Research Models Database



Back to the Top

There are many rodent models of Alzheimer’s disease, Parkinson's disease, Amyotrophic Lateral Sclerosis, and related neurodegenerative diseases. This database currently contains just a subset of the many that have been developed, with more added on a regular basis. Models were included based on a variety of factors, including prominence in the literature, availability, frequency of use, and extent of characterization. The Parkinson's disease models were selected by experts at The Michael J. Fox Foundation (MJFF).

Inclusion criteria:

  • Rodent model of AD, ALS, PD or related neurodegenerative disease
  • Availability of characterization data describing disease-related phenotypes
  • Genetic models (i.e., not pharmacological, e.g., Aβ infusion, 6-OHDA)

The majority of the models currently in the database have modifications to disease-related genes, including genes known to harbor autosomal dominant mutations (such as APP, MAPT, PSEN1, PSEN2) as well as genes associated with disease risk (e.g., APOE, TREM2). The database includes transgenic models, knock-ins, knock-outs, and animals expressing multiple transgenes, and any combination of the above.

Data sources:

Descriptions are based on several sources, including:

  • Published literature, including primary papers, reviews, and book chapters
  • Alzforum news articles
  • The Jackson Laboratory
  • The Mouse Genome Informatics (MGI) database
  • Company websites (e.g Taconic, Horizon, etc.)
  • Researchers who developed or chracterized the models

Curation strategy:

Entries focus on model characterization rather than on research findings generated from the model. Data related to preclinical studies are generally not included. In general, the initial characterization of the model serves as the foundation of each entry and is supplemented with data from follow-up papers when available.

In an effort to provide the most relevant information, we have targetted our curation effort to address specific core disease-related phenotypes, which are frequently characterized, such as motor impairment and gliosis. Summarized information about each phenotype is presented alongside the "earliest reported occurrence", which is plotted on a line representing the rodent lifespan. It is worth noting that the age of “earliest reported occurrence” may not correspond with the true onset of the phenotype. Furthermore, the development and progression of a phenotype may vary considerably from animal to animal and from lab to lab. Often there are differences depending on the sex of the animal or environmental factors, such as diet.

Within this database, a phenotype may be categorized as “Absent.” This means that the phenotype was investigated in at least one study and not observed. However, “Absent” should be taken with a grain of salt: It does not mean that this phenotype will not, or cannot, be observed under other circumstances, such as at a more advanced age, under different environmental conditions, or with more sensitive assays. Within this database, a phenotype may also be categorized as having “No Data.” This means that to the best of our knowledge the phenotype has not yet been described in the literature.

AD-related phenotypes:

Plaques - Amyloid plaques of any shape or stage, in any brain region
Tangles - Neurofibrillary tangles composed of abnormally phosphorylated tau
Neuronal Loss - Neuronal loss in any brain region
Gliosis - Astrogliosis or microgliosis, usually measured by immunohistochemistry
Changes in LTP/LTD - Altered electrophysiological properties indicative of impaired or elevated LTP or LTD
Cognitive Impairment - Reduced learning and memory based on any number of behavioral tests

ALS-related phenotypes:

Cortical Neuron Loss - Neuronal loss in the brain, usually in the motor cortex
Lower Motor Neuron Loss - Neuronal loss in the spinal cord, usually in the ventral horn
Cytoplasmic Inclusions - Inclusions or aggregates in the cytoplasm (includes proteinaceous entities such as TDP-43, SOD-1, ubiquitin, and dipeptide repeats) and entities like eosinophilic aggregates
Gliosis - Astrogliosis or microgliosis
NMJ Abnormalities - Abnormalities at the neuromuscular junction, e.g. morphological changes associated with denervation
Muscle Atrophy - Reduced muscle mass, usually accompanied by changes in muscle architecture
Motor Impairment - Tremors, changes in gait, strength, or coordination indicative of motor impairment; includes paralysis
Body Weight - Reduced body weight, usually reflecting weight loss compared with controls, but may also refer to reduced weight gain compared with controls
Premature Death - Reduced average lifespan compared with controls, includes spontaneous death and euthanasia at end stage

PD-related phenotypes:

Neuronal Loss - Neuronal loss in any brain region
Dopamine Deficiency - Low levels of dopamine and/or its primary metabolites in the brain
α-synuclein inclusions - Inclusions or aggregations in brain cells, nuclear or cytoplasmic
Neuroinflammation - Greater numbers of reactive astrocytes and/or microglia in the brain and/or elevated levels of proinflammatory cytokines
Motor Impairment - Any motor abnormality, including differences in spontaneous activity, changes in coordination, strength, tremor, etc.
Mitochondrial Abnormalities - Abnormalities in mitochondrial structure or function, including ultrastructure, ATP levels, fission/fusion deficits, membrane potential, etc.
Cognitive Dysfunction - Memory or learning difficulties as assessed by a variety of behavioral tests, as well as changes in attention, anxiety, and social behavior

To confirm the accuracy of curated data and obtain current availability information, we attempted to contact the lead scientist(s) involved in generating the models. However, this was not possible in all cases.