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  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
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In a medical emergency, call 911. More numbers, and what each line does, on the help page.

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.

  1. Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2011-09-08 Inflammation and the immune system

    Alzheimer disease is characterized by neuronal loss and brain plaques of extracellular amyloid β (Aβ), but the means by which Aβ may induce neuronal loss is not entirely clear.

    Why it matters

    In rat cell cultures, low concentrations of amyloid beta caused neurons to be lost through a process in which microglia engulfed them, rather than through direct toxicity or classic cell death. This is laboratory work in cells, so it is early and does not establish a treatment or prevention approach for patients.

  2. Comprehension of insincere communication in neurodegenerative disease: lies, sarcasm, and theory of mind

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Cortex; a journal devoted to the study of the nervous system and behavior 2011-09-01 Digital health tools

    Comprehension of insincere communication is an important aspect of social cognition requiring visual perspective taking, emotion reading, and understanding others' thoughts, opinions, and intentions.

    Why it matters

    Among 102 patients with four neurodegenerative diseases and 77 healthy older adults, behavioral variant frontotemporal dementia patients showed impaired comprehension of lies and sarcasm compared with controls, while other groups' impairment tracked general cognitive impairment. This concerns social cognition testing, not treating, curing, or preventing Alzheimer's disease.

  3. Understanding the role of TDP-43 and FUS/TLS in ALS and beyond

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Current opinion in neurobiology 2011-08-02 Brain tissue and pathology

    Dominant mutations in two DNA/RNA binding proteins, TDP-43 and FUS/TLS, are causes of inherited Amyotrophic Lateral Sclerosis (ALS).

    Why it matters

    This review discusses how mutations in the RNA-binding proteins TDP-43 and FUS/TLS cause inherited ALS and how altered RNA processing may be central to the disease. It concerns ALS, not Alzheimer's disease, and does not report any treatment, cure, or prevention for Alzheimer's.

  4. CX3CR1 protein signaling modulates microglial activation and protects against plaque-independent cognitive deficits in a mouse model of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2011-07-19 Risk genes beyond APOE

    Aberrant microglial activation has been proposed to contribute to the cognitive decline in Alzheimer disease (AD), but the underlying molecular mechanisms remain enigmatic.

    Why it matters

    In a mouse model of Alzheimer's disease, CX3CR1 deficiency worsened neuronal and behavioral deficits, and these effects were associated with cytokine production but not with plaque deposition. This is animal research and does not yet show a treatment for people.

  5. Expansion of intronic GGCCTG hexanucleotide repeat in NOP56 causes SCA36, a type of spinocerebellar ataxia accompanied by motor neuron involvement

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. American journal of human genetics 2011-06-16 Genetics

    Autosomal-dominant spinocerebellar ataxias (SCAs) are a heterogeneous group of neurodegenerative disorders.

    Why it matters

    This genetic study linked an expanded repeat in the NOP56 gene to a spinocerebellar ataxia, and that expansion was not found in the Alzheimer disease cases tested. It concerns a different disease and provides no information about treating, curing or preventing Alzheimer's.

  6. APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The EMBO journal 2011-04-26 Risk genes beyond APOE

    Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and its proteolytic fragments are still poorly understood.

    Why it matters

    In mice, the secreted fragment APPsα was able to rescue most APP/APLP2 double knockout mice from death after birth, but surviving mice still had impaired nerve-to-muscle signaling and problems with learning and synaptic strengthening. These findings come from genetically modified animals and describe basic biology, not a treatment for people.

  7. Exercise-induced myokines and their role in chronic diseases

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain, behavior, and immunity 2011-02-25 Prevention and risk

    Physical inactivity has recently been identified as a major and independent risk factor for the development of dementia and cognitive decline.

    Why it matters

    This review proposes that physical inactivity is a risk factor for dementia and that muscles release myokines during exercise that may have anti-inflammatory effects. The evidence is still accumulating and no direct trial in humans showing that myokines prevent dementia is presented.

  8. Synaptic loss in the inferior temporal gyrus in mild cognitive impairment and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Journal of Alzheimer's disease : JAD 2011-01-01 Mild cognitive impairment

    Alzheimer's disease (AD) is a slowly progressing form of dementia characterized in its earliest stages as a loss of memory.

    Why it matters

    People with amnestic mild cognitive impairment had significantly fewer synapses in the inferior temporal gyrus compared to those with no cognitive impairment, similar to people with Alzheimer's disease. This shows synaptic loss occurs early, but the study does not test any treatment.

  9. Loss of white matter integrity is associated with gait disorders in cerebral small vessel disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain : a journal of neurology 2010-12-14 Vascular contributions

    Pathological studies have demonstrated abnormalities in white matter that may appear normal on brain imaging.

  10. Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1-42

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Annals of neurology 2010-12-01 Genetics

    Forty of 105 (38%) were classified as NC-low, and 65 (62%) as NC-high.

    Why it matters

    Among 105 cognitively normal older adults, 38% had low cerebrospinal fluid Aβ1-42 and this group had higher tau and p-tau and increased rates of brain atrophy, suggesting they may be in the earliest stages of neurodegeneration. This supports using brain atrophy as an outcome measure in prevention studies and does not test any treatment, cure, or prevention.

  11. Apolipoprotein E4 domain interaction mediates detrimental effects on mitochondria and is a potential therapeutic target for Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2010-11-30 Genetics

    Apolipoprotein (apo) E4 is the major genetic risk factor for late-onset Alzheimer disease (AD).

    Why it matters

    In mice and cells, the APOE4 protein's internal domain interaction was linked to lower levels of mitochondrial respiratory complexes and reduced mitochondrial function in neurons. This identifies a possible therapeutic target, but it is laboratory research and not yet a treatment for people.

  12. TDP-43 mediates degeneration in a novel Drosophila model of disease caused by mutations in VCP/p97

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2010-06-01 Brain tissue and pathology

    Inclusion body myopathy associated with Paget's disease of bone and frontotemporal dementia (IBMPFD) is a dominantly inherited degenerative disorder caused by mutations in the valosin-containing protein (VCP7) gene.

    Why it matters

    This study developed a fruit fly model of IBMPFD caused by VCP mutations and found that TDP-43 mediates degeneration in that model. It is animal research, so it does not establish a treatment or cure for people.

  13. Astrocytic expression of Parkinson's disease-related A53T alpha-synuclein causes neurodegeneration in mice

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular brain 2010-04-21 Inflammation and the immune system

    Parkinson's disease (PD) is the most common movement disorder.

    Why it matters

    Mice engineered to express mutant alpha-synuclein in astrocytes developed rapidly progressive paralysis. This is animal research on Parkinson's-related protein, not a treatment or prevention for Alzheimer's disease.

  14. LEAP: learning embeddings for atlas propagation

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. NeuroImage 2009-10-06 Long-term cohort studies

    We propose a novel framework for the automatic propagation of a set of manually labeled brain atlases to a diverse set of images of a population of subjects.

    Why it matters

    This paper proposes a method for automatically propagating labeled brain atlases to many different brain images. It is a technical imaging method, not a finding about treating, curing or preventing Alzheimer's disease.

  15. Differential placental gene expression in severe preeclampsia

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Placenta 2009-02-26 Brain tissue and pathology

    We investigated the global placental gene expression profile in severe preeclampsia.

    Why it matters

    This study compared placental gene expression between women with severe preeclampsia and uncomplicated pregnancies. It is about pregnancy complications and contains no information about treating, curing or preventing Alzheimer's disease.

  16. TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of Cell Biology 2009-01-26 TREM2 and immune genetics

    Phagocytosis, which is essential for the immune response to pathogens, is initiated by specific interactions between pathogens and cell surface receptors expressed by phagocytes.

    Why it matters

    Finds that TREM-2, together with its signaling partner DAP12, promotes the uptake (phagocytosis) of bacteria by cells. In these lab experiments, depleting TREM-2 reduced both binding and uptake of bacteria. It does not study Alzheimer's disease.

  17. Understanding white matter disease: imaging-pathological correlations in vascular cognitive impairment

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Stroke 2008-12-08 Biomarkers

    Most strokes are covert and observed incidentally on brain scans, but their presence increases risk of overt stroke and dementia.

    Why it matters

    This paper describes how small strokes and diffuse white matter disease, including amyloid angiopathy, can lower the threshold for dementia when they coexist with Alzheimer's disease. It calls for further research to understand and treat this chronic subcortical vascular disease and offers no proven treatment or prevention.

  18. Incidence and extent of Lewy body-related alpha-synucleinopathy in aging human olfactory bulb

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Journal of neuropathology and experimental neurology 2008-11-01 Disease mechanisms

    We investigated the incidence and extent of Lewy body (LB)-related alpha-synucleinopathy (LBAS) in the olfactory bulb (OB) in 320 consecutive autopsy patients from a general geriatric hospital (mean age, 81.5 +/- 8.5 years).

  19. Hydrogen peroxide promotes Abeta production through JNK-dependent activation of gamma-secretase

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of biological chemistry 2008-04-23 Risk genes beyond APOE

    Accumulation of senile plaques composed of amyloid beta-peptide (Abeta) is a pathological hallmark of Alzheimer disease (AD), and Abeta is generated through the sequential cleavage of amyloid precursor protein (APP) by beta- and gamma-secretase.

    Why it matters

    In human neuroblastoma cells, hydrogen peroxide increased amyloid beta production through JNK-dependent activation of gamma-secretase. This is cell-based laboratory work on a possible mechanism and does not show any treatment, cure or prevention for Alzheimer's disease.

  20. Cortical alpha-synuclein load is associated with amyloid-beta plaque burden in a subset of Parkinson's disease patients

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2008-01-08 Caregiving

    Amyloid-beta (Abeta) peptide pathology in Alzheimer's disease (AD) comprises extracellular plaques and cerebral amyloid angiopathy (CAA).

    Why it matters

    This study found a strong association between amyloid-beta plaque burden and cortical alpha-synuclein load in a subset of Parkinson's disease patients, with the APOE epsilon4 allele over-represented in that subgroup. It is a pathological association study in Parkinson's disease and does not test any treatment, cure, or prevention for Alzheimer's disease.

  21. Some phytochemical, pharmacological and toxicological properties of ginger (Zingiber officinale Roscoe): a review of recent research

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association 2007-09-18 Risk factors

    Ginger (Zingiber officinale Roscoe, Zingiberacae) is a medicinal plant that has been widely used in Chinese, Ayurvedic and Tibb-Unani herbal medicines all over the world, since antiquity, for a wide array of unrelated ailments that include arthritis, rheumatism, sprains, muscular aches, pains, sore throats, cramps, constipation, indigestion, vomiting, hypertension, dementia, fever, infectious diseases and helminthiasis.

    Why it matters

    This review of ginger notes it has been used traditionally for many ailments including dementia and describes its pharmacological actions such as anti-inflammatory and anti-oxidant effects. It states that more studies are required in animals and humans on the kinetics of ginger and its constituents and the effects of their consumption.

  22. ESCRT-III dysfunction causes autophagosome accumulation and neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Current biology : CB 2007-08-02 Lewy body dementia

    Defects in the endosomal-lysosomal pathway have been implicated in a number of neurodegenerative disorders.

    Why it matters

    In cortical neurons and flies, loss of the ESCRT-III component mSnf7-2 or expression of mutant CHMP2B caused dendrite retraction, neuron loss, and autophagosome accumulation. This suggests ESCRT-III dysfunction and autophagy may be involved in frontotemporal dementia, but it is laboratory research, not a therapy.

  23. Immunotherapy targeting pathological tau conformers in a tangle mouse model reduces brain pathology with associated functional improvements

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2007-08-01 Lewy body dementia

    Immunotherapies for various neurodegenerative diseases have recently emerged as a promising approach for clearing pathological protein conformers in these disorders.

    Why it matters

    In P301L tangle model mice, active immunization against a phosphorylated tau epitope reduced aggregated tau in the brain and slowed progression of the tangle-related behavioral phenotype. This is animal research and does not yet show that tau immunotherapy works in people with Alzheimer's disease or frontotemporal dementia.

  24. Nicotinic acetylcholine receptors and nicotinic cholinergic mechanisms of the central nervous system

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Annual review of pharmacology and toxicology 2007-01-01 Disparities

    Subtypes of neuronal nicotinic acetylcholine receptors (nAChRs) are constructed from numerous subunit combinations that compose channel-receptor complexes with varied functional and pharmacological characteristics.

    Why it matters

    This review describes how nicotinic acetylcholine receptors in the brain help regulate learning, memory and attention, and notes that changes in these mechanisms are seen in Alzheimer's disease and other conditions. It reports no trial or treatment, so it does not show that targeting these receptors would cure or prevent Alzheimer's.

  25. Oxidative stress and the pathogenesis of neurodegenerative disorders

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. International review of neurobiology 2007-01-01 How common it is

    Microglia-derived inflammatory neurotoxins play a principal role in the pathogenesis of neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and HIV-associated dementia; chief among these is reactive oxygen species.

    Why it matters

    This review describes how oxidative stress and inflammation from microglia are involved in the pathogenesis of neurodegenerative disorders including Alzheimer's disease. It discusses possible therapeutic directions but reports no tested treatment or cure.

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.

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