Dr. James J Lah MD PHD
Neurologist | Neurology
1841 Clifton Rd Ne Atlanta GA, 30329About
Dr. James Lah is a distinguished Neurologist in Atlanta, GA. Dr. Lah specializes in diagnosing, treating, and managing disorders of the brain and nervous system. With expertise in handling complex conditions like epilepsy, multiple sclerosis, and migraines, Dr. Lah employs advanced techniques and personalized treatment plans to improve patient outcomes. As a neurologist, Dr. Lah is committed to staying abreast of the latest developments in neurological research and therapies.
Board Certification
Psychiatry and NeurologyAmerican Board of Psychiatry and NeurologyABPN
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Loss of apolipoprotein E receptor LR11 in Alzheimer disease.
- The lipoprotein receptor LR11 regulates amyloid beta production and amyloid precursor protein traffic in endosomal compartments.
- Sortilin, SorCS1b, and SorLA Vps10p sorting receptors, are novel gamma-secretase substrates.
- LR11/SorLA expression is reduced in sporadic Alzheimer disease but not in familial Alzheimer disease.
- Neuronal LR11/sorLA expression is reduced in mild cognitive impairment.
- Development of transgenic rats producing human beta-amyloid precursor protein as a model for Alzheimer's disease: transgene and endogenous APP genes are regulated tissue-specifically.
- Development of a rapid screening instrument for mild cognitive impairment and
- Loss of LR11/SORLA enhances early pathology in a mouse model of amyloidosis: evidence for a proximal role in Alzheimer's disease.
- Deficient high-affinity binding of Pittsburgh compound B in a case of Alzheimer's disease.
- DHA diet reduces AD pathology in young APPswe/PS1 Delta E9 transgenic mice: possible gender effects.
- Rho kinase II phosphorylation of the lipoprotein receptor LR11/SORLA alters amyloid-beta production.
- Exogenous seeding of cerebral beta-amyloid deposition in betaAPP-transgenic rats.
- Aberrant septin 11 is associated with sporadic frontotemporal lobar degeneration.
- GGA1-mediated endocytic traffic of LR11/SorLA alters APP intracellular distribution and amyloid-β production.
- Neuronal LR11 expression does not differentiate between clinically-defined Alzheimer's disease and control brains.
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