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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The extracellular deposition of β-amyloid (Aβ) is one of the major characteristics in Alzheimer´s disease (AD).
Why it matters
In organotypic mouse brain slices, human Aβ42 spread into adjacent areas and activated glial cells, with most spread Aβ42 taken up by microglia and no degeneration of cholinergic neurons. This is laboratory research on how amyloid may spread, not a treatment or prevention for people.
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These data point to significant reductions in KLC1 in AD and AD-DS.
Why it matters
This study found normal levels of KIF5 but reduced levels of KLC1 in the brains of people with Alzheimer disease and with Alzheimer disease in Down syndrome, pointing to possible defects in anterograde transport. This is laboratory brain tissue work and does not show a treatment or cure.
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Alzheimer disease (AD) is characterized by the accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated tau, which together lead to neurodegeneration and cognitive decline.
Why it matters
In Tau22/5xFAD bigenic mice, a combination vaccine targeting both amyloid-beta and tau was tested to reduce pathology. This is preclinical animal work, and the text notes that phase 3 trials of approaches targeting either protein alone have so far failed to delay disease progression in humans.
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Activated Caspase-6 (Casp6) is associated with age-dependent cognitive impairment and Alzheimer disease (AD).
Why it matters
In aged mice with Caspase-6-induced cognitive impairment, methylene blue treatment reversed memory deficits and improved synaptic function and neuroinflammation. This is an animal study, so it does not show that methylene blue benefits people with Alzheimer disease.
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The control of viral infections in the brain involves the activation of microglial cells, the macrophages of the brain that are constantly surveying the central nervous system, and the production of amyloid-beta (Aβ) as an anti-microbial molecule.
Why it matters
In microglial cell models, HHV-6A infection induced amyloid-beta expression and microglial activation. This is laboratory cell work and does not establish a treatment or prevention for Alzheimer's disease.
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The heterogeneous functions of dermal myeloid cells in antigen presentation, and scavenging pathogens and cell debris places them centrally in cutaneous inflammation.
Why it matters
This study used single-cell RNA sequencing to describe myeloid cell diversity in healthy human skin. It does not study Alzheimer's disease and provides no information on treating, curing or preventing it.
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Microglia transform from homeostatic to disease-associated-microglia (DAM) profiles in neurodegeneration.
Why it matters
Using siRNA in primary microglia, this study examined how IRF1, LXRβ, and CEBPα regulate homeostatic and disease-associated microglial genes. This is a laboratory study of gene regulation and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Epilepsy is a chronic and severe neurological disorder that has negative effects on the autonomous activities of patients.
Why it matters
In a mouse hippocampal neuron model of epilepsy, up-regulating Trem2 inhibited neuronal apoptosis and reduced oxidative stress via the PI3K/Akt pathway. It does not test any treatment, cure, or prevention for Alzheimer's disease.
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Aggregation of the hyperphosphorylated protein tau into neurofibrillary tangles and neuropil threads is a hallmark of Alzheimer disease (AD).
Why it matters
This study characterized a tau-specific monoclonal antibody, CBTAU-24.1, isolated from the human memory B cell repertoire, and reported its crystal structure with a phospho-tau epitope. The work is laboratory-based and aims to shed light on molecular mechanisms of Alzheimer's disease pathogenesis, not to demonstrate a treatment.
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39/100
As a recently identified susceptibility gene for Alzheimer's disease (AD), triggering receptor expressed on myeloid cells 2 (TREM2) encodes an immune receptor that is uniquely expressed on microglia, functioning as a modulator of microglial functions including phagocytosis and inflammatory response.
Why it matters
In mice, reducing TREM2 made tau hyperphosphorylation worse, suggesting TREM2 may protect against tau pathology. This is early animal work, and the precise mechanisms remain largely unclear.
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Traumatic brain injury (TBI) is one of the leading causes of death and disability worldwide, and has emerged as a critical risk factor for multiple neurodegenerative diseases, particularly Alzheimer's disease (AD).
Why it matters
This review discusses how neuroinflammation after traumatic brain injury may contribute to Alzheimer's-like disease and notes that drug targets are being sought. It does not test a treatment or cure.
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Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD).
Why it matters
In mice and in people, plasma levels of neuronal pentraxin 1 were elevated in early Alzheimer's disease and mild cognitive impairment, and in mice the protein was reduced by dietary DHA supplementation. The authors propose NP1 as a possible synapse-related blood biomarker, but this is early research and does not establish any treatment.
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a member of the immunoglobulin superfamily and associates with TYRO protein tyrosine kinase-binding protein at the cell membrane to form a receptor signaling complex.
Why it matters
This study is about gastric cancer, not Alzheimer's disease. It found high TREM2 expression correlated with poor prognosis in gastric cancer, which does not inform Alzheimer's treatment.
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Recent genome-wide association studies revealed that Triggering receptor expressed on myeloid cells 2 (TREM2) was associated with Alzheimer's disease (AD) and other neurodegenerative diseases.
Why it matters
In 50 people with Alzheimer's disease and matched controls, the study examined DNA methylation of TREM2 and its gene expression in leukocytes. It is a small human study of a marker, not a test of any treatment, so it does not show how to treat, cure or prevent Alzheimer's.
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Genetic analyses showed that the triggering receptor expressed in myeloid cells 2 (TREM2) p.R47H variant increases the risk for Alzheimer's disease (AD).
Why it matters
This study measured mRNA and protein profiles of wild-type and p.R47H TREM2 in human brains to see whether the mutation affects expression or function. It is descriptive human tissue research and does not test a treatment.
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Current immunohistochemical techniques have made the identification of microglia possible in routinely processed tissue sections from human brains.
Why it matters
This review discusses microglia and brain macrophages and argues that microglial activation is not always the same as neuroinflammation. It offers no treatment or prevention findings for Alzheimer's disease.
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Accruing data indicate that radiation-induced consequences resemble pathologies of neurodegenerative diseases such as Alzheimer´s. The aim of this study was to elucidate the effect on hippocampus of chronic low-dose-rate radiation exposure (1 mGy/day or 20 mGy/day) given over 300 days with cumulative doses of 0.3 Gy and 6.0 Gy, respectively.
Why it matters
In an Alzheimer's mouse model, chronic low-dose-rate radiation changed the hippocampal phosphoproteome in ways that overlapped with Alzheimer's pathology, including inhibition of CREB signalling. This is animal work suggesting radiation may be a contributing risk factor, and it does not test any treatment, cure or prevention for people.
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PET amyloid imaging is increasingly used in research trials related to Alzheimer disease and has potential as a quantitative biomarker.
Why it matters
This describes a semiautomated method for measuring amyloid plaque binding on PET scans without needing a separate MRI scan for each person. The method's measurements correlated with amyloid levels measured at autopsy, which could help standardize how amyloid scans are read in research.
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Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a rare recessively inherited disease that is associated with early dementia and bone cysts with fractures.
Why it matters
This review describes how loss-of-function mutations in TYROBP or TREM2 cause Nasu-Hakola disease, a rare inherited condition with early dementia and bone cysts. It explains a genetic mechanism and does not report any treatment, cure, or prevention for Alzheimer's disease.
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39/100
Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) is conceived as a potential target for therapies against Alzheimer disease (AD) which is characterized by the accumulation of plaques formed of short β-amyloid (APPβ) peptides.
Why it matters
This study evaluated miR-29c and BACE1 expression in sporadic Alzheimer's disease brain tissues and examined miR-29c regulation of BACE1 in human neuroblastoma cells. It reports a correlation between downregulated miR-29c and increased BACE1 expression, but this is not a treatment trial and does not show that changing miR-29c helps patients.
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Impaired insulin signaling pathway in the brain in type 2 diabetes (T2D) is a risk factor for Alzheimer disease (AD).
Why it matters
In rats with type 2 diabetes, exendin-4 reduced Alzheimer disease-associated tau hyperphosphorylation in the hippocampus. This is animal research only and does not show any treatment, cure or prevention benefit in people.
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It was found that the acupuncture stimulation could modulate the DMN activity in AD.
Why it matters
In 14 people with Alzheimer disease and 14 normal controls, acupuncture at two acupoints was followed by changes in default mode network connectivity, including improved connectivity in some impaired regions. This is a small imaging study of acupuncture's effect on brain network activity, not evidence that acupuncture treats, cures or prevents Alzheimer's disease.
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We propose that amyotrophic lateral sclerosis (ALS), and frontotemporal dementia may be viewed as a failure of interlinked functional complexes having their origins in key evolutionary adaptations.
Why it matters
This paper proposes that amyotrophic lateral sclerosis and frontotemporal dementia can be viewed as a failure of interlinked functional complexes with origins in evolutionary adaptations related to hand-arm function, locomotion, brainstem function and cognition. It is a theoretical evolutionary perspective and reports no treatment, cure or prevention.
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Decline of cognition and increasing risk of neurodegenerative diseases are major problems associated with aging in humans.
Why it matters
In mice, the brain's clearance system for toxic proteins like amyloid-beta works much faster during sleep than when awake, and this clearance can also be boosted by anesthesia or by blocking certain signaling. The authors note that clinical studies suggest sleep quality and duration may predict Alzheimer's onset and that good sleep may reduce risk.
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Caspase cleaved amyloid precursor protein (APPcc) and SET are increased and mislocalized in the neuronal cytoplasm in Alzheimer Disease (AD) brains.
Why it matters
In brain tissue from a small number of Alzheimer and Down syndrome patients, and in mice, increased caspase cleaved amyloid precursor protein in one hippocampal region was linked to SET translocation and tau hyperphosphorylation. This suggests a possible early step in disease progression, but no treatment, cure or prevention is demonstrated.
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.
- Cerebral extracellular preamyloid deposits in Alzheimer's disease, Down syndrome and nondemented elderly individuals
- Cellular reservoirs of HIV-1 in the central nervous system of infected individuals: identification by the combination of in situ polymerase chain reaction and immunohistochemistry
- Chemokine receptors in the central nervous system: role in brain inflammation and neurodegenerative diseases
- Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in a tauopathy mouse model reduces C1q and normalizes clinical phenotype while increasing spread and state of phosphorylation of tau
- Cerebellar dysfunction in frontotemporal dementia: intra-cerebellar pathology and cerebellar network degeneration
- Exercise-induced irisin ameliorates cognitive impairment following chronic cerebral hypoperfusion by suppressing neuroinflammation and hippocampal neuronal apoptosis
- Cytoplasmic expression of trans-active response DNA-binding protein-43 in aged mice display hippocampal sclerosis-like degeneration and neuronal loss with reduced lifespan
- Membrane breakdown in acute and chronic neurodegeneration: focus on choline-containing phospholipids
- Association of BDNF Val66Met With Tau Hyperphosphorylation and Cognition in Dominantly Inherited Alzheimer Disease
- Bioenergetic mechanisms in astrocytes may contribute to amyloid plaque deposition and toxicity