are consistent with the presence of smaller hippocampal and amygdalar volumes in patients with dissociative identity disorder, compared with healthy subjects.
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Neurodegenerative diseases are often classified based on the abnormal accumulation of synuclein or tau.
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The mind involves the whole body and two-way communication between the brain and the cardiovascular, immune, and other systems via neural and endocrine mechanisms.
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The presence of activated microglia in postmortem Alzheimer disease specimens is used to support the argument that inflammation contributes to Alzheimer pathogenesis.
Why it matters
This review of transgenic mouse models notes that microglial activation and inflammation increase with age alongside amyloid plaques, but that boosting these inflammatory reactions sometimes reduced pathology rather than worsening it. It is based on animal models and reports no treatment, cure or prevention for people.
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Amyloid-beta peptide is elevated in the brains of patients with Alzheimer disease and is believed to be causative in the disease process.
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40/100
In fetuses with Down syndrome, neurons fail to show normal dendritic development, yielding a "tree in winter" appearance.
Why it matters
This review discusses how beta-amyloid precursor protein and S100B, both from chromosome 21, are implicated in the neuronal and plaque changes in Down syndrome, with betaAPP gene triplication necessary but perhaps not sufficient for Alzheimer pathology. It is a mechanistic review and tests no treatment or prevention.
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Cholinesterase inhibitors positively affect cognition in Alzheimer's disease (AD) and other conditions, but no controlled functional MRI studies have examined where their effects occur in the brain.
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40/100
Roles for excitotoxicity and inflammation in Alzheimer's disease have been hypothesized.
Why it matters
This laboratory study found that amyloid beta-peptide caused cultured microglia to release D-serine, a coagonist at NMDA glutamate receptors, and tested effects on rat hippocampal neurons. It is early cell-culture work and does not show any treatment, cure or prevention for Alzheimer's disease in people.
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Thorn-shaped astrocytes (TSA) are glial fibrillary tangles that contain abnormally phosphorylated and aggregated microtubule-associated tau protein.
Why it matters
This autopsy study found that thorn-shaped astrocytes, a form of tau pathology in glial cells, become more common with age and were present in about half of people aged 75-98. The development of this pathology was not correlated with the severity of Alzheimer-related cortical pathology, so it appears to be a distinct age-related change rather than a direct driver of Alzheimer's disease.
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40/100
We report a case of rapidly progressive frontotemporal dementia presenting at age 33 years.
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Dementia of the Alzheimer type (DAT) is common in older persons with Down syndrome (DS).
Why it matters
In 55 older people with Down syndrome, this study found an association in females between apolipoprotein E type and thyroid status, with E2 linked to lower and E4 to higher rates of hypothyroidism. It did not test any treatment or prevention for Alzheimer's disease.
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Twelve patients with refractory temporal lobe epilepsy and unilateral hippocampal sclerosis had repeat volumetric magnetic resonance imaging scans after a mean of 3.4 years to determine whether progressive hippocampal volume loss occurred.
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High-resolution magnetic resonance microscopy (MRM) was used to determine regional brain volumetric changes in a mouse model of Alzheimer's disease.
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We describe a right-handed man who developed progressive nonfluent aphasia and apraxia of speech beginning at age 71.
Why it matters
This case report describes a man with progressive nonfluent aphasia and subsequent aphasic dementia who was found at autopsy to have atypical progressive supranuclear palsy pathology. It concerns diagnosis and pathology of a single case, not treating, curing, or preventing Alzheimer's disease.
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Neuregulin-1 (NRG-1) regulates developmental neuronal survival and synaptogenesis, astrocytic differentiation, and microglial activation.
Why it matters
This study found that neuregulin-1 and erbB4 immunoreactivity is associated with neuritic plaques in Alzheimer's brain and in a transgenic mouse model. It is observational work and does not test any treatment or show how to prevent the disease.
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40/100
The novel Drosophila mutant löchrig (loe) shows progressive neurodegeneration and neuronal cell death, in addition to a low level of cholesterol ester. loe affects a specific isoform of the gamma-subunit of AMP-activated protein kinase (AMPK), a negative regulator of hydroxymethylglutaryl (HMG)-CoA reductase and cholesterol synthesis in vertebrates.
Why it matters
In a Drosophila mutant, the neurodegenerative phenotype was modified by HMG-CoA reductase levels and suppressed by statin, and enhanced by a mutation in the fly amyloid precursor protein-like gene. This is a fruit fly study and does not show any treatment, cure, or prevention for Alzheimer's disease in humans.
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Within the last few years, there has been a growing interest in the neuroprotective effects of estrogen and the possible beneficial effects of estrogen in neurodegenerative diseases such as stroke, Alzheimer disease, and Parkinson disease.
Why it matters
This review discusses whether estrogen and selective estrogen receptor modulators such as tamoxifen and raloxifene can protect the brain, noting the mechanism is not clearly resolved. It reports no treatment, cure, or prevention for Alzheimer's disease.
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To address the question of whether beta-amyloid peptides also affect cholinergic neurotransmission in vivo, brain tissue from transgenic Tg2576 mice with Alzheimer plaque pathology at ages ranging from 7 to 24 months were examined by immuno- and histochemical staining for choline acetyltransferase (ChAT) and acetycholinesterase (AChE), by assaying cholinergic enzyme activities and high-affinity choline uptake as well muscarinic and nicotinic cholinergic receptor binding levels by quantitative autoradiography.
Why it matters
In Tg2576 mice, cortical and hippocampal activities of AChE and ChAT did not differ from non-transgenic mice, though high-affinity choline uptake was reduced in the hippocampus of 21-month-old transgenic mice. This was an animal study and reports no treatment, cure or prevention for Alzheimer's disease.
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.
- APOE ε4 carriers share immune-related proteomic changes across neurodegenerative diseases
- Differential effects of apolipoprotein E isoforms on metal-induced aggregation of A beta using physiological concentrations
- Association between insomnia and cognitive performance, gray matter volume, and white matter microstructure in cognitively unimpaired adults
- Improved accuracy of clinical diagnosis of Lewy body Parkinson's disease
- Tissue-specific expression patterns of the RAGE receptor and its soluble forms--a result of regulated alternative splicing?
- Loss of VPS13C Function in Autosomal-Recessive Parkinsonism Causes Mitochondrial Dysfunction and Increases PINK1/Parkin-Dependent Mitophagy
- Alpha-synuclein locus duplication as a cause of familial Parkinson's disease
- TauIQ: A Canonical Image Based Algorithm to Quantify Tau PET Scans
- Landscape of Intercellular Crosstalk in Healthy and NASH Liver Revealed by Single-Cell Secretome Gene Analysis
- Exaggerated inflammation, impaired host defense, and neuropathology in progranulin-deficient mice