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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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.
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The amyloidogenic pathway leading to the production and deposition of Abeta peptides, major constituents of Alzheimer disease senile plaques, is linked to neuronal metal homeostasis.
Why it matters
This laboratory study showed that BACE1 interacts with the copper chaperone for superoxide dismutase-1 and binds copper. It describes a molecular interaction related to metal handling and does not test any treatment, cure, or prevention.
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Single-gene mutations can produce human progeroid syndromes--phenotypes that mimic usual or "normative" aging.
Why it matters
This review discusses single-gene mutations that cause human progeroid syndromes, such as Werner syndrome, which mimic aspects of aging. It does not report a treatment, cure or prevention for Alzheimer's disease.
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Converging lines of research suggest that the hippocampal complex (HC) may have a role in the pathophysiology of major depressive disorder (MDD).
Why it matters
This review suggests the hippocampus may be involved in major depression, with animal studies indicating that stress hormones can reduce neurogenesis and that antidepressants may increase it. It does not report any treatment or prevention for Alzheimer's disease.
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Inhaled anesthetics enhance oligomerization and cytotoxicity of Alzheimer disease-associated peptides.
Why it matters
In laboratory experiments, the inhaled anesthetics halothane and isoflurane increased the clumping and toxicity of amyloid beta, a protein linked to Alzheimer's disease. This is early in-vitro work, and the authors call for further evaluation of the interaction between neurodegenerative disorders, dementia, and inhalational anesthesia.
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Autism is a neurodevelopmental disorder characterized by impairments in reciprocal social interaction, deficits in verbal and nonverbal communication, and a restricted repertoire of activities or interests.
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APP is an important locus predicting the age at onset of dementia in people with Down syndrome.
Why it matters
In people with Down syndrome, the number of tetranucleotide repeat alleles in the APP gene was associated with a 13-year difference in the age at onset of dementia. The authors conclude that APP is an important locus predicting the age at onset of dementia in people with Down syndrome, but the study does not test a treatment or cure.
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43/100
Beta-amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology.
Why it matters
In fruit flies engineered to express APP, BACE and presenilins, beta-amyloid plaques and age-dependent neurodegeneration appeared, and secretase inhibitors changed the severity of these effects. This is an animal model, so it does not show that such inhibitors help people with Alzheimer's disease.
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43/100
Diffusion tensor measurements correlate better with cognition than conventional MRI measures.
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These data show a new role for DAP12 signaling in regulating formation of multinucleated osteoclasts.
Why it matters
This study found that the signaling protein DAP12 helps regulate the formation of multinucleated osteoclasts, which are bone cells. It concerns bone biology in mice and cells, not Alzheimer's disease, so it does not directly inform Alzheimer's treatment, cure or prevention.
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Aged individuals with Down syndrome (DS) develop senile plaques and neurofibrillary tangles consistent with Alzheimer disease (AD).
Why it matters
In hippocampal tissue from 15 people with Down syndrome aged 5 months to 67 years, the earliest tau accumulation in middle age occurred in the outer molecular layer, followed later by an increase in GAP-43 associated with entorhinal neuron loss. The authors suggest compensatory growth responses may occur before extensive Alzheimer's pathology, but this is an observational tissue study and does not test a treatment.
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Compared with controls, relatives, particularly from multiplex families, had significantly smaller left hippocampi.
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.
- Optical Coherence Tomography Reveals Retinal Neuroaxonal Thinning in Frontotemporal Dementia as in Alzheimer's Disease
- TREM2 Modulation Remodels the Tumor Myeloid Landscape Enhancing Anti-PD-1 Immunotherapy
- Tau, Amyloid Beta and Deep Brain Stimulation: Aiming to Restore Cognitive Deficit in Alzheimer's Disease
- Genome-wide association studies of cerebral white matter lesion burden: the CHARGE consortium
- Cyclophilin D deficiency improves mitochondrial function and learning/memory in aging Alzheimer disease mouse model
- Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease
- ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import
- Rapamycin alleviates toxicity of different aggregate-prone proteins
- Efficacy and safety of programmable compared with fixed anti-siphon devices for treating idiopathic normal-pressure hydrocephalus (iNPH) in adults - SYGRAVA: study protocol for a randomized trial
- Biomagnification of cyanobacterial neurotoxins and neurodegenerative disease among the Chamorro people of Guam