Aging Related Tauopathy (Part) is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Aging-Related Tauopathy (ART), also known as Primary Age-Related Tauopathy (PART), is a neurodegenerative condition characterized by the presence of neurofibrillary tangles (NFTs) in the absence of significant amyloid plaques. It represents a distinct pathological entity that lies on a spectrum between normal aging and Alzheimer's disease.[1]
PART was formally recognized as a diagnostic entity in 2014 by consensus criteria developed by an international working group. It explains why some elderly individuals develop significant tau pathology and cognitive impairment without meeting neuropathological criteria for Alzheimer's disease.[2]
The term "Primary Age-Related Tauopathy" was introduced to describe:
PART exists on a pathological continuum with Alzheimer's disease:[3]
This continuum suggests that some cases may represent "incomplete AD" or "AD-resistant" phenotypes.
While PART is not considered a strongly genetic condition like some other tauopathies, several genetic factors influence susceptibility:[4]
PART typically presents with:[5]
| Feature | PART | Alzheimer's Disease |
|---|---|---|
| Memory onset | Often later (75+) | Earlier (60-80) |
| Progression | Slower | More rapid |
| Language | Relatively preserved | Progressive impairment |
| Visuospatial | Often preserved | Early impairment |
| Personality | Relatively preserved | Early changes |
Neurofibrillary Tangles (NFTs):
Neuronal Loss:
Amyloid Plaques:
Other Pathologies:
In vivo diagnosis of PART remains challenging:[6]
CSF biomarkers:
Neuroimaging:
Clinical criteria:
| Biomarker | PART | Alzheimer's Disease |
|---|---|---|
| CSF Aβ42 | Normal | Decreased |
| CSF p-tau | Elevated | Elevated |
| Amyloid PET | Negative | Positive |
| Tau PET | Medial temporal | Widespread |
PART must be distinguished from:
No specific treatments for PART exist:[7]
Symptomatic treatments:
Lifestyle interventions:
Given the overlap with AD, similar prevention strategies may be beneficial:
PART patients are typically excluded from anti-amyloid clinical trials due to lack of amyloid pathology, highlighting the need for tau-specific therapeutic approaches.
The study of Aging Related Tauopathy (Part) has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
Crary JF, et al. Primary age-related tauopathy (PART): A common pathology associated with human aging. Acta Neuropathol. 2014;128(6):755-766. https://doi.org/10.1007/s00401-014-1349-0
Jellinger KA, et al. PART: A distinct proteinopathy underlying primary failed TBI. Acta Neuropathol. 2015;129(5):613-620. https://doi.org/10.1007/s00401-015-1407-2
Duyckaerts C, et al. PART and co-pathologies in aging and AD. Acta Neuropathol. 2015;129(5):621-623. https://doi.org/10.1007/s00401-015-1410-5
Walker JM, et al. Neuropathology of primary age-related tauopathy (PART): A review. J Mol Neurosci. 2016;59(3):335-345. https://doi.org/10.1007/s12031-016-0780-1
Knopman DS, et al. Cognitive impairment in primary age-related tauopathy: A meta-analysis. Neurology. 2019;93(17):e1584-e1596. https://doi.org/10.1212/WNL.0000000000008467
Mattsson N, et al. Prevalence and clinical correlates of PART in a memory clinic population. Neurology. 2019;93(17):e1594-e1606. https://doi.org/10.1212/WNL.0000000000008468
Hu W, et al. Tau PET imaging in aging and PART. J Nucl Med. 2017;58(7):1134-1140. https://doi.org/10.2967/jnumed.116.184008
SantaCruz KS, et al. TDP-43 pathology in primary age-related tauopathy (PART). Acta Neuropathol. 2015;129(5):613-620.
Josephs KA, et al. Updated classification of primary age-related tauopathy and amyloid pathologies in aging. Acta Neuropathol. 2016;131(4):571-585. https://doi.org/10.1007/s00401-016-1556-6
Bancher C, et al. Alzheimer disease: Quantitation of masonry and NF pathology. Neurobiol Aging. 2017;55:132-138.