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You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • 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.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

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. Molecular landscapes of human hippocampal immature neurons across lifespan

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2022-07-06 Genetics

    Immature dentate granule cells (imGCs) arising from adult hippocampal neurogenesis contribute to plasticity and unique brain functions in rodents 1,2 and are dysregulated in multiple human neurological disorders 3-5 .

  2. Genome-wide association studies for Alzheimer's disease: bigger is not always better

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain communications 2022-05-17 Genetics

    As the size of genome-wide association studies increase, the number of associated trait loci identified inevitably increase.

  3. Somatic genomic changes in single Alzheimer's disease neurons

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2022-04-20 Genetics

    Dementia in Alzheimer's disease progresses alongside neurodegeneration 1-4 , but the specific events that cause neuronal dysfunction and death remain poorly understood.

  4. Brain integrity is altered by hepatic APOE ε4 in humanized-liver mice

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2022-04-13 Genetics

    Liver-generated plasma apolipoprotein E (apoE) does not enter the brain but nonetheless correlates with Alzheimer's disease (AD) risk and AD biomarker levels.

  5. A human brain vascular atlas reveals diverse mediators of Alzheimer's risk

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2022-02-14 Genetics

    The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 .

  6. A human-based multi-gene signature enables quantitative drug repurposing for metabolic disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. eLife 2022-01-17 Drug development

    Insulin resistance (IR) contributes to the pathophysiology of diabetes, dementia, viral infection, and cardiovascular disease.

  7. Causal association of cognitive reserve on Alzheimer's disease with putative sex difference

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2021-12-31 Genetics

    AD was associated with lower PRS for premorbid cognitive performance, intelligence, and educational attainment.

  8. Apolipoprotein E regulates lipid metabolism and α-synuclein pathology in human iPSC-derived cerebral organoids

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Acta neuropathologica 2021-08-28 Genetics

    APOE4 is a strong genetic risk factor for Alzheimer's disease and Dementia with Lewy bodies; however, how its expression impacts pathogenic pathways in a human-relevant system is not clear.

  9. Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2021-07-28 Risk genes beyond APOE

    Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD.

  10. APP, PSEN1, and PSEN2 Variants in Alzheimer's Disease: Systematic Re-evaluation According to ACMG Guidelines

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Frontiers in aging neuroscience 2021-06-18 Risk genes beyond APOE

    The strategies of classifying APP, PSEN1, and PSEN2 variants varied substantially in the previous studies.

  11. TMEM106B and CPOX are genetic determinants of cerebrospinal fluid Alzheimer's disease biomarker levels

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-05-14 Genetics

    We identify novel genome-wide significant associations between DNA variants in TMEM106B and CSF levels of NfL, and between CPOX and YKL-40.

  12. Retinal imaging demonstrates reduced capillary density in clinically unimpaired APOE ε4 gene carriers

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Alzheimer's & dementia (Amsterdam, Netherlands) 2021-05-11 Brain scans and imaging

    Our analyses demonstrate lower retinal capillary densities in early disease, in cognitively normal APOE ε4 gene carriers.

  13. An integrated multi-omics approach identifies epigenetic alterations associated with Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature genetics 2020-09-28 Genetics

    Protein aggregation is the hallmark of neurodegeneration, but the molecular mechanisms underlying late-onset Alzheimer's disease (AD) are unclear.

  14. Risk prediction of late-onset Alzheimer's disease implies an oligogenic architecture

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature communications 2020-09-23 Genetics

    Genetic association studies have identified 44 common genome-wide significant risk loci for late-onset Alzheimer's disease (LOAD).

  15. A single-cell atlas of the human substantia nigra reveals cell-specific pathways associated with neurological disorders

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature communications 2020-08-21 Genetics

    We describe a human single-nuclei transcriptomic atlas for the substantia nigra (SN), generated by sequencing approximately 17,000 nuclei from matched cortical and SN samples.

  16. Integrated analysis of ultra-deep proteomes in cortex, cerebrospinal fluid and serum reveals a mitochondrial signature in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular neurodegeneration 2020-07-25 Biomarkers

    Our results demonstrate that novel AD biomarker candidates are identified and confirmed by proteomic studies of brain tissue and biofluids, providing a rich resource for large-scale biomarker validation for the AD community.

  17. Older molecular brain age in severe mental illness

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2020-07-06 Genetics

    Psychiatric disorders are associated with accelerated aging and enhanced risk for neurodegenerative disorders.

  18. Disease-associated astrocytes in Alzheimer's disease and aging

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature neuroscience 2020-04-27 Genetics

    The role of non-neuronal cells in Alzheimer's disease progression has not been fully elucidated.

  19. Incomplete penetrance in familial Alzheimer's disease with PSEN1 Ala260Gly mutation

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 2020-04-23 Risk genes beyond APOE

    Presenilin1 (PSEN1) gene is the most common known genetic cause of early-onset familial Alzheimer's disease.

  20. A pathogenic PSEN1 Trp165Cys mutation associated with early-onset Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. BMC neurology 2019-08-07 Risk genes beyond APOE

    We report a case of EOAD having a pathogenic PSEN1 (Trp165Cys) confirmed with in silico and in vitro predictions.

  21. Handedness, language areas and neuropsychiatric diseases: insights from brain imaging and genetics

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain 2019-08-07 Genetics

    Ninety per cent of the human population has been right-handed since the Paleolithic, yet the brain signature and genetic basis of handedness remain poorly characterized.

  22. Long Non-coding RNA BACE1-AS May Serve as an Alzheimer's Disease Blood-Based Biomarker

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of molecular neuroscience : MN 2019-07-01 Biomarkers

    Circulating long noncoding RNAs (lncRNAs) might serve as biomarkers for different pathological conditions.

  23. The role of ABCA7 in Alzheimer's disease: evidence from genomics, transcriptomics and methylomics

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Acta neuropathologica 2019-03-22 Genetics

    Genome-wide association studies (GWAS) originally identified ATP-binding cassette, sub-family A, member 7 (ABCA7), as a novel risk gene of Alzheimer's disease (AD).

  24. Genomics of 1 million parent lifespans implicates novel pathways and common diseases and distinguishes survival chances

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. eLife 2019-01-15 Genetics

    We use a genome-wide association of 1 million parental lifespans of genotyped subjects and data on mortality risk factors to validate previously unreplicated findings near CDKN2B-AS1 , ATXN2/BRAP , FURIN/FES , ZW10 , PSORS1C3 , and 13q21.31, and identify and replicate novel findings near ABO , ZC3HC1 , and IGF2R .

  25. Leukocyte Telomere Length Shortening and Alzheimer's Disease Etiology

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Journal of Alzheimer's disease : JAD 2019 Genetics

    The genetic risk score for TL was associated with higher risk of AD [log-odds ratio (OR) = 0.003 for per TL-decreasing allele; 95% confidence interval (CI): 0.001, 0.005, p = 0.005].

From across this topic

9 of the 933 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.

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