Thomas D. Bird

48.9k citations
263 papers · 38.5k · 16 hit papers · h-index 81

Impact in

  • Neurology top 0.02%
    • Amyotrophic Lateral Sclerosis Research
    • Parkinson's Disease Mechanisms and Treatments
    • Neuroinflammation and Neurodegeneration Mechanisms
    • Neurological diseases and metabolism
  • Physiology top 0.01%
    • Alzheimer's disease research and treatments

Papers in

    • Alzheimer's disease research and treatments 112
    • Parkinson's Disease Mechanisms and Treatments 25
    • Amyotrophic Lateral Sclerosis Research 20

Thomas D. Bird

258 papers receiving 37.0k citations

Thomas D. Bird's Hit Papers

New insights into the genetic etiology of Alzheimer’s disease and related dementias 2022 · 1.4k citations
1.4k0+11+22Years since publication2.0k4.0k6.0k

Peers

Thomas D. Bird
Comparison fields: 5 of 179
  • Neurology 7.4k
  • Physiology 17.8k
  • Neurology 10.2k
  • Biological Psychiatry 1.0k
  • Cellular and Molecular Neuroscience 6.1k
Replace Eileen H. Bigio with:
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Citations per field
00.5×1.5×
Eileen H. Bigio · 1×
Citations per year

Countries citing papers authored by Thomas D. Bird

Since Specialization
Citations

This map shows the geographic impact of Thomas D. Bird's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Thomas D. Bird with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Thomas D. Bird more than expected).

Fields of papers citing papers by Thomas D. Bird

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Thomas D. Bird. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Thomas D. Bird. The network helps show where Thomas D. Bird may publish in the future.

Co-authors

The 25 scholars most cited alongside Thomas D. Bird, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with Thomas D. Bird Line = papers co-authored together Thomas D. Bird links everyone, so they are left out of the graph.

All Works

20 of 20 papers shown

Showing the 20 most-cited of 263 papers — load more, or switch the sort, to bring in the rest.

#Work
1
Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis
Hit paper breakdown →
19936107
2
Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease
Hit paper breakdown →
19962231
3
Candidate Gene for the Chromosome 1 Familial Alzheimer's Disease Locus
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19952157
4
Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing
Hit paper breakdown →
20192087
5
Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease
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20111594
6
New insights into the genetic etiology of Alzheimer’s disease and related dementias
Hit paper breakdown →
20221436
7
Tau is a candidate gene for chromosome 17 frontotemporal dementia
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19981195
8
Genetic Linkage Evidence for a Familial Alzheimer's Disease Locus on Chromosome 14
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1992783
9
Review Article: Genetics of Alzheimer Disease
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2010781
10
Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease
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2017749
11
A Familial Alzheimer's Disease Locus on Chromosome 1
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1995657
12
TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy
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2016645
13
TARDBP mutations in amyotrophic lateral sclerosis with TDP-43 neuropathology: a genetic and histopathological analysis
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2008630
14 2002587
15
Upregulated function of mitochondria‐associated ER membranes in Alzheimer disease
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2012549
16 2010483
17 1998472
18 1999431
19 1998424
20 1998408

About Thomas D. Bird

Thomas D. Bird is a scholar working on Physiology, Neurology, Neurology, Cellular and Molecular Neuroscience and Psychiatry and Mental health, having authored 263 papers that have together received 38.5k indexed citations. Recurring topics across this work include Alzheimer's disease research and treatments (112 papers), Dementia and Cognitive Impairment Research (25 papers), Parkinson's Disease Mechanisms and Treatments (25 papers), Bioinformatics and Genomic Networks (25 papers), Prion Diseases and Protein Misfolding (23 papers), Amyotrophic Lateral Sclerosis Research (20 papers), Cholinesterase and Neurodegenerative Diseases (19 papers) and Nuclear Receptors and Signaling (18 papers). The work is most often cited by research in Neurology (7.4k citations), Physiology (17.8k citations), Neurology (10.2k citations), Biological Psychiatry (1.0k citations) and Cellular and Molecular Neuroscience (6.1k citations). Thomas D. Bird has collaborated with scholars based in United States, United Kingdom and Japan. Frequent co-authors include Gerard D. Schellenberg, Ellen M. Wijsman, Ellen J. Nemens, Parvoneh Poorkaj, David Nochlin, Debby W. Tsuang, Ephrat Levy‐Lahad, S. M. Sumi, Leojean Anderson and Murray A. Raskind. Their work appears in journals such as Annals of Neurology, Neurology, American Journal of Medical Genetics Part B Neuropsychiatric Genetics, Alzheimer s & Dementia and Human Molecular Genetics.

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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