Primary age-related tauopathy (PART) is a neuropathological designation introduced in 2014 to describe the neurofibrillary tangles (NFT) that are commonly observed in the brains of normally aged and cognitively impaired individuals that can occur independently of the amyloid plaques of Alzheimer's disease (AD).
At autopsy, the hallmark of PART is the presence of Alzheimer-type neurofibrillary tangles (NFTs) composed of abnormal tau protein in neurons in the medial temporal lobe, but no amyloid-beta (Aβ42) peptide accumulation in plaques.
[2] Patients with PART display neurofibrillary tangles that are essentially identical to those occurring in mild to moderate-stage Alzheimer's disease and other tauopathies.
[9][7] Specifically, higher stages of tangle burden (i.e. Braak III or IV) in PART have been found to be associated with more rapid decline on tasks involving episodic and semantic memory along with tests of processing speed and attention.
[7][6] One current hypothesis suggests that PART related dementia could be infrequent in younger populations, but may show symptomatic onset within oldest old (people greater than 90 years old).
[11] Given that the elderly represent a fast growing segment of the population worldwide, further research is needed to understand how PART related pathological process can manifest in specific clinical symptoms.
[20] Tau protein stabilize the microtubules and are involved in fast dendrite growth, retrograde and antegrade transport intracellularly and neuron maintenance.
[21] These options listed below have not been yet linked or specified for PART treatment since the disease is yet to gain acceptance as a unique abnormality case by the medical community.
[18] Staurosporine, Methylene blue and other kinase inhibitors can pass the blood brain barrier and inhibit MARK which consequently down regulation tau protein hyper-phosphorylation and ultimately its detachment from microtubules.