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Table 1 Summary of the pathophysiology, disease indicators, current treatment strategies and drugs used in neurodegenerative tauopathies

From: Chinese nutraceuticals and physical activity; their role in neurodegenerative tauopathies

Tauopathies

Patophysiology

Disease indicator

Current treatment strategies

Drugs

Alzehimer’s diseases

Characterized by a defined pattern of tangles from the trans-entorhinal cortex → entorhinal cortex → CA1 region of hippocampus and finally to the frontal, temporal, and parietal cortices, thus leading to neuronal loss and atrophy which induces inflammation and amyloid plaques deposition [125]

Formation of senile plaques (SP) [126]

Amyloid-β-peptide vaccination

Secretase inhibitors

Anti-inflammatory agents

Cholesterol reducing drugs [127]

Donepezil

Galantamine

Memantine

Rivastigmine [128]

Progressive supranuclear palsy

Characterized by development of NFT in astrocytes with the diffusion of plaques and lewy bodies in the brainstem cell nuclei & cerebral cortex. However, in long standing cases, the purkinje cells of the cerebellum are affected leading to the dilation of the third & fourth ventricles [129, 130]

Gait difficulty and falls

Dystonia and personality change

Non-specific dizziness

Palilalia

Compulsive spitting [131]

Drug therapy

Electroconvulsive therapy [PSP]

Levodopa

Dopamine agonists

Pergolide

Physostigmine

Zolpidem

Benztropine [PSP]

Corticobasal degenration

Characterized by asymmetric frontoparietal cortical atrophy and asymmetric hyperexcitability of the motor cortex, thus leads to the progression of astrocytic plaques

Ataxic gait

Myoclonus

Dystonia

Dysphagia

Dysarthria

Imaging techniques such as computerized tonography scanning (CTS) & Magnetic Resonance Imaging (MRI)

Clinical testing and work up (Electroencephalogram; EEG)

Baclofen

Botulinum toxin

Clonazepam

Benzodiazepines

Argyrophilic disease

At the anterior entorhinal cortex, there is mild involvement of the cortical and basolateral nuclei of the amygdala. There is also mild involvement of mammary bodies, nucleus accubens and rare grains in the mid brain, thus leading to impaired UPS function. [132]

Episodic memory loss

Cognitive decline and dementia

Behavioral abnormalities

Emotional imbalances [133, 134]

Anti-phosphorylation strategies

Anti-aggregation strategies

Rhodamines

Thiacarbocyanines

N-phenylalanimes

Anthraquinones

Levodopa