Stroke/Alzheimer’s Disease and Related

FIGURE 32-2. Treatment algorithm for Alzheimer s disease. A. Cognitive treatment. B. Treatment of psychiatric or behavioral symptoms. AD, Alzheimer s disease MMSE, Mini Mental Status Examination NINCDS-ADRDA National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer s Disease and Related Disorders Association. (From Faulkner JD, Bartlett J, Hicks P. Alzheimer s disease. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 1164, with permission.)... 

Female or male 50-85 years old with a caregiver Mini Mental Status (MMS) test between 16 and 26 inclusive Clinical Dementia Rating (CDR) test inferior or equal to 1 National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer s Disease and Related Disorders Association (NINCDS/ADRDA) test positive for Alzheimer s disease Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV) test positive for dementia Exclusion Criteria ... 

Careful sample selection and preparation are the prerequisites for a successful analysis (Boguski and McIntosh, 2003). Postmortem brain samples for our studies were obtained from the M RC London Brain Bank for Neruodegenerative Diseases, Institute of Psychiatry. The AD patients fulfilled the National Institute of Neurological and Communicative Disorders and Stroke and Alzheimer s Disease and Related Disorders Association (NINCDS/ADRDA) criteria for probable AD (Mirra et al., 1991). A definite diagnosis of AD was performed by historical analysis of the brain samples, which was consistent with the CERAD criteria (Tierney et al., 1988). The brain regions temporal, frontal, occipital, parietal cortex, and cerebellum of patients with AD (72.3 7.6 years old) and controls (72.6 9.6 years old) (Seidl et al., 1997) were used for the studies at the protein level. The... 

The ability of conotoxins to selectively block ion channels and neuronal receptors has led to their development into therapeutic agents. So far, most conotoxin applications as therapeutics have been concentrated on the treatment of different forms of pain. The first drug of marine origin is based on the w-conotoxin MVIIA for the treatment of chronic pain (see helow). Other therapeutic applications of conotoxins include treatment of schizophrenia, epilepsy, neuromuscular disorders, certain types of cancer, urinary dysfunction, Parkinson s disease, Alzheimer s disease, stroke, and related hrain injuries. Other uses include muscle relaxants, anesthetics, and antiseizure compounds. As the demand for new painkillers and other neuropharmacological agents is expected to increase, the value of the discovery and testing of new conotoxins is expected to continue to expand. 

At this time, however, we are not aware of any compounds selected primarily by their neuroprotection activity on rodent models that have established clinical efficacy for dementias or related neurodegenerative diseases. This may be partially explained by their priority development for stroke, and clinicians have found it is difficult or unlikely to slow the ischemia in patients if they are not treated aggressively within 3 h of the initial ischemic event. The speed of neurodegeneration in stroke (cerebral ischemia) makes it a much more difficult target for drug intervention than neurodegeneration from slower pathologies such as Alzheimer s, Parkinson s, and malfunctions in neurotransmitters. 

Since the late 1990s, the publication rate of the supercritical phase related work is increasing significantly. The extraction of bioactive compounds from plants is still the subject with major production. And fortunately, some of the works are dedicated to evaluating the extraets as potential elements of therapies for various diseases like stroke, eaneer, Alzheimer s, infections, depression, inflammatory processes, acute and ehronic pain, among others. 

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