If G protein-linked glutamate receptors are an important component through neural cell excitation, and transpositioning of said receptors is an important finding (such as in cerebellar ataxia), then a cognitive behavioral approach in conjunction with appropriate drug treatment would offer some neural protection. Keep in mind that synapse-associated polyribosome complexes (SPRCs) discovered by Oswald Steward are also important variables here.

Without proper dendritic spine synthesis, cognitive decline is guaranteed. We witness this severe deficiency in reasoning ability in persons with Down syndrome. It is now well known that stimulating thought and problem-solving over the long term greatly enhances long-term potentiation. It is also known that SPRCs are enhanced to facilitate this increase in neuronal communication through greater protein synthesis at the base of synapses in dendrites at both ionotropic signal-gated neurons and the metabotropic receptors mentioned in the previous paper.

We see much similarity between Alzheimer disease risk and Down syndrome: Presenilin...  Read more

If G protein-linked glutamate receptors are an important component through neural cell excitation, and transpositioning of said receptors is an important finding (such as in cerebellar ataxia), then a cognitive behavioral approach in conjunction with appropriate drug treatment would offer some neural protection. Keep in mind that synapse-associated polyribosome complexes (SPRCs) discovered by Oswald Steward are also important variables here.

Without proper dendritic spine synthesis, cognitive decline is guaranteed. We witness this severe deficiency in reasoning ability in persons with Down syndrome. It is now well known that stimulating thought and problem-solving over the long term greatly enhances long-term potentiation. It is also known that SPRCs are enhanced to facilitate this increase in neuronal communication through greater protein synthesis at the base of synapses in dendrites at both ionotropic signal-gated neurons and the metabotropic receptors mentioned in the previous paper.

We see much similarity between Alzheimer disease risk and Down syndrome: Presenilin genes 1 and 2 handle important enzyme manufacture and still-unknown protein modification processes. What we do know is that problems in these genes can and do increase amyloid-β 42 and cause conformational changes at both synapses (dendritic spines, varicose axons). A host of intracellular cascade modifications occur at G protein-linked receptors. Glutamate overexcitation is seen, as well as damaged transport mediums, which do not permit enough glutamate transport to critical areas of cognition and motor movement such as cerebellum, frontal lobe, Broca's, etc.)

References:
Neuroscience Exploring the Brain, second edition. Mark F. Bear, Barry W, Connors, Michael A. Paradiso, 2001 Lippincott Williams & Wilkins. pp.42-43; 44-45;154-158.

(see )Ataxia—Rare Spectrin Mutations and a Rarer Pedigree

View all comments by Jacob Mack

Sampling and expression of amyloid-β (Aβ) peptides in vascular dementia (VD) brains and Alzheimer disease (AD) brains may explain the difference in learning and memory and not genetic differences, entirely. Since the effects of VD and AD on learning and memory are similar, but Aβ extractions differ between VD and AD, the so called IMAG scores will differ accordingly. However, this difference may be related to extraction variation as a function of VD.

References:
Lewis H, Beher D, Cookson N, Oakley A, Piggott M, Morris CM, Jaros E, Perry R, Ince P, Kenny RA, Ballard CG, Shearman MS, Kalaria RN. Quantification of Alzheimer pathology in ageing and dementia: age-related accumulation of amyloid-beta(42) peptide in vascular dementia. Neuropathology & Applied Neurobiology. 2006;32(2):103-118.

View all comments by Kiumars Lalezarzadeh