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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Amyloid beta-peptide (Abeta) accumulation leads to neurodegeneration and Alzheimer disease; however, amyloid metabolism is a dynamic process and enzymic mechanisms exist for Abeta removal.
Why it matters
In two neuroblastoma cell lines, the amyloid precursor protein intracellular domain bound directly to the neprilysin promoter in high-expressing cells but not in low-expressing cells. This is a cell-based finding about amyloid removal and does not show that altering neprilysin treats or prevents Alzheimer's disease.
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The receptor for advanced glycation end products (RAGE) is a 55-kDa type I membrane glycoprotein of the immunoglobulin superfamily.
Why it matters
This study describes how the RAGE receptor is shed from cells by metalloproteinases, a process relevant to conditions including Alzheimer's disease. It is laboratory cell research and does not test any treatment or cure.
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Inclusion body myopathy (IBM) associated with Paget disease of the bone (PDB) and frontotemporal dementia (FTD) (now called IBMPFD), is a progressive autosomal dominant disorder that was recently identified as being caused by mutations in the VCP (p97 or CDC48) gene which plays a key role in the ubiquitin-proteasome dependent degradation of cytosolic proteins and in the retro translocation of misfolded proteins from the endoplasmic reticulum into the cytoplasm.
Why it matters
This review describes inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia, caused by mutations in the VCP gene, with myopathy in about 90% of affected people and premature frontotemporal dementia in a third. It concerns a distinct inherited disorder and does not address treating, curing or preventing Alzheimer's disease.
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Amyloid precursor protein (APP) mis-processing and aberrant tau hyperphosphorylation are causally related to the pathogenesis and neurodegenerative processes that characterize Alzheimer's disease (AD).
Why it matters
In a rat neuronal cell line expressing human tau, glucocorticoids triggered Alzheimer's-like changes including abnormal amyloid precursor protein processing and tau hyperphosphorylation. This is cell-based work on a possible contributing factor and does not test any treatment, cure, or prevention.
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Autopsy studies have shown that about 55% of patients with frontotemporal lobar degeneration (FTLD) and 25% of patients with Alzheimer's disease (AD) harbour TDP-43 immunoreactive pathological changes in their brains.
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Abnormal deposition of alpha-synuclein in neurons and glia is implicated in many neurological diseases, such as Parkinson's disease and Dementia with Lewy bodies.
Why it matters
This laboratory study shows that neurons, astrocytes and microglia can clear extracellular alpha-synuclein aggregates, with microglia degrading them fastest, and that LPS activation slowed degradation. It concerns alpha-synuclein, linked to Parkinson's disease and dementia with Lewy bodies, and reports no Alzheimer's treatment or outcome.
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Temporal lobe epilepsy (TLE) is considered primarily a limbic disorder.
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DNA damage is a form of cell stress and injury that has been implicated in the pathogenesis of many neurologic disorders, including amyotrophic lateral sclerosis, Alzheimer disease, Down syndrome, Parkinson disease, cerebral ischemia, and head trauma.
Why it matters
This review notes that DNA damage has been linked to Alzheimer disease and other neurologic disorders, but that most data show only associations and its role as a direct cause of neuron death remains unclear. It identifies no treatment or prevention for Alzheimer's disease.
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Exercise is a treatment paradigm that can ameliorate cognitive dysfunction in Alzheimer disease (AD) and AD mouse models.
Why it matters
In aged Tg2576 mice with existing Alzheimer's-like pathology, short-term voluntary exercise improved cognition and altered neuroinflammation. Because this was done in mice, it does not establish that exercise produces the same cognitive benefit in people with Alzheimer's disease.
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As the average ages of North Americans and Europeans continue to rise; similarly the incidence of "old age" associated illnesses likewise increases.
Why it matters
Alzheimer's disease, Parkinson's disease and stroke affect different brain regions and cell types early on, but their final stages may share similar cellular and molecular processes leading to neuronal death. The paper discusses TNF-alpha inhibition as a possible treatment strategy, but no trial results in patients are reported here.
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In a previous study, we found that human neural stem cells (HNSCs) exposed to high concentrations of secreted amyloid-precursor protein (sAPP) in vitro differentiated into mainly astrocytes, suggesting that pathological alterations in APP processing during neurodegenerative conditions such as Alzheimer's disease (AD) may prevent neuronal differentiation of HNSCs.
Why it matters
In this mouse study, treatment with (+)-phenserine reduced amyloid precursor protein and GFAP levels in the hippocampus and increased neuronal differentiation of transplanted human neural stem cells. Because it is an animal study, it does not show whether this approach would work in people with Alzheimer's disease.
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Mutation of the amyloid precursor protein (APP), presenilin-1, or presenilin-2 results in the development of early onset autosomal dominant forms of Alzheimer disease (AD).
Why it matters
This laboratory work found that the amount of substrate affects the ratio of Abeta42 to Abeta40 produced by gamma-secretase, and that different mutations show distinct reaction behaviors. It describes a mechanism and reports no treatment, cure or prevention for Alzheimer's disease.
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Immunotherapy against beta-amyloid peptide (Abeta) is a leading therapeutic direction for Alzheimer disease (AD).
Why it matters
Treating Alzheimer's disease mutant cells or primary neurons with amyloid-beta antibodies decreased intracellular amyloid-beta levels. This is a laboratory cell study and does not demonstrate any treatment, cure, or prevention for Alzheimer's disease in people.
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Ectodomain shedding and intramembrane proteolysis of the amyloid precursor protein (APP) by alpha-, beta- and gamma-secretase are involved in the pathogenesis of Alzheimer disease (AD).
Why it matters
The study shows that interleukin-1 receptor II can be proteolytically processed by alpha-, beta-, and gamma-secretase in a manner similar to amyloid precursor protein. This is a laboratory finding about processing and does not establish any treatment, cure, or prevention for Alzheimer's disease.
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Aberrations in hippocampal asymmetry and left hippocampal volumes were found for adolescent heavy drinkers.
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43/100
In chronic liver failure, manganese accumulation is responsible for the pallidal MRI T1 hyperintensity.
Why it matters
In seven chronic liver failure cases, pallidal T1 hyperintensity was linked to sevenfold higher pallidal manganese concentrations, with manganese also elevated in other brain regions and mostly negative alpha-synuclein and tau staining. This concerns manganese accumulation in liver failure rather than Alzheimer's disease, and offers no treatment, cure or prevention for it.
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43/100
These results provide a link between tau autoimmunity and tauopathy-like abnormalities and indicate potential dangers of using tau for immunotherapy.
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Type 2 diabetes is associated with cognitive dysfunction and increases the risk of dementia in the elderly.
Why it matters
In 95 non-demented elderly people with type 2 diabetes, this study explored relationships between diabetes clinical profiles, cognitive function, white matter hyperintensities and subcortical brain atrophy. The available text does not report whether any intervention affected cognition or dementia risk.
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Defects in mitochondrial oxidative metabolism, in particular decreased activity of cytochrome c oxidase, have been reported in Alzheimer disease tissue and in cultured cells that overexpress amyloid precursor protein.
Why it matters
This laboratory study examined heat shock proteins and related molecular chaperones in preventing intracellular beta-amyloid-induced inhibition of complex IV and limiting apoptosis in cultured neurons. It is cell-based work and does not show that these chaperones treat, cure or prevent Alzheimer's disease in people.
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Gamma-secretase is a multiprotein complex responsible for the intramembranous cleavage of the amyloid precursor protein and other type I transmembrane proteins.
Why it matters
This laboratory work examines how parts of presenilin may form a water-containing cavity needed for γ-secretase to cut proteins inside the membrane. It is basic structural research and does not show any treatment, cure, or prevention for Alzheimer's disease.
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Elevated levels of NO produced within the central nervous system (CNS) are associated with the pathogenesis of neuroinflammatory and neurodegenerative human diseases such as multiple sclerosis, HIV dementia, brain ischemia, trauma, Parkinson's disease, and Alzheimer's disease.
Why it matters
This review describes how glial cells express inducible nitric oxide synthase and produce high levels of nitric oxide in response to inflammatory stimuli, a process linked to several neurodegenerative diseases including Alzheimer's disease. It is a mechanistic review and reports no treatment or patient outcome.
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43/100
Emerging evidence indicates that cholesterol metabolism affects the pathogenesis of Alzheimer's disease (AD).
Why it matters
In Tg2576 mice, lacking the LDL receptor led to high cholesterol, more amyloid deposits and worse spatial learning after amyloid appeared. This is animal work, so it does not yet show whether targeting the LDL receptor would help people.
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Familial frontotemporal dementia (FTD), characterized by tau-negative, ubiquitin-positive inclusions at autopsy, is linked to a chromosomal region at 17q21 (FTDU-17), encompassing the gene encoding the microtubule associated protein tau, MAPT.
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It is well established that oxidative stress plays a key role in the degenerative neuronal death and progression of Alzheimer's disease (AD), although it is not clear if it is the primary triggering event in the pathogenesis of this disorder.
Why it matters
This study found more DNA damage, including oxidative damage, in blood cells of people with MCI and Alzheimer's disease than in controls. It supports the idea that oxidative stress occurs early but does not test any treatment or show that antioxidants help.
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43/100
The amyloid precursor protein (APP) is proteolytically processed by beta- and gamma-secretases to release amyloid beta, the main component in senile plaques found in the brains of patients with Alzheimer disease.
Why it matters
This laboratory study found that activating the P2Y2 nucleotide receptor enhances alpha-secretase-dependent processing of the amyloid precursor protein. This is cell-based work and does not test whether this approach treats or prevents Alzheimer's disease in people.
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.
- Intersection of pathological tau and microglia at the synapse
- Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration
- Expression of intercellular adhesion molecule (ICAM)-1 by a subset of astrocytes in Alzheimer disease and some other degenerative neurological disorders
- Corticostriatal synaptic function in mouse models of Huntington's disease: early effects of huntingtin repeat length and protein load
- Dissociable contribution of plasma NfL and p-tau181 to cognitive impairment in Parkinson's disease
- Associations between tau PET and CSF MTBR243 do not vary by sex
- TREM2 Function in Alzheimer's Disease and Neurodegeneration
- Controlled cortical impact results in an extensive loss of dendritic spines that is not mediated by injury-induced amyloid-beta accumulation
- Brain Functional Magnetic Resonance Imaging Highlights Altered Connections and Functional Networks in Patients With Hypertension
- Brain-derived neurotrophic factor val66met polymorphism and volume of the hippocampal formation