Neuroimaging shows dramatic brain cell loss in Alzheimer'sBrain cells
disappear quickly and steadily in patients with Alzheimer's disease, an international
team of researchers reported on Thursday. Neuroimaging studies (MRI) indicated
a 5% annual loss of brain cells in Alzheimer's patients, and what more alarming,
up to 10% in the frotal lobe, the key memory areas. In contrast, healthy volunteers
monitored in the study lost less than 1% of their brain cells a year. Neurologists
at UCLA, in Britain and in Australia scanned the brains of 12 Alzheimer's patients
and 14 healthy volunteers very three months. Now the doctors could, for
the first time ever, see Alzheimer's disease progressing in living patients. MRI
gives a finer image of bodily structures than x-rays. The rearchers were stunned
to see a spreading wave of tissue loss. Initially confined to memory areas, this
loss moved across the brain like a lava flow, destroying more and more tissue
as the disease progressed, the investigators decribe writing in the Journal of
Neuroscience. Memory
systems go first and then the frontal areas involved in inhibition and self-control
and later areas involved in emotion. Another feature is that some parts of the
brain are completely spared. One example is the visual area. Why it is, is a mystery,
theu autors say.
The researchers said their findings would help doctors
check to see if treatments are helping, and perhaps help chart the course of the
disease. Alzheimer's is assessed using standard tests of a patient's behavior
and performance, rather than any physical evidence. This will probably continue
to be the case. "The diagnosis of Alzheimer's disease really depends
upon demonstration of cognitive dysfunction," Gilman said in an interview
with Reuters Health. Reference:
Thompson P, Hayashi K, de Zubicaray G, et al. Dynamics of gray matter loss in
Alzheimer´s. Journal of Neuroscience. 2003 February Carnosine Therapy
in Alzheimer's DiseaseThe main reason for brain cell destruction is probably
the inhibition of the proteasome, a protein which removes damaged and denaturated
proteins from the brain cells. The causes of proteasome inhibition are explained
in a separate
review. Carnosine protects the
proteasome and hence fights Alzheimer´s disease. Carnosine is a dipeptide,
also called a neuropeptide and neurotransmitter. Patients with Alzheimer´s
disease develop extracellular deposits of amyloid protein and microscopic tangles
of fibrils inside nerve cells. In experiments, treatment with carnosine was found
to reduce or completely prevent cell damage caused by ß-amyloid. Carnosine
blocks and inactivates ß-amyloid, so it protects neural tissues against
dementia. Moreover, carnosine protects the brain cells by fighting the
highly toxic alpha, beta-unsaturated aldehyde acrolein which is formed during
the peroxidation of polyunsaturated lipids, raising the possibility that it functions
as a 'toxicological second messenger' during oxidative cell injury. Recent
research also confirms that the toxic unsaturated aldehyde crotonaldehyde (CA)
contributes to carbonylation
resulting in protein damage during lipid peroxidation. As carnosine combats all
aldehydes, it offers another explanation for its benefits in prevention of Alzheimer´s
disease and other conditions with oxidative stress. Moreover, Carnosine protects
proteasomes,
protein molecules which detoxify the brain cells, and Carnosine removes toxic
heavy metals from the brain cells in a biochemical process called chelation.
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