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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Elimination of extracellular aggregates and apoptotic neural membranes without inflammation is crucial for brain tissue homeostasis.
Why it matters
This review describes microglial immunoreceptor ITAM and inhibition motif signaling in neuroinflammation, including TREM2 signaling via DAP12 to activate phagocytosis. It is a review of mechanisms and reports no treatment, cure or prevention for Alzheimer's disease.
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Patients with Alzheimer's disease (AD) exhibit substantial accumulation of amyloid-beta (Abeta) plaques in the brain.
Why it matters
In a mouse model of Alzheimer's disease, immunization with amyloid-beta caused T cells to gather at plaques and enhanced plaque clearance. This is an early animal study and does not yet show that this approach treats Alzheimer's disease in people.
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BACE1 (beta-site amyloid precursor protein-cleaving enzyme 1) is a membrane-tethered member of the aspartyl proteases, essential for the production of beta-amyloid, a toxic peptide that accumulates in the brain of subjects affected by Alzheimer disease.
Why it matters
This laboratory study describes how ubiquitin regulates GGA3-mediated degradation of BACE1, the enzyme essential for producing beta-amyloid. It is cell and molecular work and does not show that altering this pathway treats, cures or prevents Alzheimer's disease in patients.
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As brain testosterone plays both androgenic and estrogenic actions due to its conversion into estrogen via aromatase naturally, it is unclear that the age-related reduction of testosterone increased risk of Alzheimer's disease (AD) in men is mediated through androgen alone or both androgen and estrogen mechanisms.
Why it matters
In a mouse model of Alzheimer's disease, blocking the conversion of testosterone into estrogen reduced brain plaques and improved cognitive function. These are animal results, so it is not yet known whether the same approach would work or be safe in people.
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The results suggest a broad impairment in EF in adolescents with DS, and are consistent with several similar studies conducted with adults with DS.
Why it matters
This study found that adolescents with Down syndrome performed worse than typically developing children on several tests of executive function, such as planning and working memory. The results are about thinking skills in adolescents and do not test or propose a treatment for Alzheimer's disease.
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For studying rare hereditary Alzheimer's disease (AD), transgenic (Tg) animal models overexpressing amyloid-beta protein precursor (AbetaPP) followed by increased amyloid-beta (Abeta) formation are used.
Why it matters
In a transgenic mouse model of Alzheimer's disease, an insulin-resistant brain state induced by streptozotocin worsened Alzheimer-like changes. This is animal research and does not establish any treatment, cure, or prevention for people.
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Both sporadic and familial Alzheimer's disease (AD) patients exhibit increased chromosome aneuploidy, particularly trisomy 21, in neurons and other cells.
Why it matters
In transgenic mice and transfected cells, familial Alzheimer's disease mutations in APP induced chromosome mis-segregation and aneuploidy, and adding synthetic amyloid-beta peptide to cultured cells caused rapid chromosome mis-segregation including trisomy 21. The authors conclude that amyloid-beta-induced microtubule dysfunction leads to aneuploid neurons and may contribute to the pathogenesis of Alzheimer's disease.
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The human GFAP splice variants GFAPDelta164 and GFAPDeltaexon6 both result in a GFAP protein isoform with a unique out-of-frame carboxy-terminus that can be detected by the GFAP+1 antibody.
Why it matters
This study found that an antibody previously thought to detect a GFAP form in neurons was actually cross-reacting with neurofilament-L, and a purified version revealed a specific astrocyte subtype in human brain. It is a laboratory methods study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system (CNS) can result in neurological dysfunction with devastating consequences in a significant proportion of individuals with acquired immune deficiency syndrome.
Why it matters
This review describes how HIV-1 infection in the central nervous system causes damage indirectly through activated macrophage/microglia cells that release neurotoxic mediators. It concerns HIV-related neurological dysfunction and reports no treatment, cure or prevention for Alzheimer's disease.
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The amyloid precursor protein (APP) plays a central role in Alzheimer disease (AD) pathogenesis because sequential cleavages by beta- and gamma-secretase lead to the generation of the amyloid-beta (Abeta) peptide, a key constituent in the amyloid plaques present in brains of AD individuals.
Why it matters
Forcing the amyloid precursor protein to form dimers decreased amyloid-beta production in this laboratory study. This points to amyloid precursor protein dimerization as a possible way to lower amyloid-beta, but it is early cell-based work and not a treatment.
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We assessed the regional brain atrophy in mouse lemur primates from 4.7T T2-weighted magnetic resonance images.
Why it matters
This study in mouse lemur primates described age-related brain atrophy on MRI and suggested intracellular amyloid deposition was more closely linked to it than extracellular amyloid or tau. It is animal research and does not test any treatment, cure or prevention for Alzheimer's disease in people.
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Down syndrome (DS) is the most frequent cause of mental retardation in man.
Why it matters
This review concludes that the immune system in children with Down syndrome is likely deficient from the beginning, rather than only showing early aging. It discusses immune findings and does not report a treatment or cure for Alzheimer's disease.
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The proteinopathy sporadic Parkinson's disease (sPD) is the second most frequent degenerative disorder of the human nervous system after Alzheimer's disease.
Why it matters
This review describes the distribution of Lewy body pathology in sporadic Parkinson's disease and notes that cognitive decline and dementia can occur. It is about the pathology of Parkinson's disease and does not test any treatment or prevention for Alzheimer's disease.
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We have recently identified a novel form of post-translational regulation of BACE1 (beta-site amyloid precursor protein-cleaving enzyme 1), a membrane protein that acts as the rate-limiting enzyme in the generation of the Alzheimer disease amyloid beta-peptide.
Why it matters
Two acetyltransferases, ATase1 and ATase2, were identified that acetylate nascent BACE1 and protect it from degradation by PCSK9/NARC-1, allowing it to reach the Golgi apparatus. This is basic cell biology on how BACE1 levels are regulated and offers no treatment or prevention.
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The brain-derived neurotrophic factor gene (BDNF) is one of many genes thought to influence synaptic plasticity in the adult brain and shows a common single nucleotide polymorphism (BDNF Val66Met) in the normal population that is associated with differences in hippocampal volume and episodic memory.
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Osteoporosis (OP) is a common age-related systemic skeletal disease, with a strong genetic component, characterised by loss of bone mass and strength, which leads to increased bone fragility and susceptibility to fracture.
Why it matters
This study used microarrays to compare gene expression in bone from people with hip fragility fractures and age-matched controls, in the context of osteoporosis. It is not about Alzheimer's disease and reports no treatment, cure, or prevention for it.
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We have recently identified a new form of post-translational regulation of BACE1 (beta-site amyloid precursor protein (APP)-cleaving enzyme 1), a membrane protein that acts as the rate-limiting enzyme in the generation of the Alzheimer disease amyloid beta-peptide (Abeta).
Why it matters
This laboratory work describes how the enzyme PCSK9 helps dispose of non-acetylated BACE1, the enzyme that limits production of amyloid beta-peptide. It identifies a basic cell mechanism, not a treatment, and was not tested in patients.
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Pharmacological modulation of the GABA(A) receptor has gained increasing attention as a potential treatment for central processes affected in Alzheimer disease (AD), including neuronal survival and cognition.
Why it matters
In laboratory work, the drug etazolate acted through GABA(A) receptors to increase the nonamyloidogenic alpha-secretase pathway and release sAPPalpha. This is early pharmacological research and does not yet show a treatment, cure, or prevention for Alzheimer's disease.
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An enigmatic feature of age-related neurodegenerative diseases is that they seldom, if ever, are fully manifested in nonhuman species under natural conditions.
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Central nervous system (CNS) human immunodeficiency virus type 1 (HIV-1) infection begins during primary viremia and continues throughout the course of untreated systemic infection.
Why it matters
Combination antiretroviral therapy usually suppresses HIV in cerebrospinal fluid, reduces the incidence of AIDS dementia complex, and can prevent neurological progression or lead to recovery in those who have it. This concerns HIV-associated dementia, not Alzheimer's disease, and does not address treating, curing, or preventing Alzheimer's.
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Macrophage recognition of Salmonella enterica serovar Typhimurium leads to a cascade of signaling events, including the activation of Src family and Syk kinases and the production of reactive oxygen species (ROS), which are critical for host innate defense during early stages of bacterial infection.
Why it matters
This study showed that the innate immune response of macrophages to Salmonella Typhimurium, including reactive oxygen species production, requires TREM2 and DAP12. It is about bacterial infection in mice and does not address treating, curing or preventing Alzheimer's disease.
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An 82-year-old man presented with progressive changes in personality, social conduct, and executive function with preservation of memory, deteriorating from baseline to requiring acute hospitalization within 6 months.
Why it matters
This case report describes one patient with frontotemporal-dementia-like symptoms who had elevated antibodies to neuronal voltage-gated potassium channels, suggesting a potentially reversible autoimmune encephalopathy. It is a single case and does not establish a treatment, cure, or prevention for Alzheimer's disease.
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Intracellular aggregation of the microtubule-associated protein tau into filamentous inclusions is a defining characteristic of Alzheimer disease.
Why it matters
This cell culture study used a small molecule to drive tau aggregation in order to test whether tau aggregates are directly toxic to cells. It is early laboratory work and does not test any treatment, cure, or prevention in people.
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Selective increases in soluble Abeta(1-42) after TBI may predispose individuals with a brain injury to Alzheimer disease pathology.
Why it matters
In brain tissue from people who had severe traumatic brain injury, those with cortical amyloid plaques had higher levels of soluble amyloid-beta42 but not amyloid-beta40. This small human tissue study links severe head injury to changes in a form of amyloid, but it does not show that these changes cause Alzheimer's disease or that treating them would help.
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Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging.
Why it matters
This review lists dementia and Alzheimer's disease among many disorders sharing underlying mechanisms of reactive oxygen species production and accumulation of mitochondrial DNA damage. It suggests antioxidant therapies hold promise for improving mitochondrial performance, but reports no tested treatment, cure or prevention for Alzheimer's disease.
From across this topic
9 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 9. The same 9 appear here every time.
- Microglial histone H3K18 crotonylation promotes STAT1 expression and induces cognitive deficit in Alzheimer disease
- Glial Fibrillary Acidic Protein and Neurofilament Light Reference Intervals in Healthy Individuals
- A fibril-specific, conformation-dependent antibody recognizes a subset of Abeta plaques in Alzheimer disease, Down syndrome and Tg2576 transgenic mouse brain
- β-Secretase Cleavage of Alzheimer's Amyloid Precursor Protein by the Transmembrane Aspartic Protease BACE
- Integrated bio-cooperative robotic platform for virtual cognitive training in Parkinson's disease: design and methodology of the OPERA project
- Tau protein in cerebrospinal fluid: a biochemical marker for axonal degeneration in Alzheimer disease?
- Tau protein isoforms, phosphorylation and role in neurodegenerative disorders
- Differential effects of partial and complete loss of TREM2 on microglial injury response and tauopathy
- Fine Particle Exposure and Clinical Aggravation in Neurodegenerative Diseases in New York State